--- _id: '163' abstract: - lang: eng text: For ultrafast fixation of biological samples to avoid artifacts, high-pressure freezing (HPF) followed by freeze substitution (FS) is preferred over chemical fixation at room temperature. After HPF, samples are maintained at low temperature during dehydration and fixation, while avoiding damaging recrystallization. This is a notoriously slow process. McDonald and Webb demonstrated, in 2011, that sample agitation during FS dramatically reduces the necessary time. Then, in 2015, we (H.G. and S.R.) introduced an agitation module into the cryochamber of an automated FS unit and demonstrated that the preparation of algae could be shortened from days to a couple of hours. We argued that variability in the processing, reproducibility, and safety issues are better addressed using automated FS units. For dissemination, we started low-cost manufacturing of agitation modules for two of the most widely used FS units, the Automatic Freeze Substitution Systems, AFS(1) and AFS2, from Leica Microsystems, using three dimensional (3D)-printing of the major components. To test them, several labs independently used the modules on a wide variety of specimens that had previously been processed by manual agitation, or without agitation. We demonstrate that automated processing with sample agitation saves time, increases flexibility with respect to sample requirements and protocols, and produces data of at least as good quality as other approaches. article_processing_charge: No article_type: original author: - first_name: Siegfried full_name: Reipert, Siegfried last_name: Reipert - first_name: Helmuth full_name: Goldammer, Helmuth last_name: Goldammer - first_name: Christine full_name: Richardson, Christine last_name: Richardson - first_name: Martin full_name: Goldberg, Martin last_name: Goldberg - first_name: Timothy full_name: Hawkins, Timothy last_name: Hawkins - first_name: Elena full_name: Hollergschwandtner, Elena id: 3C054040-F248-11E8-B48F-1D18A9856A87 last_name: Hollergschwandtner - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Sebastian full_name: Antreich, Sebastian last_name: Antreich - first_name: York full_name: Stierhof, York last_name: Stierhof citation: ama: 'Reipert S, Goldammer H, Richardson C, et al. Agitation modules: Flexible means to accelerate automated freeze substitution. Journal of Histochemistry and Cytochemistry. 2018;66(12):903-921. doi:10.1369/0022155418786698' apa: 'Reipert, S., Goldammer, H., Richardson, C., Goldberg, M., Hawkins, T., Saeckl, E., … Stierhof, Y. (2018). Agitation modules: Flexible means to accelerate automated freeze substitution. Journal of Histochemistry and Cytochemistry. SAGE Publications. https://doi.org/10.1369/0022155418786698' chicago: 'Reipert, Siegfried, Helmuth Goldammer, Christine Richardson, Martin Goldberg, Timothy Hawkins, Elena Saeckl, Walter Kaufmann, Sebastian Antreich, and York Stierhof. “Agitation Modules: Flexible Means to Accelerate Automated Freeze Substitution.” Journal of Histochemistry and Cytochemistry. SAGE Publications, 2018. https://doi.org/10.1369/0022155418786698.' ieee: 'S. Reipert et al., “Agitation modules: Flexible means to accelerate automated freeze substitution,” Journal of Histochemistry and Cytochemistry, vol. 66, no. 12. SAGE Publications, pp. 903–921, 2018.' ista: 'Reipert S, Goldammer H, Richardson C, Goldberg M, Hawkins T, Saeckl E, Kaufmann W, Antreich S, Stierhof Y. 2018. Agitation modules: Flexible means to accelerate automated freeze substitution. Journal of Histochemistry and Cytochemistry. 66(12), 903–921.' mla: 'Reipert, Siegfried, et al. “Agitation Modules: Flexible Means to Accelerate Automated Freeze Substitution.” Journal of Histochemistry and Cytochemistry, vol. 66, no. 12, SAGE Publications, 2018, pp. 903–21, doi:10.1369/0022155418786698.' short: S. Reipert, H. Goldammer, C. Richardson, M. Goldberg, T. Hawkins, E. Saeckl, W. Kaufmann, S. Antreich, Y. Stierhof, Journal of Histochemistry and Cytochemistry 66 (2018) 903–921. date_created: 2018-12-11T11:44:57Z date_published: 2018-12-01T00:00:00Z date_updated: 2023-10-17T08:42:24Z day: '01' department: - _id: RySh - _id: EM-Fac doi: 10.1369/0022155418786698 external_id: isi: - '000452277700005' pmid: - '29969056' intvolume: ' 66' isi: 1 issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1369/0022155418786698 month: '12' oa: 1 oa_version: Published Version page: 903-921 pmid: 1 publication: Journal of Histochemistry and Cytochemistry publication_identifier: issn: - 0022-1554 publication_status: published publisher: SAGE Publications quality_controlled: '1' scopus_import: '1' status: public title: 'Agitation modules: Flexible means to accelerate automated freeze substitution' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 66 year: '2018' ... --- _id: '51' abstract: - lang: eng text: Asymmetries have long been known about in the central nervous system. From gross anatomical differences, such as the presence of the parapineal organ in only one hemisphere of the developing zebrafish, to more subtle differences in activity between both hemispheres, as seen in freely roaming animals or human participants under PET and fMRI imaging analysis. The presence of asymmetries has been demonstrated to have huge behavioural implications, with their disruption often leading to the generation of neurological disorders, memory problems, changes in personality, and in an organism's health and well-being. For my Ph.D. work I aimed to tackle two important avenues of research. The first being the process of input-side dependency in the hippocampus, with the goal of finding a key gene responsible for its development (Gene X). The second project was to do with experience-induced laterality formation in the hippocampus. Specifically, how laterality in the synapse density of the CA1 stratum radiatum (s.r.) could be induced purely through environmental enrichment. Through unilateral tracer injections into the CA3, I was able to selectively measure the properties of synapses within the CA1 and investigate how they differed based upon which hemisphere the presynaptic neurone originated. Having found the existence of a previously unreported reversed (left-isomerism) i.v. mutant, through morpholocal examination of labelled terminals in the CA1 s.r., I aimed to elucidate a key gene responsible for the process of left or right determination of inputs to the CA1 s.r.. This work relates to the previous finding of input-side dependent asymmetry in the wild-type rodent, where the origin of the projecting neurone to the CA1 will determine the morphology of a synapse, to a greater degree than the hemisphere in which the projection terminates. Using left- and right-isomerism i.v. mice, in combination with whole genome sequence analysis, I highlight Ena/VASP-like (Evl) as a potential target for Gene X. In relation to this topic, I also highlight my work in the recently published paper of how knockout of PirB can lead to a lack of input-side dependency in the murine hippocampus. For the second question, I show that the environmental enrichment paradigm will lead to an asymmetry in the synapse densities in the hippocampus of mice. I also highlight that the nature of the enrichment is of less consequence than the process of enrichment itself. I demonstrate that the CA3 region will dramatically alter its projection targets, in relation to environmental stimulation, with the asymmetry in synaptic density, caused by enrichment, relying heavily on commissural fibres. I also highlight the vital importance of input-side dependent asymmetry, as a necessary component of experience-dependent laterality formation in the CA1 s.r.. However, my results suggest that it isn't the only cause, as there appears to be a CA1 dependent mechanism also at play. Upon further investigation, I highlight the significant, and highly important, finding that the changes seen in the CA1 s.r. were predominantly caused through projections from the left-CA3, with the right-CA3 having less involvement in this mechanism. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Matthew J full_name: Case, Matthew J id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87 last_name: Case citation: ama: 'Case MJ. From the left to the right: A tale of asymmetries, environments, and hippocampal development. 2018. doi:10.15479/AT:ISTA:th_1032' apa: 'Case, M. J. (2018). From the left to the right: A tale of asymmetries, environments, and hippocampal development. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th_1032' chicago: 'Case, Matthew J. “From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development.” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th_1032.' ieee: 'M. J. Case, “From the left to the right: A tale of asymmetries, environments, and hippocampal development,” Institute of Science and Technology Austria, 2018.' ista: 'Case MJ. 2018. From the left to the right: A tale of asymmetries, environments, and hippocampal development. Institute of Science and Technology Austria.' mla: 'Case, Matthew J. From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development. Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th_1032.' short: 'M.J. Case, From the Left to the Right: A Tale of Asymmetries, Environments, and Hippocampal Development, Institute of Science and Technology Austria, 2018.' date_created: 2018-12-11T11:44:22Z date_published: 2018-06-27T00:00:00Z date_updated: 2023-09-07T12:39:22Z day: '27' ddc: - '571' - '576' degree_awarded: PhD department: - _id: RySh doi: 10.15479/AT:ISTA:th_1032 file: - access_level: closed checksum: dcc7b55619d8509dd62b8e99d6cdee44 content_type: application/msword creator: dernst date_created: 2019-04-09T07:16:26Z date_updated: 2021-02-11T23:30:13Z embargo_to: open_access file_id: '6251' file_name: 2018_Thesis_Case_Source.doc file_size: 141270528 relation: source_file - access_level: open_access checksum: f69fdd5c8709c4e618aa8c1a1221153d content_type: application/pdf creator: dernst date_created: 2019-04-09T07:16:23Z date_updated: 2021-02-11T11:17:14Z embargo: 2019-07-05 file_id: '6252' file_name: 2018_Thesis_Case.pdf file_size: 15193621 relation: main_file file_date_updated: 2021-02-11T23:30:13Z has_accepted_license: '1' language: - iso: eng month: '06' oa: 1 oa_version: Published Version page: '186' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '8003' pubrep_id: '1032' related_material: record: - id: '682' relation: part_of_dissertation status: public status: public supervisor: - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 title: 'From the left to the right: A tale of asymmetries, environments, and hippocampal development' type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2018' ... --- _id: '612' abstract: - lang: eng text: Metabotropic GABAB receptors mediate slow inhibitory effects presynaptically and postsynaptically through the modulation of different effector signalling pathways. Here, we analysed the distribution of GABAB receptors using highly sensitive SDS-digested freeze-fracture replica labelling in mouse cerebellar Purkinje cells. Immunoreactivity for GABAB1 was observed on presynaptic and, more abundantly, on postsynaptic compartments, showing both scattered and clustered distribution patterns. Quantitative analysis of immunoparticles revealed a somato-dendritic gradient, with the density of immunoparticles increasing 26-fold from somata to dendritic spines. To understand the spatial relationship of GABAB receptors with two key effector ion channels, the G protein-gated inwardly rectifying K+ (GIRK/Kir3) channel and the voltage-dependent Ca2+ channel, biochemical and immunohistochemical approaches were performed. Co-immunoprecipitation analysis demonstrated that GABAB receptors co-assembled with GIRK and CaV2.1 channels in the cerebellum. Using double-labelling immunoelectron microscopic techniques, co-clustering between GABAB1 and GIRK2 was detected in dendritic spines, whereas they were mainly segregated in the dendritic shafts. In contrast, co-clustering of GABAB1 and CaV2.1 was detected in dendritic shafts but not spines. Presynaptically, although no significant co-clustering of GABAB1 and GIRK2 or CaV2.1 channels was detected, inter-cluster distance for GABAB1 and GIRK2 was significantly smaller in the active zone than in the dendritic shafts, and that for GABAB1 and CaV2.1 was significantly smaller in the active zone than in the dendritic shafts and spines. Thus, GABAB receptors are associated with GIRK and CaV2.1 channels in different subcellular compartments. These data provide a better framework for understanding the different roles played by GABAB receptors and their effector ion channels in the cerebellar network. article_processing_charge: No article_type: original author: - first_name: Rafael full_name: Luján, Rafael last_name: Luján - first_name: Carolina full_name: Aguado, Carolina last_name: Aguado - first_name: Francisco full_name: Ciruela, Francisco last_name: Ciruela - first_name: Javier full_name: Cózar, Javier last_name: Cózar - first_name: David full_name: Kleindienst, David id: 42E121A4-F248-11E8-B48F-1D18A9856A87 last_name: Kleindienst - first_name: Luis full_name: De La Ossa, Luis last_name: De La Ossa - first_name: Bernhard full_name: Bettler, Bernhard last_name: Bettler - first_name: Kevin full_name: Wickman, Kevin last_name: Wickman - first_name: Masahiko full_name: Watanabe, Masahiko last_name: Watanabe - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Yugo full_name: Fukazawa, Yugo last_name: Fukazawa citation: ama: Luján R, Aguado C, Ciruela F, et al. Differential association of GABAB receptors with their effector ion channels in Purkinje cells. Brain Structure and Function. 2018;223(3):1565-1587. doi:10.1007/s00429-017-1568-y apa: Luján, R., Aguado, C., Ciruela, F., Cózar, J., Kleindienst, D., De La Ossa, L., … Fukazawa, Y. (2018). Differential association of GABAB receptors with their effector ion channels in Purkinje cells. Brain Structure and Function. Springer. https://doi.org/10.1007/s00429-017-1568-y chicago: Luján, Rafael, Carolina Aguado, Francisco Ciruela, Javier Cózar, David Kleindienst, Luis De La Ossa, Bernhard Bettler, et al. “Differential Association of GABAB Receptors with Their Effector Ion Channels in Purkinje Cells.” Brain Structure and Function. Springer, 2018. https://doi.org/10.1007/s00429-017-1568-y. ieee: R. Luján et al., “Differential association of GABAB receptors with their effector ion channels in Purkinje cells,” Brain Structure and Function, vol. 223, no. 3. Springer, pp. 1565–1587, 2018. ista: Luján R, Aguado C, Ciruela F, Cózar J, Kleindienst D, De La Ossa L, Bettler B, Wickman K, Watanabe M, Shigemoto R, Fukazawa Y. 2018. Differential association of GABAB receptors with their effector ion channels in Purkinje cells. Brain Structure and Function. 223(3), 1565–1587. mla: Luján, Rafael, et al. “Differential Association of GABAB Receptors with Their Effector Ion Channels in Purkinje Cells.” Brain Structure and Function, vol. 223, no. 3, Springer, 2018, pp. 1565–87, doi:10.1007/s00429-017-1568-y. short: R. Luján, C. Aguado, F. Ciruela, J. Cózar, D. Kleindienst, L. De La Ossa, B. Bettler, K. Wickman, M. Watanabe, R. Shigemoto, Y. Fukazawa, Brain Structure and Function 223 (2018) 1565–1587. date_created: 2018-12-11T11:47:29Z date_published: 2018-04-01T00:00:00Z date_updated: 2024-03-28T23:30:31Z day: '01' ddc: - '571' department: - _id: RySh doi: 10.1007/s00429-017-1568-y ec_funded: 1 external_id: isi: - '000428419500030' file: - access_level: open_access checksum: a55b3103476ecb5f4f983d8801807e8b content_type: application/pdf creator: system date_created: 2018-12-12T10:15:36Z date_updated: 2020-07-14T12:47:20Z file_id: '5157' file_name: IST-2018-1013-v1+1_2018_Kleindienst_Differential.pdf file_size: 5542926 relation: main_file file_date_updated: 2020-07-14T12:47:20Z has_accepted_license: '1' intvolume: ' 223' isi: 1 issue: '3' language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ month: '04' oa: 1 oa_version: Published Version page: 1565 - 1587 project: - _id: 25CBA828-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '720270' name: Human Brain Project Specific Grant Agreement 1 (HBP SGA 1) - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme publication: Brain Structure and Function publication_status: published publisher: Springer publist_id: '7192' pubrep_id: '1013' quality_controlled: '1' related_material: record: - id: '9562' relation: dissertation_contains status: public scopus_import: '1' status: public title: Differential association of GABAB receptors with their effector ion channels in Purkinje cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 223 year: '2018' ... --- _id: '643' abstract: - lang: eng text: It has been reported that nicotinamide-overload induces oxidative stress associated with insulin resistance, the key feature of type 2 diabetes mellitus (T2DM). This study aimed to investigate the effects of B vitamins in T2DM. Glucose tolerance tests (GTT) were carried out in adult Sprague-Dawley rats treated with or without cumulative doses of B vitamins. More specifically, insulin tolerance tests (ITT) were also carried out in adult Sprague-Dawley rats treated with or without cumulative doses of Vitamin B3. We found that cumulative Vitamin B1 and Vitamin B3 administration significantly increased the plasma H2O2 levels associated with high insulin levels. Only Vitamin B3 reduced muscular and hepatic glycogen contents. Cumulative administration of nicotinic acid, another form of Vitamin B3, also significantly increased plasma insulin level and H2O2 generation. Moreover, cumulative administration of nicotinic acid or nicotinamide impaired glucose metabolism. This study suggested that excess Vitamin B1 and Vitamin B3 caused oxidative stress and insulin resistance. article_processing_charge: No article_type: original author: - first_name: Wuping full_name: Sun, Wuping last_name: Sun - first_name: Ming-Zhu full_name: Zhai, Ming-Zhu id: 34009CFA-F248-11E8-B48F-1D18A9856A87 last_name: Zhai - first_name: Qian full_name: Zhou, Qian last_name: Zhou - first_name: Chengrui full_name: Qian, Chengrui last_name: Qian - first_name: Changyu full_name: Jiang, Changyu last_name: Jiang citation: ama: Sun W, Zhai M-Z, Zhou Q, Qian C, Jiang C. Effects of B vitamins overload on plasma insulin level and hydrogen peroxide generation in rats. Chinese Journal of Physiology. 2017;60(4):207-214. doi:10.4077/CJP.2017.BAF469 apa: Sun, W., Zhai, M.-Z., Zhou, Q., Qian, C., & Jiang, C. (2017). Effects of B vitamins overload on plasma insulin level and hydrogen peroxide generation in rats. Chinese Journal of Physiology. Chinese Physiological Society. https://doi.org/10.4077/CJP.2017.BAF469 chicago: Sun, Wuping, Ming-Zhu Zhai, Qian Zhou, Chengrui Qian, and Changyu Jiang. “Effects of B Vitamins Overload on Plasma Insulin Level and Hydrogen Peroxide Generation in Rats.” Chinese Journal of Physiology. Chinese Physiological Society, 2017. https://doi.org/10.4077/CJP.2017.BAF469. ieee: W. Sun, M.-Z. Zhai, Q. Zhou, C. Qian, and C. Jiang, “Effects of B vitamins overload on plasma insulin level and hydrogen peroxide generation in rats,” Chinese Journal of Physiology, vol. 60, no. 4. Chinese Physiological Society, pp. 207–214, 2017. ista: Sun W, Zhai M-Z, Zhou Q, Qian C, Jiang C. 2017. Effects of B vitamins overload on plasma insulin level and hydrogen peroxide generation in rats. Chinese Journal of Physiology. 60(4), 207–214. mla: Sun, Wuping, et al. “Effects of B Vitamins Overload on Plasma Insulin Level and Hydrogen Peroxide Generation in Rats.” Chinese Journal of Physiology, vol. 60, no. 4, Chinese Physiological Society, 2017, pp. 207–14, doi:10.4077/CJP.2017.BAF469. short: W. Sun, M.-Z. Zhai, Q. Zhou, C. Qian, C. Jiang, Chinese Journal of Physiology 60 (2017) 207–214. date_created: 2018-12-11T11:47:40Z date_published: 2017-08-31T00:00:00Z date_updated: 2021-01-12T08:07:28Z day: '31' ddc: - '570' department: - _id: RySh doi: 10.4077/CJP.2017.BAF469 external_id: pmid: - '28847140' intvolume: ' 60' issue: '4' language: - iso: eng month: '08' oa_version: Published Version page: 207 - 214 pmid: 1 publication: Chinese Journal of Physiology publication_identifier: issn: - '03044920' publication_status: published publisher: Chinese Physiological Society publist_id: '7142' quality_controlled: '1' scopus_import: 1 status: public title: Effects of B vitamins overload on plasma insulin level and hydrogen peroxide generation in rats type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 60 year: '2017' ... --- _id: '693' abstract: - lang: eng text: 'Many central synapses contain a single presynaptic active zone and a single postsynaptic density. Vesicular release statistics at such “simple synapses” indicate that they contain a small complement of docking sites where vesicles repetitively dock and fuse. In this work, we investigate functional and morphological aspects of docking sites at simple synapses made between cerebellar parallel fibers and molecular layer interneurons. Using immunogold labeling of SDS-treated freeze-fracture replicas, we find that Cav2.1 channels form several clusters per active zone with about nine channels per cluster. The mean value and range of intersynaptic variation are similar for Cav2.1 cluster numbers and for functional estimates of docking-site numbers obtained from the maximum numbers of released vesicles per action potential. Both numbers grow in relation with synaptic size and decrease by a similar extent with age between 2 wk and 4 wk postnatal. Thus, the mean docking-site numbers were 3.15 at 2 wk (range: 1–10) and 2.03 at 4 wk (range: 1–4), whereas the mean numbers of Cav2.1 clusters were 2.84 at 2 wk (range: 1–8) and 2.37 at 4 wk (range: 1–5). These changes were accompanied by decreases of miniature current amplitude (from 93 pA to 56 pA), active-zone surface area (from 0.0427 μm2 to 0.0234 μm2), and initial success rate (from 0.609 to 0.353), indicating a tightening of synaptic transmission with development. Altogether, these results suggest a close correspondence between the number of functionally defined vesicular docking sites and that of clusters of voltage-gated calcium channels. ' article_processing_charge: Yes (in subscription journal) author: - first_name: Takafumi full_name: Miki, Takafumi last_name: Miki - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Gerardo full_name: Malagon, Gerardo last_name: Malagon - first_name: Laura full_name: Gomez, Laura last_name: Gomez - first_name: Katsuhiko full_name: Tabuchi, Katsuhiko last_name: Tabuchi - first_name: Masahiko full_name: Watanabe, Masahiko last_name: Watanabe - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Alain full_name: Marty, Alain last_name: Marty citation: ama: Miki T, Kaufmann W, Malagon G, et al. Numbers of presynaptic Ca2+ channel clusters match those of functionally defined vesicular docking sites in single central synapses. PNAS. 2017;114(26):E5246-E5255. doi:10.1073/pnas.1704470114 apa: Miki, T., Kaufmann, W., Malagon, G., Gomez, L., Tabuchi, K., Watanabe, M., … Marty, A. (2017). Numbers of presynaptic Ca2+ channel clusters match those of functionally defined vesicular docking sites in single central synapses. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1704470114 chicago: Miki, Takafumi, Walter Kaufmann, Gerardo Malagon, Laura Gomez, Katsuhiko Tabuchi, Masahiko Watanabe, Ryuichi Shigemoto, and Alain Marty. “Numbers of Presynaptic Ca2+ Channel Clusters Match Those of Functionally Defined Vesicular Docking Sites in Single Central Synapses.” PNAS. National Academy of Sciences, 2017. https://doi.org/10.1073/pnas.1704470114. ieee: T. Miki et al., “Numbers of presynaptic Ca2+ channel clusters match those of functionally defined vesicular docking sites in single central synapses,” PNAS, vol. 114, no. 26. National Academy of Sciences, pp. E5246–E5255, 2017. ista: Miki T, Kaufmann W, Malagon G, Gomez L, Tabuchi K, Watanabe M, Shigemoto R, Marty A. 2017. Numbers of presynaptic Ca2+ channel clusters match those of functionally defined vesicular docking sites in single central synapses. PNAS. 114(26), E5246–E5255. mla: Miki, Takafumi, et al. “Numbers of Presynaptic Ca2+ Channel Clusters Match Those of Functionally Defined Vesicular Docking Sites in Single Central Synapses.” PNAS, vol. 114, no. 26, National Academy of Sciences, 2017, pp. E5246–55, doi:10.1073/pnas.1704470114. short: T. Miki, W. Kaufmann, G. Malagon, L. Gomez, K. Tabuchi, M. Watanabe, R. Shigemoto, A. Marty, PNAS 114 (2017) E5246–E5255. date_created: 2018-12-11T11:47:57Z date_published: 2017-06-27T00:00:00Z date_updated: 2023-02-23T12:54:57Z day: '27' ddc: - '570' department: - _id: EM-Fac - _id: RySh doi: 10.1073/pnas.1704470114 external_id: pmid: - '28607047' file: - access_level: open_access checksum: 2ab75d554f3df4a34d20fa8040589b7e content_type: application/pdf creator: kschuh date_created: 2020-01-03T13:27:29Z date_updated: 2020-07-14T12:47:44Z file_id: '7223' file_name: 2017_PNAS_Miki.pdf file_size: 2721544 relation: main_file file_date_updated: 2020-07-14T12:47:44Z has_accepted_license: '1' intvolume: ' 114' issue: '26' language: - iso: eng month: '06' oa: 1 oa_version: Published Version page: E5246 - E5255 pmid: 1 publication: PNAS publication_identifier: issn: - '00278424' publication_status: published publisher: National Academy of Sciences publist_id: '7013' quality_controlled: '1' scopus_import: 1 status: public title: Numbers of presynaptic Ca2+ channel clusters match those of functionally defined vesicular docking sites in single central synapses type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 114 year: '2017' ... --- _id: '709' abstract: - lang: eng text: Adipose tissues play key roles in energy homeostasis. Brown adipocytes and beige adipocytes in white adipose tissue (WAT) share the similar characters of thermogenesis, both of them could be potential targets for obesity management. Several thermo-sensitive transient receptor potential channels (thermoTRPs) are shown to be involved in adipocyte biology. However, the expression pattern of thermoTRPs in adipose tissues from obese mice is still unknown. The mRNA expression of thermoTRPs in subcutaneous WAT (sWAT) and interscapular brown adipose tissue (iBAT) from lean and obese mice were measured using reverse transcriptase-quantitative PCRs (RT-qPCR). The results demonstrated that all 10 thermoTRPs are expressed in both iBAT and sWAT, and without significant difference in the mRNA expression level of thermoTRPs between these two tissues. Moreover, Trpv1 and Trpv3 mRNA expression levels in both iBAT and sWAT were significantly decreased in high fat diet (HFD)-induced obese mice and db/db (leptin receptor deficient) mice. Trpm2 mRNA expression level was significantly decreased only in sWAT from HFD-induced obese mice and db/db mice. On the other hand, Trpv2 and Trpv4 mRNA expression levels in iBAT and sWAT were significantly increased in HFD-induced obese mice and db/db mice. Taken together, we conclude that all 10 thermoTRPs are expressed in iBAT and sWAT. And several thermoTRPs differentially expressed in adipose tissues from HFD-induced obese mice and db/db mice, suggesting a potential involvement in anti-obesity regulations. author: - first_name: Wuping full_name: Sun, Wuping last_name: Sun - first_name: Chen full_name: Li, Chen last_name: Li - first_name: Yonghong full_name: Zhang, Yonghong last_name: Zhang - first_name: Changyu full_name: Jiang, Changyu last_name: Jiang - first_name: Ming-Zhu full_name: Zhai, Ming-Zhu id: 34009CFA-F248-11E8-B48F-1D18A9856A87 last_name: Zhai - first_name: Qian full_name: Zhou, Qian last_name: Zhou - first_name: Lizu full_name: Xiao, Lizu last_name: Xiao - first_name: Qiwen full_name: Deng, Qiwen last_name: Deng citation: ama: Sun W, Li C, Zhang Y, et al. Gene expression changes of thermo sensitive transient receptor potential channels in obese mice. Cell Biology International. 2017;41(8):908-913. doi:10.1002/cbin.10783 apa: Sun, W., Li, C., Zhang, Y., Jiang, C., Zhai, M.-Z., Zhou, Q., … Deng, Q. (2017). Gene expression changes of thermo sensitive transient receptor potential channels in obese mice. Cell Biology International. Wiley-Blackwell. https://doi.org/10.1002/cbin.10783 chicago: Sun, Wuping, Chen Li, Yonghong Zhang, Changyu Jiang, Ming-Zhu Zhai, Qian Zhou, Lizu Xiao, and Qiwen Deng. “Gene Expression Changes of Thermo Sensitive Transient Receptor Potential Channels in Obese Mice.” Cell Biology International. Wiley-Blackwell, 2017. https://doi.org/10.1002/cbin.10783. ieee: W. Sun et al., “Gene expression changes of thermo sensitive transient receptor potential channels in obese mice,” Cell Biology International, vol. 41, no. 8. Wiley-Blackwell, pp. 908–913, 2017. ista: Sun W, Li C, Zhang Y, Jiang C, Zhai M-Z, Zhou Q, Xiao L, Deng Q. 2017. Gene expression changes of thermo sensitive transient receptor potential channels in obese mice. Cell Biology International. 41(8), 908–913. mla: Sun, Wuping, et al. “Gene Expression Changes of Thermo Sensitive Transient Receptor Potential Channels in Obese Mice.” Cell Biology International, vol. 41, no. 8, Wiley-Blackwell, 2017, pp. 908–13, doi:10.1002/cbin.10783. short: W. Sun, C. Li, Y. Zhang, C. Jiang, M.-Z. Zhai, Q. Zhou, L. Xiao, Q. Deng, Cell Biology International 41 (2017) 908–913. date_created: 2018-12-11T11:48:04Z date_published: 2017-08-01T00:00:00Z date_updated: 2021-01-12T08:11:47Z day: '01' department: - _id: RySh doi: 10.1002/cbin.10783 intvolume: ' 41' issue: '8' language: - iso: eng month: '08' oa_version: None page: 908 - 913 publication: Cell Biology International publication_identifier: issn: - '10656995' publication_status: published publisher: Wiley-Blackwell publist_id: '6981' quality_controlled: '1' scopus_import: 1 status: public title: Gene expression changes of thermo sensitive transient receptor potential channels in obese mice type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 41 year: '2017' ... --- _id: '736' abstract: - lang: eng text: The neurotransmitter receptor subtype, number, density, and distribution relative to the location of transmitter release sites are key determinants of signal transmission. AMPA-type ionotropic glutamate receptors (AMPARs) containing GluA3 and GluA4 subunits are prominently expressed in subsets of neurons capable of firing action potentials at high frequencies, such as auditory relay neurons. The auditory nerve (AN) forms glutamatergic synapses on two types of relay neurons, bushy cells (BCs) and fusiform cells (FCs) of the cochlear nucleus. AN-BC and AN-FC synapses have distinct kinetics; thus, we investigated whether the number, density, and localization of GluA3 and GluA4 subunits in these synapses are differentially organized using quantitative freeze-fracture replica immunogold labeling. We identify a positive correlation between the number of AMPARs and the size of AN-BC and AN-FC synapses. Both types of AN synapses have similar numbers of AMPARs; however, the AN-BC have a higher density of AMPARs than AN-FC synapses, because the AN-BC synapses are smaller. A higher number and density of GluA3 subunits are observed at AN-BC synapses, whereas a higher number and density of GluA4 subunits are observed at AN-FC synapses. The intrasynaptic distribution of immunogold labeling revealed that AMPAR subunits, particularly GluA3, are concentrated at the center of the AN-BC synapses. The central distribution of AMPARs is absent in GluA3-knockout mice, and gold particles are evenly distributed along the postsynaptic density. GluA4 gold labeling was homogenously distributed along both synapse types. Thus, GluA3 and GluA4 subunits are distributed at AN synapses in a target-cell-dependent manner. article_processing_charge: No author: - first_name: María full_name: Rubio, María last_name: Rubio - first_name: Ko full_name: Matsui, Ko last_name: Matsui - first_name: Yugo full_name: Fukazawa, Yugo last_name: Fukazawa - first_name: Naomi full_name: Kamasawa, Naomi last_name: Kamasawa - first_name: Harumi full_name: Harada, Harumi id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87 last_name: Harada orcid: 0000-0001-7429-7896 - first_name: Makoto full_name: Itakura, Makoto last_name: Itakura - first_name: Elek full_name: Molnár, Elek last_name: Molnár - first_name: Manabu full_name: Abe, Manabu last_name: Abe - first_name: Kenji full_name: Sakimura, Kenji last_name: Sakimura - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 citation: ama: Rubio M, Matsui K, Fukazawa Y, et al. The number and distribution of AMPA receptor channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells. Brain Structure and Function. 2017;222(8):3375-3393. doi:10.1007/s00429-017-1408-0 apa: Rubio, M., Matsui, K., Fukazawa, Y., Kamasawa, N., Harada, H., Itakura, M., … Shigemoto, R. (2017). The number and distribution of AMPA receptor channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells. Brain Structure and Function. Springer. https://doi.org/10.1007/s00429-017-1408-0 chicago: Rubio, María, Ko Matsui, Yugo Fukazawa, Naomi Kamasawa, Harumi Harada, Makoto Itakura, Elek Molnár, Manabu Abe, Kenji Sakimura, and Ryuichi Shigemoto. “The Number and Distribution of AMPA Receptor Channels Containing Fast Kinetic GluA3 and GluA4 Subunits at Auditory Nerve Synapses Depend on the Target Cells.” Brain Structure and Function. Springer, 2017. https://doi.org/10.1007/s00429-017-1408-0. ieee: M. Rubio et al., “The number and distribution of AMPA receptor channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells,” Brain Structure and Function, vol. 222, no. 8. Springer, pp. 3375–3393, 2017. ista: Rubio M, Matsui K, Fukazawa Y, Kamasawa N, Harada H, Itakura M, Molnár E, Abe M, Sakimura K, Shigemoto R. 2017. The number and distribution of AMPA receptor channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells. Brain Structure and Function. 222(8), 3375–3393. mla: Rubio, María, et al. “The Number and Distribution of AMPA Receptor Channels Containing Fast Kinetic GluA3 and GluA4 Subunits at Auditory Nerve Synapses Depend on the Target Cells.” Brain Structure and Function, vol. 222, no. 8, Springer, 2017, pp. 3375–93, doi:10.1007/s00429-017-1408-0. short: M. Rubio, K. Matsui, Y. Fukazawa, N. Kamasawa, H. Harada, M. Itakura, E. Molnár, M. Abe, K. Sakimura, R. Shigemoto, Brain Structure and Function 222 (2017) 3375–3393. date_created: 2018-12-11T11:48:14Z date_published: 2017-11-01T00:00:00Z date_updated: 2023-09-27T14:14:51Z day: '01' ddc: - '571' department: - _id: RySh doi: 10.1007/s00429-017-1408-0 external_id: isi: - '000414761700002' file: - access_level: open_access checksum: 73787a22507de8fb585bb598e1418ca7 content_type: application/pdf creator: system date_created: 2018-12-12T10:10:20Z date_updated: 2020-07-14T12:47:56Z file_id: '4806' file_name: IST-2017-881-v1+1_s00429-017-1408-0.pdf file_size: 4011126 relation: main_file file_date_updated: 2020-07-14T12:47:56Z has_accepted_license: '1' intvolume: ' 222' isi: 1 issue: '8' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 3375 - 3393 publication: Brain Structure and Function publication_identifier: issn: - '18632653' publication_status: published publisher: Springer publist_id: '6932' pubrep_id: '881' quality_controlled: '1' scopus_import: '1' status: public title: The number and distribution of AMPA receptor channels containing fast kinetic GluA3 and GluA4 subunits at auditory nerve synapses depend on the target cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 222 year: '2017' ... --- _id: '740' abstract: - lang: eng text: 'Developments in bioengineering and molecular biology have introduced a palette of genetically encoded probes for identification of specific cell populations in electron microscopy. These probes can be targeted to distinct cellular compartments, rendering them electron dense through a subsequent chemical reaction. These electron densities strongly increase the local contrast in samples prepared for electron microscopy, allowing three major advances in ultrastructural mapping of circuits: genetic identification of circuit components, targeted imaging of regions of interest and automated analysis of the tagged circuits. Together, the gains from these advances can decrease the time required for the analysis of targeted circuit motifs by over two orders of magnitude. These genetic encoded tags for electron microscopy promise to simplify the analysis of circuit motifs and become a central tool for structure‐function studies of synaptic connections in the brain. We review the current state‐of‐the‐art with an emphasis on connectomics, the quantitative analysis of neuronal structures and motifs.' article_number: e288 article_processing_charge: No article_type: original author: - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Maximilian A full_name: Jösch, Maximilian A id: 2BD278E6-F248-11E8-B48F-1D18A9856A87 last_name: Jösch orcid: 0000-0002-3937-1330 citation: ama: Shigemoto R, Jösch MA. The genetic encoded toolbox for electron microscopy and connectomics. WIREs Developmental Biology. 2017;6(6). doi:10.1002/wdev.288 apa: Shigemoto, R., & Jösch, M. A. (2017). The genetic encoded toolbox for electron microscopy and connectomics. WIREs Developmental Biology. Wiley-Blackwell. https://doi.org/10.1002/wdev.288 chicago: Shigemoto, Ryuichi, and Maximilian A Jösch. “The Genetic Encoded Toolbox for Electron Microscopy and Connectomics.” WIREs Developmental Biology. Wiley-Blackwell, 2017. https://doi.org/10.1002/wdev.288. ieee: R. Shigemoto and M. A. Jösch, “The genetic encoded toolbox for electron microscopy and connectomics,” WIREs Developmental Biology, vol. 6, no. 6. Wiley-Blackwell, 2017. ista: Shigemoto R, Jösch MA. 2017. The genetic encoded toolbox for electron microscopy and connectomics. WIREs Developmental Biology. 6(6), e288. mla: Shigemoto, Ryuichi, and Maximilian A. Jösch. “The Genetic Encoded Toolbox for Electron Microscopy and Connectomics.” WIREs Developmental Biology, vol. 6, no. 6, e288, Wiley-Blackwell, 2017, doi:10.1002/wdev.288. short: R. Shigemoto, M.A. Jösch, WIREs Developmental Biology 6 (2017). date_created: 2018-12-11T11:48:15Z date_published: 2017-08-11T00:00:00Z date_updated: 2023-09-27T12:51:41Z day: '11' ddc: - '570' department: - _id: RySh - _id: MaJö doi: 10.1002/wdev.288 external_id: isi: - '000412827400005' pmid: - '28800674' file: - access_level: open_access checksum: a9370f27b1591773b7a0de299bc81c8c content_type: application/pdf creator: dernst date_created: 2019-11-19T07:36:18Z date_updated: 2020-07-14T12:47:57Z file_id: '7045' file_name: 2017_WIREs_Shigemoto.pdf file_size: 1647787 relation: main_file file_date_updated: 2020-07-14T12:47:57Z has_accepted_license: '1' intvolume: ' 6' isi: 1 issue: '6' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '08' oa: 1 oa_version: Submitted Version pmid: 1 publication: WIREs Developmental Biology publication_identifier: issn: - '17597684' publication_status: published publisher: Wiley-Blackwell publist_id: '6927' quality_controlled: '1' scopus_import: '1' status: public title: The genetic encoded toolbox for electron microscopy and connectomics tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 6 year: '2017' ... --- _id: '746' abstract: - lang: eng text: Metabotropic glutamate receptor subtype 5 (mGluR5) is crucially implicated in the pathophysiology of Fragile X Syndrome (FXS); however, its dysfunction at the sub-cellular level, and related synaptic and cognitive phenotypes are unexplored. Here, we probed the consequences of mGluR5/Homer scaffold disruption for mGluR5 cell-surface mobility, synaptic N-methyl-D-Aspartate receptor (NMDAR) function, and behavioral phenotypes in the second-generation Fmr1 knockout (KO) mouse. Using single-molecule tracking, we found that mGluR5 was significantly more mobile at synapses in hippocampal Fmr1 KO neurons, causing an increased synaptic surface co-clustering of mGluR5 and NMDAR. This correlated with a reduced amplitude of synaptic NMDAR currents, a lack of their mGluR5-Activated long-Term depression, and NMDAR/hippocampus dependent cognitive deficits. These synaptic and behavioral phenomena were reversed by knocking down Homer1a in Fmr1 KO mice. Our study provides a mechanistic link between changes of mGluR5 dynamics and pathological phenotypes of FXS, unveiling novel targets for mGluR5-based therapeutics. article_number: '1103' article_processing_charge: No author: - first_name: Elisabetta full_name: Aloisi, Elisabetta last_name: Aloisi - first_name: Katy full_name: Le Corf, Katy last_name: Le Corf - first_name: Julien full_name: Dupuis, Julien last_name: Dupuis - first_name: Pei full_name: Zhang, Pei last_name: Zhang - first_name: Melanie full_name: Ginger, Melanie last_name: Ginger - first_name: Virginie full_name: Labrousse, Virginie last_name: Labrousse - first_name: Michela full_name: Spatuzza, Michela last_name: Spatuzza - first_name: Matthias full_name: Georg Haberl, Matthias last_name: Georg Haberl - first_name: Lara full_name: Costa, Lara last_name: Costa - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Anke full_name: Tappe Theodor, Anke last_name: Tappe Theodor - first_name: Fillippo full_name: Drago, Fillippo last_name: Drago - first_name: Pier full_name: Vincenzo Piazza, Pier last_name: Vincenzo Piazza - first_name: Christophe full_name: Mulle, Christophe last_name: Mulle - first_name: Laurent full_name: Groc, Laurent last_name: Groc - first_name: Lucia full_name: Ciranna, Lucia last_name: Ciranna - first_name: Maria full_name: Catania, Maria last_name: Catania - first_name: Andreas full_name: Frick, Andreas last_name: Frick citation: ama: Aloisi E, Le Corf K, Dupuis J, et al. Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice. Nature Communications. 2017;8(1). doi:10.1038/s41467-017-01191-2 apa: Aloisi, E., Le Corf, K., Dupuis, J., Zhang, P., Ginger, M., Labrousse, V., … Frick, A. (2017). Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-017-01191-2 chicago: Aloisi, Elisabetta, Katy Le Corf, Julien Dupuis, Pei Zhang, Melanie Ginger, Virginie Labrousse, Michela Spatuzza, et al. “Altered Surface MGluR5 Dynamics Provoke Synaptic NMDAR Dysfunction and Cognitive Defects in Fmr1 Knockout Mice.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/s41467-017-01191-2. ieee: E. Aloisi et al., “Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice,” Nature Communications, vol. 8, no. 1. Nature Publishing Group, 2017. ista: Aloisi E, Le Corf K, Dupuis J, Zhang P, Ginger M, Labrousse V, Spatuzza M, Georg Haberl M, Costa L, Shigemoto R, Tappe Theodor A, Drago F, Vincenzo Piazza P, Mulle C, Groc L, Ciranna L, Catania M, Frick A. 2017. Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice. Nature Communications. 8(1), 1103. mla: Aloisi, Elisabetta, et al. “Altered Surface MGluR5 Dynamics Provoke Synaptic NMDAR Dysfunction and Cognitive Defects in Fmr1 Knockout Mice.” Nature Communications, vol. 8, no. 1, 1103, Nature Publishing Group, 2017, doi:10.1038/s41467-017-01191-2. short: E. Aloisi, K. Le Corf, J. Dupuis, P. Zhang, M. Ginger, V. Labrousse, M. Spatuzza, M. Georg Haberl, L. Costa, R. Shigemoto, A. Tappe Theodor, F. Drago, P. Vincenzo Piazza, C. Mulle, L. Groc, L. Ciranna, M. Catania, A. Frick, Nature Communications 8 (2017). date_created: 2018-12-11T11:48:17Z date_published: 2017-12-01T00:00:00Z date_updated: 2023-09-27T12:27:30Z day: '01' ddc: - '571' department: - _id: RySh doi: 10.1038/s41467-017-01191-2 external_id: isi: - '000413571300004' file: - access_level: open_access checksum: 99ceee57549dc0461e3adfc037ec70a9 content_type: application/pdf creator: system date_created: 2018-12-12T10:17:32Z date_updated: 2020-07-14T12:47:58Z file_id: '5287' file_name: IST-2017-915-v1+1_s41467-017-01191-2.pdf file_size: 1841650 relation: main_file file_date_updated: 2020-07-14T12:47:58Z has_accepted_license: '1' intvolume: ' 8' isi: 1 issue: '1' language: - iso: eng month: '12' oa: 1 oa_version: Published Version publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '6921' pubrep_id: '915' quality_controlled: '1' scopus_import: '1' status: public title: Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 8 year: '2017' ... --- _id: '1146' abstract: - lang: eng text: 'Aim: The present study was to compare the effects of nicotinic acid and nicotinamide on the plasma methyl donors, choline and betaine. Methods: Thirty adult subjects were randomly divided into three groups of equal size, and orally received purified water (C group), nicotinic acid (300 mg, NA group) or nicotinamide (300 mg, NM group). Plasma nicotinamide, N 1-methylnicotinamide, homocysteine, betaine and choline levels before and 1.5-h and 3-h post-dosing, plasma normetanephrine and metanephrine concentrations at 3-h post-dosing, and the urinary excretion of N 1-methyl-2-pyridone-5-carboxamide during the test period were examined. Results: The level of 3-h plasma nicotinamide, N 1-methylnicotinamide, homocysteine, the urinary excretion of N 1-methyl-2-pyridone-5-carboxamide and pulse pressure (PP) in the NM group was 221%, 3972%, 61%, 1728% and 21.2% higher than that of the control group (P < 0.01, except homocysteine and PP P < 0.05), while the 3-h plasma betaine, normetanephrine and metanephrine level in the NM group was 24.4%, 9.4% and 11.7% lower (P < 0.05, except betaine P < 0.01), without significant difference in choline levels. Similar but less pronounced changes were observed in the NA group, with a lower level of 3-h plasma N 1-methylnicotinamide (1.90 ± 0.20 μmol/l vs. 3.62 ± 0.27 μmol/l, P < 0.01) and homocysteine (12.85 ± 1.39 μmol/l vs. 18.08 ± 1.02 μmol/l, P < 0.05) but a higher level of betaine (27.44 ± 0.71 μmol/l vs. 23.52 ± 0.61 μmol/l, P < 0.05) than that of the NM group. Conclusion: The degradation of nicotinamide consumes more betaine than that of nicotinic acid at identical doses. This difference should be taken into consideration in niacin fortification. © 2016 Elsevier Ltd and European Society for Clinical Nutrition and Metabolism.' acknowledgement: We thank all the participants for their contribution to this study and volunteers from the Nursing School of Dalian University for their supporting to collect blood and urine samples of the participants. We also thank Dr. Yasunori Takayama from National Institute for Physiological Sciences of Japan for his kind help. article_processing_charge: No author: - first_name: Wuping full_name: Sun, Wuping last_name: Sun - first_name: Ming-Zhu full_name: Zhai, Ming-Zhu id: 34009CFA-F248-11E8-B48F-1D18A9856A87 last_name: Zhai - first_name: Da full_name: Li, Da last_name: Li - first_name: Yiming full_name: Zhou, Yiming last_name: Zhou - first_name: Nana full_name: Chen, Nana last_name: Chen - first_name: Ming full_name: Guo, Ming last_name: Guo - first_name: Shisheng full_name: Zhou, Shisheng last_name: Zhou citation: ama: Sun W, Zhai M-Z, Li D, et al. Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels. Clinical Nutrition. 2017;36(4):1136-1142. doi:10.1016/j.clnu.2016.07.016 apa: Sun, W., Zhai, M.-Z., Li, D., Zhou, Y., Chen, N., Guo, M., & Zhou, S. (2017). Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels. Clinical Nutrition. Elsevier. https://doi.org/10.1016/j.clnu.2016.07.016 chicago: Sun, Wuping, Ming-Zhu Zhai, Da Li, Yiming Zhou, Nana Chen, Ming Guo, and Shisheng Zhou. “Comparison of the Effects of Nicotinic Acid and Nicotinamide Degradation on Plasma Betaine and Choline Levels.” Clinical Nutrition. Elsevier, 2017. https://doi.org/10.1016/j.clnu.2016.07.016. ieee: W. Sun et al., “Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels,” Clinical Nutrition, vol. 36, no. 4. Elsevier, pp. 1136–1142, 2017. ista: Sun W, Zhai M-Z, Li D, Zhou Y, Chen N, Guo M, Zhou S. 2017. Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels. Clinical Nutrition. 36(4), 1136–1142. mla: Sun, Wuping, et al. “Comparison of the Effects of Nicotinic Acid and Nicotinamide Degradation on Plasma Betaine and Choline Levels.” Clinical Nutrition, vol. 36, no. 4, Elsevier, 2017, pp. 1136–42, doi:10.1016/j.clnu.2016.07.016. short: W. Sun, M.-Z. Zhai, D. Li, Y. Zhou, N. Chen, M. Guo, S. Zhou, Clinical Nutrition 36 (2017) 1136–1142. date_created: 2018-12-11T11:50:24Z date_published: 2017-08-01T00:00:00Z date_updated: 2023-10-16T11:09:39Z day: '01' department: - _id: RySh doi: 10.1016/j.clnu.2016.07.016 intvolume: ' 36' issue: '4' language: - iso: eng month: '08' oa_version: None page: 1136-1142 publication: Clinical Nutrition publication_identifier: issn: - 0261-5614 publication_status: published publisher: Elsevier publist_id: '6212' quality_controlled: '1' scopus_import: '1' status: public title: Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2017' ... --- _id: '627' abstract: - lang: eng text: Beige adipocytes are a new type of recruitable brownish adipocytes, with highly mitochondrial membrane uncoupling protein 1 expression and thermogenesis. Beige adipocytes were found among white adipocytes, especially in subcutaneous white adipose tissue (sWAT). Therefore, beige adipocytes may be involved in the regulation of energy metabolism and fat deposition. Transient receptor potential melastatin 8 (TRPM8), a Ca2+-permeable non-selective cation channel, plays vital roles in the regulation of various cellular functions. It has been reported that TRPM8 activation enhanced the thermogenic function of brown adiposytes. However, the involvement of TRPM8 in the thermogenic function of WAT remains unexplored. Our data revealed that TRPM8 was expressed in mouse white adipocytes at mRNA, protein and functional levels. The mRNA expression of Trpm8 was significantly increased in the differentiated white adipocytes than pre-adipocytes. Moreover, activation of TRPM8 by menthol enhanced the expression of thermogenic genes in cultured white aidpocytes. And menthol-induced increases of the thermogenic genes in white adipocytes was inhibited by either KT5720 (a protein kinase A inhibitor) or BAPTA-AM. In addition, high fat diet (HFD)-induced obesity in mice was significantly recovered by co-treatment with menthol. Dietary menthol enhanced WAT "browning" and improved glucose metabolism in HFD-induced obesity mice as well. Therefore, we concluded that TRPM8 might be involved in WAT "browning" by increasing the expression levels of genes related to thermogenesis and energy metabolism. And dietary menthol could be a novel approach for combating human obesity and related metabolic diseases. article_processing_charge: No author: - first_name: Changyu full_name: Jiang, Changyu last_name: Jiang - first_name: Ming-Zhu full_name: Zhai, Ming-Zhu id: 34009CFA-F248-11E8-B48F-1D18A9856A87 last_name: Zhai - first_name: Dong full_name: Yan, Dong last_name: Yan - first_name: Da full_name: Li, Da last_name: Li - first_name: Chen full_name: Li, Chen last_name: Li - first_name: Yonghong full_name: Zhang, Yonghong last_name: Zhang - first_name: Lizu full_name: Xiao, Lizu last_name: Xiao - first_name: Donglin full_name: Xiong, Donglin last_name: Xiong - first_name: Qiwen full_name: Deng, Qiwen last_name: Deng - first_name: Wuping full_name: Sun, Wuping last_name: Sun citation: ama: Jiang C, Zhai M-Z, Yan D, et al. Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates diet-induced obesity. Oncotarget. 2017;8(43):75114-75126. doi:10.18632/oncotarget.20540 apa: Jiang, C., Zhai, M.-Z., Yan, D., Li, D., Li, C., Zhang, Y., … Sun, W. (2017). Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates diet-induced obesity. Oncotarget. Impact Journals. https://doi.org/10.18632/oncotarget.20540 chicago: Jiang, Changyu, Ming-Zhu Zhai, Dong Yan, Da Li, Chen Li, Yonghong Zhang, Lizu Xiao, Donglin Xiong, Qiwen Deng, and Wuping Sun. “Dietary Menthol-Induced TRPM8 Activation Enhances WAT ‘Browning’ and Ameliorates Diet-Induced Obesity.” Oncotarget. Impact Journals, 2017. https://doi.org/10.18632/oncotarget.20540. ieee: C. Jiang et al., “Dietary menthol-induced TRPM8 activation enhances WAT ‘browning’ and ameliorates diet-induced obesity,” Oncotarget, vol. 8, no. 43. Impact Journals, pp. 75114–75126, 2017. ista: Jiang C, Zhai M-Z, Yan D, Li D, Li C, Zhang Y, Xiao L, Xiong D, Deng Q, Sun W. 2017. Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates diet-induced obesity. Oncotarget. 8(43), 75114–75126. mla: Jiang, Changyu, et al. “Dietary Menthol-Induced TRPM8 Activation Enhances WAT ‘Browning’ and Ameliorates Diet-Induced Obesity.” Oncotarget, vol. 8, no. 43, Impact Journals, 2017, pp. 75114–26, doi:10.18632/oncotarget.20540. short: C. Jiang, M.-Z. Zhai, D. Yan, D. Li, C. Li, Y. Zhang, L. Xiao, D. Xiong, Q. Deng, W. Sun, Oncotarget 8 (2017) 75114–75126. date_created: 2018-12-11T11:47:34Z date_published: 2017-08-24T00:00:00Z date_updated: 2023-10-17T08:56:37Z day: '24' ddc: - '571' department: - _id: RySh doi: 10.18632/oncotarget.20540 file: - access_level: open_access checksum: 2219e5348bbfe1aac2725aa620c33280 content_type: application/pdf creator: system date_created: 2018-12-12T10:16:15Z date_updated: 2020-07-14T12:47:26Z file_id: '5201' file_name: IST-2017-907-v1+1_20540-294640-4-PB.pdf file_size: 6101606 relation: main_file file_date_updated: 2020-07-14T12:47:26Z has_accepted_license: '1' intvolume: ' 8' issue: '43' language: - iso: eng month: '08' oa: 1 oa_version: Published Version page: 75114 - 75126 publication: Oncotarget publication_identifier: issn: - 1949-2553 publication_status: published publisher: Impact Journals publist_id: '7167' pubrep_id: '907' quality_controlled: '1' scopus_import: '1' status: public title: Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates diet-induced obesity tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2017' ... --- _id: '682' abstract: - lang: eng text: Left-right asymmetry is a fundamental feature of higher-order brain structure; however, the molecular basis of brain asymmetry remains unclear. We recently identified structural and functional asymmetries in mouse hippocampal circuitry that result from the asymmetrical distribution of two distinct populations of pyramidal cell synapses that differ in the density of the NMDA receptor subunit GluRε2 (also known as NR2B, GRIN2B or GluN2B). By examining the synaptic distribution of ε2 subunits, we previously found that β2-microglobulin-deficient mice, which lack cell surface expression of the vast majority of major histocompatibility complex class I (MHCI) proteins, do not exhibit circuit asymmetry. In the present study, we conducted electrophysiological and anatomical analyses on the hippocampal circuitry of mice with a knockout of the paired immunoglobulin-like receptor B (PirB), an MHCI receptor. As in β2-microglobulin-deficient mice, the PirB-deficient hippocampus lacked circuit asymmetries. This finding that MHCI loss-of-function mice and PirB knockout mice have identical phenotypes suggests that MHCI signals that produce hippocampal asymmetries are transduced through PirB. Our results provide evidence for a critical role of the MHCI/PirB signaling system in the generation of asymmetries in hippocampal circuitry. article_number: e0179377 article_type: original author: - first_name: Hikari full_name: Ukai, Hikari last_name: Ukai - first_name: Aiko full_name: Kawahara, Aiko last_name: Kawahara - first_name: Keiko full_name: Hirayama, Keiko last_name: Hirayama - first_name: Matthew J full_name: Case, Matthew J id: 44B7CA5A-F248-11E8-B48F-1D18A9856A87 last_name: Case - first_name: Shotaro full_name: Aino, Shotaro last_name: Aino - first_name: Masahiro full_name: Miyabe, Masahiro last_name: Miyabe - first_name: Ken full_name: Wakita, Ken last_name: Wakita - first_name: Ryohei full_name: Oogi, Ryohei last_name: Oogi - first_name: Michiyo full_name: Kasayuki, Michiyo last_name: Kasayuki - first_name: Shihomi full_name: Kawashima, Shihomi last_name: Kawashima - first_name: Shunichi full_name: Sugimoto, Shunichi last_name: Sugimoto - first_name: Kanako full_name: Chikamatsu, Kanako last_name: Chikamatsu - first_name: Noritaka full_name: Nitta, Noritaka last_name: Nitta - first_name: Tsuneyuki full_name: Koga, Tsuneyuki last_name: Koga - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Toshiyuki full_name: Takai, Toshiyuki last_name: Takai - first_name: Isao full_name: Ito, Isao last_name: Ito citation: ama: Ukai H, Kawahara A, Hirayama K, et al. PirB regulates asymmetries in hippocampal circuitry. PLoS One. 2017;12(6). doi:10.1371/journal.pone.0179377 apa: Ukai, H., Kawahara, A., Hirayama, K., Case, M. J., Aino, S., Miyabe, M., … Ito, I. (2017). PirB regulates asymmetries in hippocampal circuitry. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0179377 chicago: Ukai, Hikari, Aiko Kawahara, Keiko Hirayama, Matthew J Case, Shotaro Aino, Masahiro Miyabe, Ken Wakita, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.” PLoS One. Public Library of Science, 2017. https://doi.org/10.1371/journal.pone.0179377. ieee: H. Ukai et al., “PirB regulates asymmetries in hippocampal circuitry,” PLoS One, vol. 12, no. 6. Public Library of Science, 2017. ista: Ukai H, Kawahara A, Hirayama K, Case MJ, Aino S, Miyabe M, Wakita K, Oogi R, Kasayuki M, Kawashima S, Sugimoto S, Chikamatsu K, Nitta N, Koga T, Shigemoto R, Takai T, Ito I. 2017. PirB regulates asymmetries in hippocampal circuitry. PLoS One. 12(6), e0179377. mla: Ukai, Hikari, et al. “PirB Regulates Asymmetries in Hippocampal Circuitry.” PLoS One, vol. 12, no. 6, e0179377, Public Library of Science, 2017, doi:10.1371/journal.pone.0179377. short: H. Ukai, A. Kawahara, K. Hirayama, M.J. Case, S. Aino, M. Miyabe, K. Wakita, R. Oogi, M. Kasayuki, S. Kawashima, S. Sugimoto, K. Chikamatsu, N. Nitta, T. Koga, R. Shigemoto, T. Takai, I. Ito, PLoS One 12 (2017). date_created: 2018-12-11T11:47:54Z date_published: 2017-06-01T00:00:00Z date_updated: 2024-03-28T23:30:12Z day: '01' ddc: - '571' department: - _id: RySh doi: 10.1371/journal.pone.0179377 file: - access_level: open_access checksum: 24dd19c46fb1c761b0bcbbcd1025a3a8 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:16Z date_updated: 2020-07-14T12:47:40Z file_id: '4934' file_name: IST-2017-897-v1+1_journal.pone.0179377.pdf file_size: 5798454 relation: main_file file_date_updated: 2020-07-14T12:47:40Z has_accepted_license: '1' intvolume: ' 12' issue: '6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: PLoS One publication_identifier: issn: - '19326203' publication_status: published publisher: Public Library of Science publist_id: '7034' pubrep_id: '897' quality_controlled: '1' related_material: record: - id: '51' relation: dissertation_contains status: public scopus_import: 1 status: public title: PirB regulates asymmetries in hippocampal circuitry tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 12 year: '2017' ... --- _id: '1083' abstract: - lang: eng text: ' Cholecystokinin-expressing interneurons (CCK-INs) mediate behavior state-dependent inhibition in cortical circuits and themselves receive strong GABAergic input. However, it remains unclear to what extent GABABreceptors (GABABRs) contribute to their inhibitory control. Using immunoelectron microscopy, we found that CCK-INs in the rat hippocampus possessed high levels of dendritic GABABRs and KCTD12 auxiliary proteins, whereas postsynaptic effector Kir3 channels were present at lower levels. Consistently, whole-cell recordings revealed slow GABABR-mediated inhibitory postsynaptic currents (IPSCs) in most CCK-INs. In spite of the higher surface density of GABABRs in CCK-INs than in CA1 principal cells, the amplitudes of IPSCs were comparable, suggesting that the expression of Kir3 channels is the limiting factor for the GABABR currents in these INs. Morphological analysis showed that CCK-INs were diverse, comprising perisomatic-targeting basket cells (BCs), as well as dendrite-targeting (DT) interneurons, including a previously undescribed DT type. GABABR-mediated IPSCs in CCK-INs were large in BCs, but small in DT subtypes. In response to prolonged activation, GABABR-mediated currents displayed strong desensitization, which was absent in KCTD12-deficient mice. This study highlights that GABABRs differentially control CCK-IN subtypes, and the kinetics and desensitization of GABABR-mediated currents are modulated by KCTD12 proteins. ' acknowledgement: "This work was supported by the Deutsche Forschungsgemeinschaft (DFG SFB 780 A2, A.K.; SFB TR3 I.V. and EXC 257, I.V.; FOR 2143, A.K. and I.V.), Spemann Graduate School (D.A.), BIOSS-2 (A6, A.K.), the Swiss National Science Foundation (3100A0-117816, B.B.), The McNaught Bequest (S.A.B. and I.V.), and Tenovus Scotland (I.V.).\r\n\r\n\r\nWe thank Cheryl Hutton and Chinmaya Sadangi for their contributions to neuronal reconstruction as well as Natalie Wernet, Sigrun Nestel, Anikó Schneider, Ina Wolter, and Ulrich Noeller for their excellent technical support. VGAT-Venus transgenic rats were generated by Drs Y. Yanagawa, M. Hirabayashi, and Y. Kawaguchi in National Institute for Physiological Sciences, Okazaki, Japan, using pCS2-Venus provided by Dr A. Miyawaki. The monoclonal mouse CCK antibody was generously provided by Dr G.V. Ohning, CURE Center, UCLA, CA. " author: - first_name: Sam full_name: Booker, Sam last_name: Booker - first_name: Daniel full_name: Althof, Daniel last_name: Althof - first_name: Anna full_name: Gross, Anna last_name: Gross - first_name: Desiree full_name: Loreth, Desiree last_name: Loreth - first_name: Johanna full_name: Müller, Johanna last_name: Müller - first_name: Andreas full_name: Unger, Andreas last_name: Unger - first_name: Bernd full_name: Fakler, Bernd last_name: Fakler - first_name: Andrea full_name: Varro, Andrea last_name: Varro - first_name: Masahiko full_name: Watanabe, Masahiko last_name: Watanabe - first_name: Martin full_name: Gassmann, Martin last_name: Gassmann - first_name: Bernhard full_name: Bettler, Bernhard last_name: Bettler - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Imre full_name: Vida, Imre last_name: Vida - first_name: Ákos full_name: Kulik, Ákos last_name: Kulik citation: ama: Booker S, Althof D, Gross A, et al. KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex. 2016;27(3):2318-2334. doi:10.1093/cercor/bhw090 apa: Booker, S., Althof, D., Gross, A., Loreth, D., Müller, J., Unger, A., … Kulik, Á. (2016). KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bhw090 chicago: Booker, Sam, Daniel Althof, Anna Gross, Desiree Loreth, Johanna Müller, Andreas Unger, Bernd Fakler, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics of GABAB Receptor-Mediated Inhibition in Cholecystokinin-Containing Interneurons.” Cerebral Cortex. Oxford University Press, 2016. https://doi.org/10.1093/cercor/bhw090. ieee: S. Booker et al., “KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons,” Cerebral Cortex, vol. 27, no. 3. Oxford University Press, pp. 2318–2334, 2016. ista: Booker S, Althof D, Gross A, Loreth D, Müller J, Unger A, Fakler B, Varro A, Watanabe M, Gassmann M, Bettler B, Shigemoto R, Vida I, Kulik Á. 2016. KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons. Cerebral Cortex. 27(3), 2318–2334. mla: Booker, Sam, et al. “KCTD12 Auxiliary Proteins Modulate Kinetics of GABAB Receptor-Mediated Inhibition in Cholecystokinin-Containing Interneurons.” Cerebral Cortex, vol. 27, no. 3, Oxford University Press, 2016, pp. 2318–34, doi:10.1093/cercor/bhw090. short: S. Booker, D. Althof, A. Gross, D. Loreth, J. Müller, A. Unger, B. Fakler, A. Varro, M. Watanabe, M. Gassmann, B. Bettler, R. Shigemoto, I. Vida, Á. Kulik, Cerebral Cortex 27 (2016) 2318–2334. date_created: 2018-12-11T11:50:03Z date_published: 2016-04-12T00:00:00Z date_updated: 2021-01-12T06:48:09Z day: '12' department: - _id: RySh doi: 10.1093/cercor/bhw090 intvolume: ' 27' issue: '3' language: - iso: eng month: '04' oa_version: None page: 2318 - 2334 publication: Cerebral Cortex publication_status: published publisher: Oxford University Press publist_id: '6297' quality_controlled: '1' status: public title: KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 27 year: '2016' ... --- _id: '1278' abstract: - lang: eng text: Adaptations of vestibulo-ocular and optokinetic response eye movements have been studied as an experimental model of cerebellum-dependent motor learning. Several previous physiological and pharmacological studies have consistently suggested that the cerebellar flocculus (FL) Purkinje cells (P-cells) and the medial vestibular nucleus (MVN) neurons targeted by FL (FL-targeted MVN neurons) may respectively maintain the memory traces of short- and long-term adaptation. To study the basic structures of the FL-MVN synapses by light microscopy (LM) and electron microscopy (EM), we injected green florescence protein (GFP)-expressing lentivirus into FL to anterogradely label the FL P-cell axons in C57BL/6J mice. The FL P-cell axonal boutons were distributed in the magnocellular MVN and in the border region of parvocellular MVN and prepositus hypoglossi (PrH). In the magnocellular MVN, the FL-P cell axons mainly terminated on somata and proximal dendrites. On the other hand, in the parvocellular MVN/PrH, the FL P-cell axonal synaptic boutons mainly terminated on the relatively small-diameter (< 1 μm) distal dendrites of MVN neurons, forming symmetrical synapses. The majority of such parvocellular MVN/PrH neurons were determined to be glutamatergic by immunocytochemistry and in-situ hybridization of GFP expressing transgenic mice. To further examine the spatial relationship between the synapses of FL P-cells and those of vestibular nerve on the neurons of the parvocellular MVN/ PrH, we added injections of biotinylated dextran amine into the semicircular canal and anterogradely labeled vestibular nerve axons in some mice. The MVN dendrites receiving the FL P-cell axonal synaptic boutons often closely apposed vestibular nerve synaptic boutons in both LM and EM studies. Such a partial overlap of synaptic boutons of FL P-cell axons with those of vestibular nerve axons in the distal dendrites of MVN neurons suggests that inhibitory synapses of FL P-cells may influence the function of neighboring excitatory synapses of vestibular nerve in the parvocellular MVN/PrH neurons. acknowledgement: This work was supported by RIKEN [to SN]; Grant-in-Aid from the Japan Society for the Promotion of Science, https://www.jsps.go.jp/english/e-grants/ [22300112 to SN]. article_number: e0164037 article_processing_charge: No article_type: original author: - first_name: Hitomi full_name: Matsuno, Hitomi last_name: Matsuno - first_name: Moeko full_name: Kudoh, Moeko last_name: Kudoh - first_name: Akiya full_name: Watakabe, Akiya last_name: Watakabe - first_name: Tetsuo full_name: Yamamori, Tetsuo last_name: Yamamori - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Soichi full_name: Nagao, Soichi last_name: Nagao citation: ama: 'Matsuno H, Kudoh M, Watakabe A, Yamamori T, Shigemoto R, Nagao S. Distribution and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy studies. PLoS One. 2016;11(10). doi:10.1371/journal.pone.0164037' apa: 'Matsuno, H., Kudoh, M., Watakabe, A., Yamamori, T., Shigemoto, R., & Nagao, S. (2016). Distribution and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy studies. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0164037' chicago: 'Matsuno, Hitomi, Moeko Kudoh, Akiya Watakabe, Tetsuo Yamamori, Ryuichi Shigemoto, and Soichi Nagao. “Distribution and Structure of Synapses on Medial Vestibular Nuclear Neurons Targeted by Cerebellar Flocculus Purkinje Cells and Vestibular Nerve in Mice: Light and Electron Microscopy Studies.” PLoS One. Public Library of Science, 2016. https://doi.org/10.1371/journal.pone.0164037.' ieee: 'H. Matsuno, M. Kudoh, A. Watakabe, T. Yamamori, R. Shigemoto, and S. Nagao, “Distribution and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy studies,” PLoS One, vol. 11, no. 10. Public Library of Science, 2016.' ista: 'Matsuno H, Kudoh M, Watakabe A, Yamamori T, Shigemoto R, Nagao S. 2016. Distribution and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy studies. PLoS One. 11(10), e0164037.' mla: 'Matsuno, Hitomi, et al. “Distribution and Structure of Synapses on Medial Vestibular Nuclear Neurons Targeted by Cerebellar Flocculus Purkinje Cells and Vestibular Nerve in Mice: Light and Electron Microscopy Studies.” PLoS One, vol. 11, no. 10, e0164037, Public Library of Science, 2016, doi:10.1371/journal.pone.0164037.' short: H. Matsuno, M. Kudoh, A. Watakabe, T. Yamamori, R. Shigemoto, S. Nagao, PLoS One 11 (2016). date_created: 2018-12-11T11:51:06Z date_published: 2016-10-06T00:00:00Z date_updated: 2021-01-12T06:49:34Z day: '06' ddc: - '570' - '571' department: - _id: RySh doi: 10.1371/journal.pone.0164037 file: - access_level: open_access checksum: 7c0ba0ca6d79844059158059d2a38d25 content_type: application/pdf creator: system date_created: 2018-12-12T10:17:16Z date_updated: 2020-07-14T12:44:42Z file_id: '5269' file_name: IST-2016-689-v1+1_journal.pone.0164037.PDF file_size: 3657084 relation: main_file file_date_updated: 2020-07-14T12:44:42Z has_accepted_license: '1' intvolume: ' 11' issue: '10' language: - iso: eng month: '10' oa: 1 oa_version: Published Version publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '6038' pubrep_id: '689' quality_controlled: '1' scopus_import: 1 status: public title: 'Distribution and structure of synapses on medial vestibular nuclear neurons targeted by cerebellar flocculus purkinje cells and vestibular nerve in mice: Light and electron microscopy studies' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2016' ... --- _id: '1094' abstract: - lang: eng text: Immunogold labeling of freeze-fracture replicas has recently been used for high-resolution visualization of protein localization in electron microscopy. This method has higher labeling efficiency than conventional immunogold methods for membrane molecules allowing precise quantitative measurements. However, one of the limitations of freeze-fracture replica immunolabeling is difficulty in keeping structural orientation and identifying labeled profiles in complex tissues like brain. The difficulty is partly due to fragmentation of freeze-fracture replica preparations during labeling procedures and limited morphological clues on the replica surface. To overcome these issues, we introduce here a grid-glued replica method combined with SEM observation. This method allows histological staining before dissolving the tissue and easy handling of replicas during immunogold labeling, and keeps the whole replica surface intact without fragmentation. The procedure described here is also useful for matched double-replica analysis allowing further identification of labeled profiles in corresponding P-face and E-face. acknowledged_ssus: - _id: EM-Fac acknowledgement: 'We thank Prof. Elek Molnár for providing us a pan-AMPAR anti-body used in Fig.2 and Dr. Ludek Lovicar for technical assistance in scanning electron microscope imaging. This work was supported by the European Union (HBP—Project Ref. 604102). ' alternative_title: - Methods in Molecular Biology article_processing_charge: No author: - first_name: Harumi full_name: Harada, Harumi id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87 last_name: Harada orcid: 0000-0001-7429-7896 - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 citation: ama: 'Harada H, Shigemoto R. Immunogold protein localization on grid-glued freeze-fracture replicas. In: High-Resolution Imaging of Cellular Proteins. Vol 1474. Springer; 2016:203-216. doi:10.1007/978-1-4939-6352-2_12' apa: Harada, H., & Shigemoto, R. (2016). Immunogold protein localization on grid-glued freeze-fracture replicas. In High-Resolution Imaging of Cellular Proteins (Vol. 1474, pp. 203–216). Springer. https://doi.org/10.1007/978-1-4939-6352-2_12 chicago: Harada, Harumi, and Ryuichi Shigemoto. “Immunogold Protein Localization on Grid-Glued Freeze-Fracture Replicas.” In High-Resolution Imaging of Cellular Proteins, 1474:203–16. Springer, 2016. https://doi.org/10.1007/978-1-4939-6352-2_12. ieee: H. Harada and R. Shigemoto, “Immunogold protein localization on grid-glued freeze-fracture replicas,” in High-Resolution Imaging of Cellular Proteins, vol. 1474, Springer, 2016, pp. 203–216. ista: 'Harada H, Shigemoto R. 2016.Immunogold protein localization on grid-glued freeze-fracture replicas. In: High-Resolution Imaging of Cellular Proteins. Methods in Molecular Biology, vol. 1474, 203–216.' mla: Harada, Harumi, and Ryuichi Shigemoto. “Immunogold Protein Localization on Grid-Glued Freeze-Fracture Replicas.” High-Resolution Imaging of Cellular Proteins, vol. 1474, Springer, 2016, pp. 203–16, doi:10.1007/978-1-4939-6352-2_12. short: H. Harada, R. Shigemoto, in:, High-Resolution Imaging of Cellular Proteins, Springer, 2016, pp. 203–216. date_created: 2018-12-11T11:50:06Z date_published: 2016-08-12T00:00:00Z date_updated: 2023-09-05T14:09:01Z day: '12' department: - _id: RySh doi: 10.1007/978-1-4939-6352-2_12 ec_funded: 1 intvolume: ' 1474' language: - iso: eng month: '08' oa_version: None page: 203 - 216 project: - _id: 25CD3DD2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '604102' name: Localization of ion channels and receptors by two and three-dimensional immunoelectron microscopic approaches publication: High-Resolution Imaging of Cellular Proteins publication_identifier: eissn: - 1611-3349 issn: - 0302-9743 publication_status: published publisher: Springer publist_id: '6281' quality_controlled: '1' status: public title: Immunogold protein localization on grid-glued freeze-fracture replicas type: book_chapter user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 1474 year: '2016' ... --- _id: '1546' abstract: - lang: eng text: Synaptic efficacy and precision are influenced by the coupling of voltage-gated Ca2+ channels (VGCCs) to vesicles. But because the topography of VGCCs and their proximity to vesicles is unknown, a quantitative understanding of the determinants of vesicular release at nanometer scale is lacking. To investigate this, we combined freeze-fracture replica immunogold labeling of Cav2.1 channels, local [Ca2+] imaging, and patch pipette perfusion of EGTA at the calyx of Held. Between postnatal day 7 and 21, VGCCs formed variable sized clusters and vesicular release became less sensitive to EGTA, whereas fixed Ca2+ buffer properties remained constant. Experimentally constrained reaction-diffusion simulations suggest that Ca2+ sensors for vesicular release are located at the perimeter of VGCC clusters (<30nm) and predict that VGCC number per cluster determines vesicular release probability without altering release time course. This "perimeter release model" provides a unifying framework accounting for developmental changes in both synaptic efficacy and time course. acknowledgement: This work was supported by the Core Research for Evolutional Science and Technology (CREST) of Japan Science and Technology Agency to T.T. and R.S.; by the funding provided by Okinawa Institute of Science and Technology (OIST) to T.T. and Y.N.; by JSPS Core-to-Core Program, A. Advanced Networks to T.T.; by the Grant-in-Aid for Young Scientists from the Japanese Ministry of Education, Culture, Sports, Science and Technology (#23700474) to Y.N.; by the Centre National de la Recherche Scientifique through the Actions Thematiques et Initatives sur Programme, Fondation Fyssen, Fondation pour la Recherche Medicale, Federation pour la Recherche sur le Cerveau, Agence Nationale de la Recherche (ANR-2007-Neuro-008-01 and ANR-2010-BLAN-1411-01) to D.D. and Y.N.; and by the European Commission Coordination Action ENINET (LSHM-CT-2005-19063) to D.D. and R.A.S. R.A.S. and J.S.R. were funded by Wellcome Trust Senior (064413) and Principal (095667) Research Fellowship and an ERC advance grant (294667) to RAS. author: - first_name: Yukihiro full_name: Nakamura, Yukihiro last_name: Nakamura - first_name: Harumi full_name: Harada, Harumi id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87 last_name: Harada orcid: 0000-0001-7429-7896 - first_name: Naomi full_name: Kamasawa, Naomi last_name: Kamasawa - first_name: Ko full_name: Matsui, Ko last_name: Matsui - first_name: Jason full_name: Rothman, Jason last_name: Rothman - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: R Angus full_name: Silver, R Angus last_name: Silver - first_name: David full_name: Digregorio, David last_name: Digregorio - first_name: Tomoyuki full_name: Takahashi, Tomoyuki last_name: Takahashi citation: ama: Nakamura Y, Harada H, Kamasawa N, et al. Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular release during development. Neuron. 2015;85(1):145-158. doi:10.1016/j.neuron.2014.11.019 apa: Nakamura, Y., Harada, H., Kamasawa, N., Matsui, K., Rothman, J., Shigemoto, R., … Takahashi, T. (2015). Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular release during development. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2014.11.019 chicago: Nakamura, Yukihiro, Harumi Harada, Naomi Kamasawa, Ko Matsui, Jason Rothman, Ryuichi Shigemoto, R Angus Silver, David Digregorio, and Tomoyuki Takahashi. “Nanoscale Distribution of Presynaptic Ca2+ Channels and Its Impact on Vesicular Release during Development.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2014.11.019. ieee: Y. Nakamura et al., “Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular release during development,” Neuron, vol. 85, no. 1. Elsevier, pp. 145–158, 2015. ista: Nakamura Y, Harada H, Kamasawa N, Matsui K, Rothman J, Shigemoto R, Silver RA, Digregorio D, Takahashi T. 2015. Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular release during development. Neuron. 85(1), 145–158. mla: Nakamura, Yukihiro, et al. “Nanoscale Distribution of Presynaptic Ca2+ Channels and Its Impact on Vesicular Release during Development.” Neuron, vol. 85, no. 1, Elsevier, 2015, pp. 145–58, doi:10.1016/j.neuron.2014.11.019. short: Y. Nakamura, H. Harada, N. Kamasawa, K. Matsui, J. Rothman, R. Shigemoto, R.A. Silver, D. Digregorio, T. Takahashi, Neuron 85 (2015) 145–158. date_created: 2018-12-11T11:52:39Z date_published: 2015-01-07T00:00:00Z date_updated: 2021-01-12T06:51:31Z day: '07' ddc: - '570' department: - _id: RySh doi: 10.1016/j.neuron.2014.11.019 file: - access_level: open_access checksum: 725f4d5be2dbb44b283ce722645ef37d content_type: application/pdf creator: system date_created: 2018-12-12T10:15:47Z date_updated: 2020-07-14T12:45:01Z file_id: '5170' file_name: IST-2016-482-v1+1_1-s2.0-S0896627314010472-main.pdf file_size: 3080111 relation: main_file file_date_updated: 2020-07-14T12:45:01Z has_accepted_license: '1' intvolume: ' 85' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 145 - 158 publication: Neuron publication_status: published publisher: Elsevier publist_id: '5625' pubrep_id: '482' quality_controlled: '1' scopus_import: 1 status: public title: Nanoscale distribution of presynaptic Ca2+ channels and its impact on vesicular release during development tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 85 year: '2015' ... --- _id: '1557' abstract: - lang: eng text: γ-Aminobutyric acid (GABA)- and glycine-mediated hyperpolarizing inhibition is associated with a chloride influx that depends on the inwardly directed chloride electrochemical gradient. In neurons, the extrusion of chloride from the cytosol primarily depends on the expression of an isoform of potassium-chloride cotransporters (KCC2s). KCC2 is crucial in the regulation of the inhibitory tone of neural circuits, including pain processing neural assemblies. Thus we investigated the cellular distribution of KCC2 in neurons underlying pain processing in the superficial spinal dorsal horn of rats by using high-resolution immunocytochemical methods. We demonstrated that perikarya and dendrites widely expressed KCC2, but axon terminals proved to be negative for KCC2. In single ultrathin sections, silver deposits labeling KCC2 molecules showed different densities on the surface of dendritic profiles, some of which were negative for KCC2. In freeze fracture replicas and tissue sections double stained for the β3-subunit of GABAA receptors and KCC2, GABAA receptors were revealed on dendritic segments with high and also with low KCC2 densities. By measuring the distances between spots immunoreactive for gephyrin (a scaffolding protein of GABAA and glycine receptors) and KCC2 on the surface of neurokinin 1 (NK1) receptor-immunoreactive dendrites, we found that gephyrin-immunoreactive spots were located at various distances from KCC2 cotransporters; 5.7 % of them were recovered in the middle of 4-10-μm-long dendritic segments that were free of KCC2 immunostaining. The variable local densities of KCC2 may result in variable postsynaptic potentials evoked by the activation of GABAA and glycine receptors along the dendrites of spinal neurons. acknowledgement: "Funded by:\r\nHungarian Academy of Sciences. Grant Number: MTA-TKI 242\r\nHungarian Brain Research Program. Grant Number: KTIA_NAP_13-1-2013-0001\r\nSolution Oriented Research for Science and Technology from the Japan Science and Technology Agency Japanese Ministry of Education, Culture, Sports, Science and Technology" author: - first_name: Fariba full_name: Javdani, Fariba last_name: Javdani - first_name: Krisztina full_name: Holló, Krisztina last_name: Holló - first_name: Krisztina full_name: Hegedűs, Krisztina last_name: Hegedűs - first_name: Gréta full_name: Kis, Gréta last_name: Kis - first_name: Zoltán full_name: Hegyi, Zoltán last_name: Hegyi - first_name: Klaudia full_name: Dócs, Klaudia last_name: Dócs - first_name: Yu full_name: Kasugai, Yu last_name: Kasugai - first_name: Yugo full_name: Fukazawa, Yugo last_name: Fukazawa - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Miklós full_name: Antal, Miklós last_name: Antal citation: ama: Javdani F, Holló K, Hegedűs K, et al. Differential expression patterns of K+Cl- cotransporter 2 in neurons within the superficial spinal dorsal horn of rats. Journal of Comparative Neurology. 2015;523(13):1967-1983. doi:10.1002/cne.23774 apa: Javdani, F., Holló, K., Hegedűs, K., Kis, G., Hegyi, Z., Dócs, K., … Antal, M. (2015). Differential expression patterns of K+Cl- cotransporter 2 in neurons within the superficial spinal dorsal horn of rats. Journal of Comparative Neurology. Wiley-Blackwell. https://doi.org/10.1002/cne.23774 chicago: Javdani, Fariba, Krisztina Holló, Krisztina Hegedűs, Gréta Kis, Zoltán Hegyi, Klaudia Dócs, Yu Kasugai, Yugo Fukazawa, Ryuichi Shigemoto, and Miklós Antal. “Differential Expression Patterns of K+Cl- Cotransporter 2 in Neurons within the Superficial Spinal Dorsal Horn of Rats.” Journal of Comparative Neurology. Wiley-Blackwell, 2015. https://doi.org/10.1002/cne.23774. ieee: F. Javdani et al., “Differential expression patterns of K+Cl- cotransporter 2 in neurons within the superficial spinal dorsal horn of rats,” Journal of Comparative Neurology, vol. 523, no. 13. Wiley-Blackwell, pp. 1967–1983, 2015. ista: Javdani F, Holló K, Hegedűs K, Kis G, Hegyi Z, Dócs K, Kasugai Y, Fukazawa Y, Shigemoto R, Antal M. 2015. Differential expression patterns of K+Cl- cotransporter 2 in neurons within the superficial spinal dorsal horn of rats. Journal of Comparative Neurology. 523(13), 1967–1983. mla: Javdani, Fariba, et al. “Differential Expression Patterns of K+Cl- Cotransporter 2 in Neurons within the Superficial Spinal Dorsal Horn of Rats.” Journal of Comparative Neurology, vol. 523, no. 13, Wiley-Blackwell, 2015, pp. 1967–83, doi:10.1002/cne.23774. short: F. Javdani, K. Holló, K. Hegedűs, G. Kis, Z. Hegyi, K. Dócs, Y. Kasugai, Y. Fukazawa, R. Shigemoto, M. Antal, Journal of Comparative Neurology 523 (2015) 1967–1983. date_created: 2018-12-11T11:52:42Z date_published: 2015-09-01T00:00:00Z date_updated: 2021-01-12T06:51:35Z day: '01' department: - _id: RySh doi: 10.1002/cne.23774 intvolume: ' 523' issue: '13' language: - iso: eng month: '09' oa_version: None page: 1967 - 1983 publication: Journal of Comparative Neurology publication_status: published publisher: Wiley-Blackwell publist_id: '5614' quality_controlled: '1' scopus_import: 1 status: public title: Differential expression patterns of K+Cl- cotransporter 2 in neurons within the superficial spinal dorsal horn of rats type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 523 year: '2015' ... --- _id: '1895' abstract: - lang: eng text: Major histocompatibility complex class I (MHCI) molecules were recently identified as novel regulators of synaptic plasticity. These molecules are expressed in various brain areas, especially in regions undergoing activity-dependent synaptic plasticity, but their role in the nucleus accumbens (NAc) is unknown. In this study, we investigated the effects of genetic disruption of MHCI function, through deletion of β2-microblobulin, which causes lack of cell surface expression of MHCI. First, we confirmed that MHCI molecules are expressed in the NAc core in wild-type mice. Second, we performed electrophysiological recordings with NAc core slices from wild-type and β2-microglobulin knock-out mice lacking cell surface expression of MHCI. We found that low frequency stimulation induced long-term depression in wild-type but not knock-out mice, whereas high frequency stimulation induced long-term potentiation in both genotypes, with a larger magnitude in knock-out mice. Furthermore, we demonstrated that knock-out mice showed more persistent behavioral sensitization to cocaine, which is a NAc-related behavior. Using this model, we analyzed the density of total AMPA receptors and their subunits GluR1 and GluR2 in the NAc core, by SDS-digested freeze-fracture replica labeling. After repeated cocaine exposure, the density of GluR1 was increased, but there was no change in total AMPA receptors and GluR2 levels in wildtype mice. In contrast, following repeated cocaine exposure, increased densities of total AMPA receptors, GluR1 and GluR2 were observed in knock-out mice. These results indicate that functional deficiency of MHCI enhances synaptic potentiation, induced by electrical and pharmacological stimulation. acknowledgement: This work was supported in part by a Grant-in-Aid for Scientific Research on Innovative Areas (Comprehensive Brain Science Network) and (B) 17330153, from the Ministry of Education, Culture, Sports, Science and Technology of Japan. article_number: e107099 author: - first_name: Mitsuhiro full_name: Edamura, Mitsuhiro last_name: Edamura - first_name: Gen full_name: Murakami, Gen last_name: Murakami - first_name: Hongrui full_name: Meng, Hongrui last_name: Meng - first_name: Makoto full_name: Itakura, Makoto last_name: Itakura - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Atsuo full_name: Fukuda, Atsuo last_name: Fukuda - first_name: Daiichiro full_name: Nakahara, Daiichiro last_name: Nakahara citation: ama: Edamura M, Murakami G, Meng H, et al. Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice. PLoS One. 2014;9(9). doi:10.1371/journal.pone.0107099 apa: Edamura, M., Murakami, G., Meng, H., Itakura, M., Shigemoto, R., Fukuda, A., & Nakahara, D. (2014). Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0107099 chicago: Edamura, Mitsuhiro, Gen Murakami, Hongrui Meng, Makoto Itakura, Ryuichi Shigemoto, Atsuo Fukuda, and Daiichiro Nakahara. “Functional Deficiency of MHC Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0107099. ieee: M. Edamura et al., “Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice,” PLoS One, vol. 9, no. 9. Public Library of Science, 2014. ista: Edamura M, Murakami G, Meng H, Itakura M, Shigemoto R, Fukuda A, Nakahara D. 2014. Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice. PLoS One. 9(9), e107099. mla: Edamura, Mitsuhiro, et al. “Functional Deficiency of MHC Class i Enhances LTP and Abolishes LTD in the Nucleus Accumbens of Mice.” PLoS One, vol. 9, no. 9, e107099, Public Library of Science, 2014, doi:10.1371/journal.pone.0107099. short: M. Edamura, G. Murakami, H. Meng, M. Itakura, R. Shigemoto, A. Fukuda, D. Nakahara, PLoS One 9 (2014). date_created: 2018-12-11T11:54:35Z date_published: 2014-09-30T00:00:00Z date_updated: 2021-01-12T06:53:54Z day: '30' ddc: - '570' department: - _id: RySh doi: 10.1371/journal.pone.0107099 file: - access_level: open_access checksum: 1f3be936be93114596d61ba44cacee69 content_type: application/pdf creator: system date_created: 2018-12-12T10:09:01Z date_updated: 2020-07-14T12:45:20Z file_id: '4724' file_name: IST-2016-439-v1+1_journal.pone.0107099.pdf file_size: 6262085 relation: main_file file_date_updated: 2020-07-14T12:45:20Z has_accepted_license: '1' intvolume: ' 9' issue: '9' language: - iso: eng month: '09' oa: 1 oa_version: Published Version publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '5200' pubrep_id: '439' scopus_import: 1 status: public title: Functional deficiency of MHC class i enhances LTP and abolishes LTD in the nucleus accumbens of mice tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2014' ... --- _id: '1898' abstract: - lang: eng text: Fast synaptic transmission is important for rapid information processing. To explore the maximal rate of neuronal signaling and to analyze the presynaptic mechanisms, we focused on the input layer of the cerebellar cortex, where exceptionally high action potential (AP) frequencies have been reported invivo. With paired recordings between presynaptic cerebellar mossy fiber boutons and postsynaptic granule cells, we demonstrate reliable neurotransmission upto ~1 kHz. Presynaptic APs are ultrafast, with ~100μs half-duration. Both Kv1 and Kv3 potassium channels mediate the fast repolarization, rapidly inactivating sodium channels ensure metabolic efficiency, and little AP broadening occurs during bursts of up to 1.5 kHz. Presynaptic Cav2.1 (P/Q-type) calcium channels open efficiently during ultrafast APs. Furthermore, a subset of synaptic vesicles is tightly coupled to Ca2+ channels, and vesicles are rapidly recruited to the release site. These data reveal mechanisms of presynaptic AP generation and transmitter release underlying neuronal kHz signaling. author: - first_name: Andreas full_name: Ritzau Jost, Andreas last_name: Ritzau Jost - first_name: Igor full_name: Delvendahl, Igor last_name: Delvendahl - first_name: Annika full_name: Rings, Annika last_name: Rings - first_name: Niklas full_name: Byczkowicz, Niklas last_name: Byczkowicz - first_name: Harumi full_name: Harada, Harumi id: 2E55CDF2-F248-11E8-B48F-1D18A9856A87 last_name: Harada orcid: 0000-0001-7429-7896 - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 - first_name: Johannes full_name: Hirrlinger, Johannes last_name: Hirrlinger - first_name: Jens full_name: Eilers, Jens last_name: Eilers - first_name: Stefan full_name: Hallermann, Stefan last_name: Hallermann citation: ama: Ritzau Jost A, Delvendahl I, Rings A, et al. Ultrafast action potentials mediate kilohertz signaling at a central synapse. Neuron. 2014;84(1):152-163. doi:10.1016/j.neuron.2014.08.036 apa: Ritzau Jost, A., Delvendahl, I., Rings, A., Byczkowicz, N., Harada, H., Shigemoto, R., … Hallermann, S. (2014). Ultrafast action potentials mediate kilohertz signaling at a central synapse. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2014.08.036 chicago: Ritzau Jost, Andreas, Igor Delvendahl, Annika Rings, Niklas Byczkowicz, Harumi Harada, Ryuichi Shigemoto, Johannes Hirrlinger, Jens Eilers, and Stefan Hallermann. “Ultrafast Action Potentials Mediate Kilohertz Signaling at a Central Synapse.” Neuron. Elsevier, 2014. https://doi.org/10.1016/j.neuron.2014.08.036. ieee: A. Ritzau Jost et al., “Ultrafast action potentials mediate kilohertz signaling at a central synapse,” Neuron, vol. 84, no. 1. Elsevier, pp. 152–163, 2014. ista: Ritzau Jost A, Delvendahl I, Rings A, Byczkowicz N, Harada H, Shigemoto R, Hirrlinger J, Eilers J, Hallermann S. 2014. Ultrafast action potentials mediate kilohertz signaling at a central synapse. Neuron. 84(1), 152–163. mla: Ritzau Jost, Andreas, et al. “Ultrafast Action Potentials Mediate Kilohertz Signaling at a Central Synapse.” Neuron, vol. 84, no. 1, Elsevier, 2014, pp. 152–63, doi:10.1016/j.neuron.2014.08.036. short: A. Ritzau Jost, I. Delvendahl, A. Rings, N. Byczkowicz, H. Harada, R. Shigemoto, J. Hirrlinger, J. Eilers, S. Hallermann, Neuron 84 (2014) 152–163. date_created: 2018-12-11T11:54:36Z date_published: 2014-10-01T00:00:00Z date_updated: 2021-01-12T06:53:55Z day: '01' department: - _id: RySh doi: 10.1016/j.neuron.2014.08.036 intvolume: ' 84' issue: '1' language: - iso: eng month: '10' oa_version: None page: 152 - 163 publication: Neuron publication_status: published publisher: Elsevier publist_id: '5197' quality_controlled: '1' scopus_import: 1 status: public title: Ultrafast action potentials mediate kilohertz signaling at a central synapse type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 84 year: '2014' ... --- _id: '1920' abstract: - lang: eng text: Cerebellar motor learning is suggested to be caused by long-term plasticity of excitatory parallel fiber-Purkinje cell (PF-PC) synapses associated with changes in the number of synaptic AMPA-type glutamate receptors (AMPARs). However, whether the AMPARs decrease or increase in individual PF-PC synapses occurs in physiological motor learning and accounts for memory that lasts over days remains elusive. We combined quantitative SDS-digested freeze-fracture replica labeling for AMPAR and physical dissector electron microscopy with a simple model of cerebellar motor learning, adaptation of horizontal optokinetic response (HOKR) in mouse. After 1-h training of HOKR, short-term adaptation (STA) was accompanied with transient decrease in AMPARs by 28% in target PF-PC synapses. STA was well correlated with AMPAR decrease in individual animals and both STA and AMPAR decrease recovered to basal levels within 24 h. Surprisingly, long-termadaptation (LTA) after five consecutive daily trainings of 1-h HOKR did not alter the number of AMPARs in PF-PC synapses but caused gradual and persistent synapse elimination by 45%, with corresponding PC spine loss by the fifth training day. Furthermore, recovery of LTA after 2 wk was well correlated with increase of PF-PC synapses to the control level. Our findings indicate that the AMPARs decrease in PF-PC synapses and the elimination of these synapses are in vivo engrams in short- and long-term motor learning, respectively, showing a unique type of synaptic plasticity that may contribute to memory consolidation. acknowledgement: This work was supported by Solution-Oriented Research for Science and Technology from the Japan Science and Technology Agency; Ministry of Education, Culture, Sports, Science and Technology of Japan Grant 16300114 (to R.S.). author: - first_name: Wen full_name: Wang, Wen last_name: Wang - first_name: Kazuhiko full_name: Nakadate, Kazuhiko last_name: Nakadate - first_name: Miwako full_name: Masugi Tokita, Miwako last_name: Masugi Tokita - first_name: Fumihiro full_name: Shutoh, Fumihiro last_name: Shutoh - first_name: Wajeeha full_name: Aziz, Wajeeha last_name: Aziz - first_name: Etsuko full_name: Tarusawa, Etsuko last_name: Tarusawa - first_name: Andrea full_name: Lörincz, Andrea last_name: Lörincz - first_name: Elek full_name: Molnár, Elek last_name: Molnár - first_name: Sebnem full_name: Kesaf, Sebnem id: 401AB46C-F248-11E8-B48F-1D18A9856A87 last_name: Kesaf - first_name: Yunqing full_name: Li, Yunqing last_name: Li - first_name: Yugo full_name: Fukazawa, Yugo last_name: Fukazawa - first_name: Soichi full_name: Nagao, Soichi last_name: Nagao - first_name: Ryuichi full_name: Shigemoto, Ryuichi id: 499F3ABC-F248-11E8-B48F-1D18A9856A87 last_name: Shigemoto orcid: 0000-0001-8761-9444 citation: ama: Wang W, Nakadate K, Masugi Tokita M, et al. Distinct cerebellar engrams in short-term and long-term motor learning. PNAS. 2014;111(1):E188-E193. doi:10.1073/pnas.1315541111 apa: Wang, W., Nakadate, K., Masugi Tokita, M., Shutoh, F., Aziz, W., Tarusawa, E., … Shigemoto, R. (2014). Distinct cerebellar engrams in short-term and long-term motor learning. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1315541111 chicago: Wang, Wen, Kazuhiko Nakadate, Miwako Masugi Tokita, Fumihiro Shutoh, Wajeeha Aziz, Etsuko Tarusawa, Andrea Lörincz, et al. “Distinct Cerebellar Engrams in Short-Term and Long-Term Motor Learning.” PNAS. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1315541111. ieee: W. Wang et al., “Distinct cerebellar engrams in short-term and long-term motor learning,” PNAS, vol. 111, no. 1. National Academy of Sciences, pp. E188–E193, 2014. ista: Wang W, Nakadate K, Masugi Tokita M, Shutoh F, Aziz W, Tarusawa E, Lörincz A, Molnár E, Kesaf S, Li Y, Fukazawa Y, Nagao S, Shigemoto R. 2014. Distinct cerebellar engrams in short-term and long-term motor learning. PNAS. 111(1), E188–E193. mla: Wang, Wen, et al. “Distinct Cerebellar Engrams in Short-Term and Long-Term Motor Learning.” PNAS, vol. 111, no. 1, National Academy of Sciences, 2014, pp. E188–93, doi:10.1073/pnas.1315541111. short: W. Wang, K. Nakadate, M. Masugi Tokita, F. Shutoh, W. Aziz, E. Tarusawa, A. Lörincz, E. Molnár, S. Kesaf, Y. Li, Y. Fukazawa, S. Nagao, R. Shigemoto, PNAS 111 (2014) E188–E193. date_created: 2018-12-11T11:54:43Z date_published: 2014-01-07T00:00:00Z date_updated: 2021-01-12T06:54:05Z day: '07' department: - _id: RySh doi: 10.1073/pnas.1315541111 intvolume: ' 111' issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3890858/ month: '01' oa: 1 oa_version: Submitted Version page: E188 - E193 publication: PNAS publication_status: published publisher: National Academy of Sciences publist_id: '5174' scopus_import: 1 status: public title: Distinct cerebellar engrams in short-term and long-term motor learning type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 111 year: '2014' ...