[{"tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","pubrep_id":"915","status":"public","_id":"746","department":[{"_id":"RySh"}],"file_date_updated":"2020-07-14T12:47:58Z","date_updated":"2023-09-27T12:27:30Z","ddc":["571"],"scopus_import":"1","intvolume":" 8","month":"12","abstract":[{"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.","lang":"eng"}],"oa_version":"Published Version","volume":8,"issue":"1","publication_status":"published","publication_identifier":{"issn":["20411723"]},"language":[{"iso":"eng"}],"file":[{"checksum":"99ceee57549dc0461e3adfc037ec70a9","file_id":"5287","content_type":"application/pdf","relation":"main_file","access_level":"open_access","file_name":"IST-2017-915-v1+1_s41467-017-01191-2.pdf","date_created":"2018-12-12T10:17:32Z","file_size":1841650,"date_updated":"2020-07-14T12:47:58Z","creator":"system"}],"article_number":"1103","article_processing_charge":"No","external_id":{"isi":["000413571300004"]},"publist_id":"6921","author":[{"last_name":"Aloisi","full_name":"Aloisi, Elisabetta","first_name":"Elisabetta"},{"full_name":"Le Corf, Katy","last_name":"Le Corf","first_name":"Katy"},{"full_name":"Dupuis, Julien","last_name":"Dupuis","first_name":"Julien"},{"first_name":"Pei","full_name":"Zhang, Pei","last_name":"Zhang"},{"last_name":"Ginger","full_name":"Ginger, Melanie","first_name":"Melanie"},{"first_name":"Virginie","full_name":"Labrousse, Virginie","last_name":"Labrousse"},{"full_name":"Spatuzza, Michela","last_name":"Spatuzza","first_name":"Michela"},{"first_name":"Matthias","last_name":"Georg Haberl","full_name":"Georg Haberl, Matthias"},{"first_name":"Lara","full_name":"Costa, Lara","last_name":"Costa"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto"},{"last_name":"Tappe Theodor","full_name":"Tappe Theodor, Anke","first_name":"Anke"},{"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","last_name":"Groc","full_name":"Groc, Laurent"},{"last_name":"Ciranna","full_name":"Ciranna, Lucia","first_name":"Lucia"},{"full_name":"Catania, Maria","last_name":"Catania","first_name":"Maria"},{"first_name":"Andreas","last_name":"Frick","full_name":"Frick, Andreas"}],"title":"Altered surface mGluR5 dynamics provoke synaptic NMDAR dysfunction and cognitive defects in Fmr1 knockout mice","citation":{"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.","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.","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).","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.","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","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","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."},"user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","oa":1,"quality_controlled":"1","publisher":"Nature Publishing Group","date_created":"2018-12-11T11:48:17Z","doi":"10.1038/s41467-017-01191-2","date_published":"2017-12-01T00:00:00Z","year":"2017","has_accepted_license":"1","isi":1,"publication":"Nature Communications","day":"01"},{"abstract":[{"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.","lang":"eng"}],"oa_version":"None","scopus_import":"1","intvolume":" 36","month":"08","publication_status":"published","publication_identifier":{"issn":["0261-5614"]},"language":[{"iso":"eng"}],"issue":"4","volume":36,"_id":"1146","type":"journal_article","status":"public","date_updated":"2023-10-16T11:09:39Z","department":[{"_id":"RySh"}],"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.","publisher":"Elsevier","quality_controlled":"1","year":"2017","publication":"Clinical Nutrition","day":"01","page":"1136-1142","date_created":"2018-12-11T11:50:24Z","date_published":"2017-08-01T00:00:00Z","doi":"10.1016/j.clnu.2016.07.016","citation":{"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.","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.","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","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","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.","short":"W. Sun, M.-Z. Zhai, D. Li, Y. Zhou, N. Chen, M. Guo, S. Zhou, Clinical Nutrition 36 (2017) 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."},"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","article_processing_charge":"No","publist_id":"6212","author":[{"first_name":"Wuping","last_name":"Sun","full_name":"Sun, Wuping"},{"full_name":"Zhai, Ming-Zhu","last_name":"Zhai","id":"34009CFA-F248-11E8-B48F-1D18A9856A87","first_name":"Ming-Zhu"},{"full_name":"Li, Da","last_name":"Li","first_name":"Da"},{"first_name":"Yiming","full_name":"Zhou, Yiming","last_name":"Zhou"},{"first_name":"Nana","last_name":"Chen","full_name":"Chen, Nana"},{"last_name":"Guo","full_name":"Guo, Ming","first_name":"Ming"},{"first_name":"Shisheng","last_name":"Zhou","full_name":"Zhou, Shisheng"}],"title":"Comparison of the effects of nicotinic acid and nicotinamide degradation on plasma betaine and choline levels"},{"status":"public","pubrep_id":"907","type":"journal_article","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"_id":"627","file_date_updated":"2020-07-14T12:47:26Z","department":[{"_id":"RySh"}],"ddc":["571"],"date_updated":"2023-10-17T08:56:37Z","month":"08","intvolume":" 8","scopus_import":"1","oa_version":"Published Version","abstract":[{"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.","lang":"eng"}],"issue":"43","volume":8,"file":[{"file_size":6101606,"date_updated":"2020-07-14T12:47:26Z","creator":"system","file_name":"IST-2017-907-v1+1_20540-294640-4-PB.pdf","date_created":"2018-12-12T10:16:15Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","checksum":"2219e5348bbfe1aac2725aa620c33280","file_id":"5201"}],"language":[{"iso":"eng"}],"publication_identifier":{"issn":["1949-2553"]},"publication_status":"published","title":"Dietary menthol-induced TRPM8 activation enhances WAT “browning” and ameliorates diet-induced obesity","publist_id":"7167","author":[{"last_name":"Jiang","full_name":"Jiang, Changyu","first_name":"Changyu"},{"id":"34009CFA-F248-11E8-B48F-1D18A9856A87","first_name":"Ming-Zhu","full_name":"Zhai, Ming-Zhu","last_name":"Zhai"},{"full_name":"Yan, Dong","last_name":"Yan","first_name":"Dong"},{"last_name":"Li","full_name":"Li, Da","first_name":"Da"},{"first_name":"Chen","full_name":"Li, Chen","last_name":"Li"},{"full_name":"Zhang, Yonghong","last_name":"Zhang","first_name":"Yonghong"},{"full_name":"Xiao, Lizu","last_name":"Xiao","first_name":"Lizu"},{"first_name":"Donglin","last_name":"Xiong","full_name":"Xiong, Donglin"},{"last_name":"Deng","full_name":"Deng, Qiwen","first_name":"Qiwen"},{"full_name":"Sun, Wuping","last_name":"Sun","first_name":"Wuping"}],"article_processing_charge":"No","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","citation":{"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.","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.","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","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","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.","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.","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."},"publisher":"Impact Journals","quality_controlled":"1","oa":1,"doi":"10.18632/oncotarget.20540","date_published":"2017-08-24T00:00:00Z","date_created":"2018-12-11T11:47:34Z","page":"75114 - 75126","day":"24","publication":"Oncotarget","has_accepted_license":"1","year":"2017"},{"language":[{"iso":"eng"}],"file":[{"file_size":5798454,"date_updated":"2020-07-14T12:47:40Z","creator":"system","file_name":"IST-2017-897-v1+1_journal.pone.0179377.pdf","date_created":"2018-12-12T10:12:16Z","content_type":"application/pdf","relation":"main_file","access_level":"open_access","checksum":"24dd19c46fb1c761b0bcbbcd1025a3a8","file_id":"4934"}],"publication_status":"published","publication_identifier":{"issn":["19326203"]},"volume":12,"issue":"6","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"51"}]},"oa_version":"Published Version","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."}],"intvolume":" 12","month":"06","scopus_import":1,"ddc":["571"],"date_updated":"2024-03-27T23:30:12Z","file_date_updated":"2020-07-14T12:47:40Z","department":[{"_id":"RySh"}],"_id":"682","pubrep_id":"897","status":"public","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","image":"/images/cc_by.png","name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","short":"CC BY (4.0)"},"type":"journal_article","article_type":"original","publication":"PLoS One","day":"01","year":"2017","has_accepted_license":"1","date_created":"2018-12-11T11:47:54Z","date_published":"2017-06-01T00:00:00Z","doi":"10.1371/journal.pone.0179377","oa":1,"publisher":"Public Library of Science","quality_controlled":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","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","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).","ieee":"H. Ukai et al., “PirB regulates asymmetries in hippocampal circuitry,” PLoS One, vol. 12, no. 6. Public Library of Science, 2017.","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.","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.","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."},"title":"PirB regulates asymmetries in hippocampal circuitry","author":[{"first_name":"Hikari","full_name":"Ukai, Hikari","last_name":"Ukai"},{"first_name":"Aiko","last_name":"Kawahara","full_name":"Kawahara, Aiko"},{"full_name":"Hirayama, Keiko","last_name":"Hirayama","first_name":"Keiko"},{"first_name":"Matthew J","id":"44B7CA5A-F248-11E8-B48F-1D18A9856A87","last_name":"Case","full_name":"Case, Matthew J"},{"last_name":"Aino","full_name":"Aino, Shotaro","first_name":"Shotaro"},{"first_name":"Masahiro","last_name":"Miyabe","full_name":"Miyabe, Masahiro"},{"first_name":"Ken","last_name":"Wakita","full_name":"Wakita, Ken"},{"first_name":"Ryohei","full_name":"Oogi, Ryohei","last_name":"Oogi"},{"first_name":"Michiyo","last_name":"Kasayuki","full_name":"Kasayuki, Michiyo"},{"full_name":"Kawashima, Shihomi","last_name":"Kawashima","first_name":"Shihomi"},{"last_name":"Sugimoto","full_name":"Sugimoto, Shunichi","first_name":"Shunichi"},{"first_name":"Kanako","last_name":"Chikamatsu","full_name":"Chikamatsu, Kanako"},{"first_name":"Noritaka","full_name":"Nitta, Noritaka","last_name":"Nitta"},{"first_name":"Tsuneyuki","last_name":"Koga","full_name":"Koga, Tsuneyuki"},{"first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","last_name":"Shigemoto","full_name":"Shigemoto, Ryuichi","orcid":"0000-0001-8761-9444"},{"first_name":"Toshiyuki","last_name":"Takai","full_name":"Takai, Toshiyuki"},{"first_name":"Isao","last_name":"Ito","full_name":"Ito, Isao"}],"publist_id":"7034","article_number":"e0179377"},{"day":"12","language":[{"iso":"eng"}],"publication":"Cerebral Cortex","year":"2016","publication_status":"published","volume":27,"issue":"3","doi":"10.1093/cercor/bhw090","date_published":"2016-04-12T00:00:00Z","date_created":"2018-12-11T11:50:03Z","page":"2318 - 2334","oa_version":"None","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. ","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. "}],"month":"04","intvolume":" 27","publisher":"Oxford University Press","quality_controlled":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_updated":"2021-01-12T06:48:09Z","citation":{"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.","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","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.","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.","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.","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."},"title":"KCTD12 auxiliary proteins modulate kinetics of GABAB receptor-mediated inhibition in Cholecystokinin-containing interneurons","department":[{"_id":"RySh"}],"publist_id":"6297","author":[{"last_name":"Booker","full_name":"Booker, Sam","first_name":"Sam"},{"last_name":"Althof","full_name":"Althof, Daniel","first_name":"Daniel"},{"first_name":"Anna","last_name":"Gross","full_name":"Gross, Anna"},{"full_name":"Loreth, Desiree","last_name":"Loreth","first_name":"Desiree"},{"first_name":"Johanna","last_name":"Müller","full_name":"Müller, Johanna"},{"first_name":"Andreas","full_name":"Unger, Andreas","last_name":"Unger"},{"full_name":"Fakler, Bernd","last_name":"Fakler","first_name":"Bernd"},{"last_name":"Varro","full_name":"Varro, Andrea","first_name":"Andrea"},{"first_name":"Masahiko","last_name":"Watanabe","full_name":"Watanabe, Masahiko"},{"first_name":"Martin","last_name":"Gassmann","full_name":"Gassmann, Martin"},{"first_name":"Bernhard","full_name":"Bettler, Bernhard","last_name":"Bettler"},{"orcid":"0000-0001-8761-9444","full_name":"Shigemoto, Ryuichi","last_name":"Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi"},{"first_name":"Imre","full_name":"Vida, Imre","last_name":"Vida"},{"full_name":"Kulik, Ákos","last_name":"Kulik","first_name":"Ákos"}],"_id":"1083","status":"public","type":"journal_article"}]