[{"publisher":"Wiley-Blackwell","quality_controlled":0,"month":"04","intvolume":" 590","abstract":[{"lang":"eng","text":"Recently developed pharmacogenetic and optogenetic approaches, with their own advantages and disadvantages, have become indispensable tools in modern neuroscience. Here, we employed a previously described knock-in mouse line (GABA ARγ2 77Ilox) in which the γ2 subunit of the GABA A receptor (GABA AR) was mutated to become zolpidem insensitive (γ2 77I) and used viral vectors to swap γ2 77I with wild-type, zolpidem-sensitive γ2 subunits (γ2 77F). The verification of unaltered density and subcellular distribution of the virally introduced γ2 subunits requires their selective labelling. For this we generated six N- and six C-terminal-tagged γ2 subunits, with which cortical cultures of GABA ARγ2 -/- mice were transduced using lentiviruses. We found that the N-terminal AU1 tag resulted in excellent immunodetection and unimpaired synaptic localization. Unaltered kinetic properties of the AU1-tagged γ2 ( AU1γ2 77F) channels were demonstrated with whole-cell patch-clamp recordings of spontaneous IPSCs from cultured cells. Next, we carried out stereotaxic injections of lenti- and adeno-associated viruses containing Cre-recombinase and the AU1γ2 77F subunit (Cre-2A- AU1γ2 77F) into the neocortex of GABA ARγ2 77Ilox mice. Light microscopic immunofluorescence and electron microscopic freeze-fracture replica immunogold labelling demonstrated the efficient immunodetection of the AU1 tag and the normal enrichment of the AU1γ2 77F subunits in perisomatic GABAergic synapses. In line with this, miniature and action potential-evoked IPSCs whole-cell recorded from transduced cells had unaltered amplitudes, kinetics and restored zolpidem sensitivity. Our results obtained with a wide range of structural and functional verification methods reveal unaltered subcellular distributions and functional properties of γ2 77I and AU1γ2 77F GABA ARs in cortical pyramidal cells. This transgenic-viral pharmacogenetic approach has the advantage that it does not require any extrinsic protein that might endow some unforeseen alterations of the genetically modified cells. In addition, this virus-based approach opens up the possibility of modifying multiple cell types in distinct brain regions and performing alternative recombination-based intersectional genetic manipulations."}],"page":"1517 - 1534","date_published":"2012-04-07T00:00:00Z","doi":"10.1113/jphysiol.2012.227538","issue":"7","volume":590,"date_created":"2018-12-11T11:57:53Z","publication_status":"published","year":"2012","day":"07","publication":"Journal of Physiology","type":"journal_article","status":"public","_id":"2476","publist_id":"4425","author":[{"first_name":"Máté","last_name":"Sümegi","full_name":"Sümegi, Máté"},{"last_name":"Fukazawa","full_name":"Fukazawa, Yugo","first_name":"Yugo"},{"first_name":"Ko","last_name":"Matsui","full_name":"Matsui, Ko"},{"full_name":"Lörincz, Andrea","last_name":"Lörincz","first_name":"Andrea"},{"first_name":"Mark","full_name":"Eyre, Mark D","last_name":"Eyre"},{"full_name":"Nusser, Zoltán","last_name":"Nusser","first_name":"Zoltán"},{"orcid":"0000-0001-8761-9444","full_name":"Ryuichi Shigemoto","last_name":"Shigemoto","first_name":"Ryuichi","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87"}],"title":"Virus-mediated swapping of zolpidem-insensitive with zolpidem-sensitive GABA A receptors in cortical pyramidal cells","citation":{"ista":"Sümegi M, Fukazawa Y, Matsui K, Lörincz A, Eyre M, Nusser Z, Shigemoto R. 2012. Virus-mediated swapping of zolpidem-insensitive with zolpidem-sensitive GABA A receptors in cortical pyramidal cells. Journal of Physiology. 590(7), 1517–1534.","chicago":"Sümegi, Máté, Yugo Fukazawa, Ko Matsui, Andrea Lörincz, Mark Eyre, Zoltán Nusser, and Ryuichi Shigemoto. “Virus-Mediated Swapping of Zolpidem-Insensitive with Zolpidem-Sensitive GABA A Receptors in Cortical Pyramidal Cells.” Journal of Physiology. Wiley-Blackwell, 2012. https://doi.org/10.1113/jphysiol.2012.227538.","apa":"Sümegi, M., Fukazawa, Y., Matsui, K., Lörincz, A., Eyre, M., Nusser, Z., & Shigemoto, R. (2012). Virus-mediated swapping of zolpidem-insensitive with zolpidem-sensitive GABA A receptors in cortical pyramidal cells. Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/jphysiol.2012.227538","ama":"Sümegi M, Fukazawa Y, Matsui K, et al. Virus-mediated swapping of zolpidem-insensitive with zolpidem-sensitive GABA A receptors in cortical pyramidal cells. Journal of Physiology. 2012;590(7):1517-1534. doi:10.1113/jphysiol.2012.227538","short":"M. Sümegi, Y. Fukazawa, K. Matsui, A. Lörincz, M. Eyre, Z. Nusser, R. Shigemoto, Journal of Physiology 590 (2012) 1517–1534.","ieee":"M. Sümegi et al., “Virus-mediated swapping of zolpidem-insensitive with zolpidem-sensitive GABA A receptors in cortical pyramidal cells,” Journal of Physiology, vol. 590, no. 7. Wiley-Blackwell, pp. 1517–1534, 2012.","mla":"Sümegi, Máté, et al. “Virus-Mediated Swapping of Zolpidem-Insensitive with Zolpidem-Sensitive GABA A Receptors in Cortical Pyramidal Cells.” Journal of Physiology, vol. 590, no. 7, Wiley-Blackwell, 2012, pp. 1517–34, doi:10.1113/jphysiol.2012.227538."},"date_updated":"2021-01-12T06:57:43Z","extern":1},{"type":"journal_article","status":"public","_id":"2475","author":[{"full_name":"Saito, Yuhki","last_name":"Saito","first_name":"Yuhki"},{"first_name":"Tsuyoshi","last_name":"Inoue","full_name":"Inoue, Tsuyoshi"},{"last_name":"Zhu","full_name":"Zhu, Gang","first_name":"Gang"},{"first_name":"Naoki","full_name":"Kimura, Naoki","last_name":"Kimura"},{"last_name":"Okada","full_name":"Okada, Motohiro","first_name":"Motohiro"},{"full_name":"Nishimura, Masaki","last_name":"Nishimura","first_name":"Masaki"},{"first_name":"Shigeo","full_name":"Murayama, Shigeo","last_name":"Murayama"},{"first_name":"Sunao","last_name":"Kaneko","full_name":"Kaneko, Sunao"},{"orcid":"0000-0001-8761-9444","full_name":"Ryuichi Shigemoto","last_name":"Shigemoto","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi"},{"full_name":"Imoto, Keiji","last_name":"Imoto","first_name":"Keiji"},{"first_name":"Toshiharu","full_name":"Suzuki, Toshiharu","last_name":"Suzuki"}],"publist_id":"4426","title":"Hyperpolarization-activated cyclic nucleotide gated channels: A potential molecular link between epileptic seizures and Aβ generation in Alzheimer's disease","citation":{"ista":"Saito Y, Inoue T, Zhu G, Kimura N, Okada M, Nishimura M, Murayama S, Kaneko S, Shigemoto R, Imoto K, Suzuki T. 2012. Hyperpolarization-activated cyclic nucleotide gated channels: A potential molecular link between epileptic seizures and Aβ generation in Alzheimer’s disease. Molecular Neurodegeneration. 7(1).","chicago":"Saito, Yuhki, Tsuyoshi Inoue, Gang Zhu, Naoki Kimura, Motohiro Okada, Masaki Nishimura, Shigeo Murayama, et al. “Hyperpolarization-Activated Cyclic Nucleotide Gated Channels: A Potential Molecular Link between Epileptic Seizures and Aβ Generation in Alzheimer’s Disease.” Molecular Neurodegeneration. BioMed Central, 2012. https://doi.org/10.1186/1750-1326-7-50.","short":"Y. Saito, T. Inoue, G. Zhu, N. Kimura, M. Okada, M. Nishimura, S. Murayama, S. Kaneko, R. Shigemoto, K. Imoto, T. Suzuki, Molecular Neurodegeneration 7 (2012).","ieee":"Y. Saito et al., “Hyperpolarization-activated cyclic nucleotide gated channels: A potential molecular link between epileptic seizures and Aβ generation in Alzheimer’s disease,” Molecular Neurodegeneration, vol. 7, no. 1. BioMed Central, 2012.","apa":"Saito, Y., Inoue, T., Zhu, G., Kimura, N., Okada, M., Nishimura, M., … Suzuki, T. (2012). Hyperpolarization-activated cyclic nucleotide gated channels: A potential molecular link between epileptic seizures and Aβ generation in Alzheimer’s disease. Molecular Neurodegeneration. BioMed Central. https://doi.org/10.1186/1750-1326-7-50","ama":"Saito Y, Inoue T, Zhu G, et al. Hyperpolarization-activated cyclic nucleotide gated channels: A potential molecular link between epileptic seizures and Aβ generation in Alzheimer’s disease. Molecular Neurodegeneration. 2012;7(1). doi:10.1186/1750-1326-7-50","mla":"Saito, Yuhki, et al. “Hyperpolarization-Activated Cyclic Nucleotide Gated Channels: A Potential Molecular Link between Epileptic Seizures and Aβ Generation in Alzheimer’s Disease.” Molecular Neurodegeneration, vol. 7, no. 1, BioMed Central, 2012, doi:10.1186/1750-1326-7-50."},"date_updated":"2021-01-12T06:57:42Z","extern":1,"publisher":"BioMed Central","quality_controlled":0,"month":"10","intvolume":" 7","abstract":[{"text":"Background: One of the best-characterized causative factors of Alzheimer's disease (AD) is the generation of amyloid-β peptide (Aβ). AD subjects are at high risk of epileptic seizures accompanied by aberrant neuronal excitability, which in itself enhances Aβ generation. However, the molecular linkage between epileptic seizures and Aβ generation in AD remains unclear. Results: X11 and X11-like (X11L) gene knockout mice suffered from epileptic seizures, along with a malfunction of hyperpolarization-activated cyclic nucleotide gated (HCN) channels. Genetic ablation of HCN1 in mice and HCN1 channel blockage in cultured Neuro2a (N2a) cells enhanced Aβ generation. Interestingly, HCN1 levels dramatically decreased in the temporal lobe of cynomolgus monkeys (Macaca fascicularis) during aging and were significantly diminished in the temporal lobe of sporadic AD patients. Conclusion: Because HCN1 associates with amyloid-β precursor protein (APP) and X11/X11L in the brain, genetic deficiency of X11/X11L may induce aberrant HCN1 distribution along with epilepsy. Moreover, the reduction in HCN1 levels in aged primates may contribute to augmented Aβ generation. Taken together, HCN1 is proposed to play an important role in the molecular linkage between epileptic seizures and Aβ generation, and in the aggravation of sporadic AD.","lang":"eng"}],"date_published":"2012-10-03T00:00:00Z","volume":7,"issue":"1","doi":"10.1186/1750-1326-7-50","date_created":"2018-12-11T11:57:53Z","year":"2012","publication_status":"published","day":"03","publication":"Molecular Neurodegeneration"},{"date_updated":"2021-01-12T06:57:43Z","citation":{"mla":"Sasaki, Takuya, et al. “Application of an Optogenetic Byway for Perturbing Neuronal Activity via Glial Photostimulation.” PNAS, vol. 109, no. 50, National Academy of Sciences, 2012, pp. 20720–25, doi:10.1073/pnas.1213458109.","ieee":"T. Sasaki, K. Beppu, K. Tanaka, Y. Fukazawa, R. Shigemoto, and K. Matsui, “Application of an optogenetic byway for perturbing neuronal activity via glial photostimulation,” PNAS, vol. 109, no. 50. National Academy of Sciences, pp. 20720–20725, 2012.","short":"T. Sasaki, K. Beppu, K. Tanaka, Y. Fukazawa, R. Shigemoto, K. Matsui, PNAS 109 (2012) 20720–20725.","apa":"Sasaki, T., Beppu, K., Tanaka, K., Fukazawa, Y., Shigemoto, R., & Matsui, K. (2012). Application of an optogenetic byway for perturbing neuronal activity via glial photostimulation. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1213458109","ama":"Sasaki T, Beppu K, Tanaka K, Fukazawa Y, Shigemoto R, Matsui K. Application of an optogenetic byway for perturbing neuronal activity via glial photostimulation. PNAS. 2012;109(50):20720-20725. doi:10.1073/pnas.1213458109","chicago":"Sasaki, Takuya, Kaoru Beppu, Kenji Tanaka, Yugo Fukazawa, Ryuichi Shigemoto, and Ko Matsui. “Application of an Optogenetic Byway for Perturbing Neuronal Activity via Glial Photostimulation.” PNAS. National Academy of Sciences, 2012. https://doi.org/10.1073/pnas.1213458109.","ista":"Sasaki T, Beppu K, Tanaka K, Fukazawa Y, Shigemoto R, Matsui K. 2012. Application of an optogenetic byway for perturbing neuronal activity via glial photostimulation. PNAS. 109(50), 20720–20725."},"extern":1,"author":[{"first_name":"Takuya","last_name":"Sasaki","full_name":"Sasaki, Takuya"},{"last_name":"Beppu","full_name":"Beppu, Kaoru","first_name":"Kaoru"},{"last_name":"Tanaka","full_name":"Tanaka, Kenji F","first_name":"Kenji"},{"first_name":"Yugo","full_name":"Fukazawa, Yugo","last_name":"Fukazawa"},{"last_name":"Shigemoto","full_name":"Ryuichi Shigemoto","orcid":"0000-0001-8761-9444","id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi"},{"last_name":"Matsui","full_name":"Matsui, Ko","first_name":"Ko"}],"publist_id":"4424","title":"Application of an optogenetic byway for perturbing neuronal activity via glial photostimulation","_id":"2477","type":"journal_article","status":"public","year":"2012","publication_status":"published","publication":"PNAS","day":"11","page":"20720 - 20725","date_created":"2018-12-11T11:57:54Z","date_published":"2012-12-11T00:00:00Z","volume":109,"issue":"50","doi":"10.1073/pnas.1213458109","abstract":[{"text":"Dynamic activity of glia has repeatedly been demonstrated, but if such activity is independent from neuronal activity, glia would not have any role in the information processing in the brain or in the generation of animal behavior. Evidence for neurons communicating with glia is solid, but the signaling pathway leading back from glial-to-neuronal activity was often difficult to study. Here, we introduced a transgenic mouse line in which channelrhodopsin-2, a light-gated cation channel, was expressed in astrocytes. Selective photostimulation of these astrocytes in vivo triggered neuronal activation. Using slice preparations, we show that glial photostimulation leads to release of glutamate, which was sufficient to activate AMPA receptors on Purkinje cells and to induce long-term depression of parallel fiber-to-Purkinje cell synapses through activation of metabotropic glutamate receptors. In contrast to neuronal synaptic vesicular release, glial activation likely causes preferential activation of extrasynaptic receptors that appose glial membrane. Finally, we show that neuronal activation by glial stimulation can lead to perturbation of cerebellar modulated motor behavior. These findings demonstrate that glia can modulate the tone of neuronal activity and behavior. This animal model is expected to be a potentially powerful approach to study the role of glia in brain function.","lang":"eng"}],"quality_controlled":0,"publisher":"National Academy of Sciences","intvolume":" 109","month":"12"},{"title":"Thin dendrites of cerebellar interneurons confer sublinear synaptic integration and a gradient of short-term plasticity","publist_id":"4427","author":[{"first_name":"Therese","full_name":"Abrahamsson, Therese","last_name":"Abrahamsson"},{"full_name":"Cathala, Laurence","last_name":"Cathala","first_name":"Laurence"},{"full_name":"Matsui, Ko","last_name":"Matsui","first_name":"Ko"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","last_name":"Shigemoto","orcid":"0000-0001-8761-9444","full_name":"Ryuichi Shigemoto"},{"first_name":"David","full_name":"DiGregorio, David A","last_name":"Digregorio"}],"extern":1,"date_updated":"2021-01-12T06:57:42Z","citation":{"ama":"Abrahamsson T, Cathala L, Matsui K, Shigemoto R, Digregorio D. Thin dendrites of cerebellar interneurons confer sublinear synaptic integration and a gradient of short-term plasticity. Neuron. 2012;73(6):1159-1172. doi:10.1016/j.neuron.2012.01.027","apa":"Abrahamsson, T., Cathala, L., Matsui, K., Shigemoto, R., & Digregorio, D. (2012). Thin dendrites of cerebellar interneurons confer sublinear synaptic integration and a gradient of short-term plasticity. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2012.01.027","ieee":"T. Abrahamsson, L. Cathala, K. Matsui, R. Shigemoto, and D. Digregorio, “Thin dendrites of cerebellar interneurons confer sublinear synaptic integration and a gradient of short-term plasticity,” Neuron, vol. 73, no. 6. Elsevier, pp. 1159–1172, 2012.","short":"T. Abrahamsson, L. Cathala, K. Matsui, R. Shigemoto, D. Digregorio, Neuron 73 (2012) 1159–1172.","mla":"Abrahamsson, Therese, et al. “Thin Dendrites of Cerebellar Interneurons Confer Sublinear Synaptic Integration and a Gradient of Short-Term Plasticity.” Neuron, vol. 73, no. 6, Elsevier, 2012, pp. 1159–72, doi:10.1016/j.neuron.2012.01.027.","ista":"Abrahamsson T, Cathala L, Matsui K, Shigemoto R, Digregorio D. 2012. Thin dendrites of cerebellar interneurons confer sublinear synaptic integration and a gradient of short-term plasticity. Neuron. 73(6), 1159–1172.","chicago":"Abrahamsson, Therese, Laurence Cathala, Ko Matsui, Ryuichi Shigemoto, and David Digregorio. “Thin Dendrites of Cerebellar Interneurons Confer Sublinear Synaptic Integration and a Gradient of Short-Term Plasticity.” Neuron. Elsevier, 2012. https://doi.org/10.1016/j.neuron.2012.01.027."},"status":"public","type":"journal_article","_id":"2474","issue":"6","doi":"10.1016/j.neuron.2012.01.027","volume":73,"date_published":"2012-03-22T00:00:00Z","date_created":"2018-12-11T11:57:52Z","page":"1159 - 1172","day":"22","publication":"Neuron","publication_status":"published","year":"2012","month":"03","intvolume":" 73","quality_controlled":0,"publisher":"Elsevier","abstract":[{"lang":"eng","text":"Interneurons are critical for neuronal circuit function, but how their dendritic morphologies and membrane properties influence information flow within neuronal circuits is largely unknown. We studied the spatiotemporal profile of synaptic integration and short-term plasticity in dendrites of mature cerebellar stellate cells by combining two-photon guided electrical stimulation, glutamate uncaging, electron microscopy, and modeling. Synaptic activation within thin (0.4 μm) dendrites produced somatic responses that became smaller and slower with increasing distance from the soma, sublinear subthreshold input-output relationships, and a somatodendritic gradient of short-term plasticity. Unlike most studies showing that neurons employ active dendritic mechanisms, we found that passive cable properties of thin dendrites determine the sublinear integration and plasticity gradient, which both result from large dendritic depolarizations that reduce synaptic driving force. These integrative properties allow stellate cells to act as spatiotemporal filters of synaptic input patterns, thereby biasing their output in favor of sparse presynaptic activity. Stellate cells are critical sources of inhibition in the cerebellum, but how their dendrites integrate excitatory synaptic inputs is unknown. Abrahamsson et al. show that thin dendrites and passive membrane properties of SCs promote sublinear synaptic summation and distance-dependent short-term plasticity. "}]},{"page":"1467 - 1480","issue":"6","doi":"10.1002/hipo.20986","volume":22,"date_published":"2012-06-01T00:00:00Z","date_created":"2018-12-11T11:58:07Z","year":"2012","publication_status":"published","day":"01","publication":"Hippocampus","publisher":"Wiley-Blackwell","quality_controlled":0,"month":"06","intvolume":" 22","abstract":[{"lang":"eng","text":"We investigated the temporal and spatial expression of SK2 in the developing mouse hippocampus using molecular and biochemical techniques, quantitative immunogold electron microscopy, and electrophysiology. The mRNA encoding SK2 was expressed in the developing and adult hippocampus. Western blotting and immunohistochemistry showed that SK2 protein increased with age. This was accompanied by a shift in subcellular localization. Early in development (P5), SK2 was predominantly localized to the endoplasmic reticulum in the pyramidal cell layer. But by P30 SK2 was almost exclusively expressed in the dendrites and spines. The level of SK2 at the postsynaptic density (PSD) also increased during development. In the adult, SK2 expression on the spine plasma membrane showed a proximal-to-distal gradient. Consistent with this redistribution and gradient of SK2, the selective SK channel blocker apamin increased evoked excitatory postsynaptic potentials (EPSPs) only in CA1 pyramidal neurons from mice older than P15. However, the effect of apamin on EPSPs was not different between synapses in proximal or distal stratum radiatum or stratum lacunosum-moleculare in adult. These results show a developmental increase and gradient in SK2-containing channel surface expression that underlie their influence on neurotransmission, and that may contribute to increased memory acquisition during early development."}],"publist_id":"4386","author":[{"first_name":"Carmen","last_name":"Ballesteros Merino","full_name":"Ballesteros-Merino, Carmen"},{"full_name":"Lin, Michael","last_name":"Lin","first_name":"Michael"},{"first_name":"Wendy","last_name":"Wu","full_name":"Wu, Wendy W"},{"last_name":"Ferrándiz Huertas","full_name":"Ferrándiz-Huertas, Clotilde","first_name":"Clotilde"},{"first_name":"María","full_name":"Cabañero, María José","last_name":"Cabañero"},{"first_name":"Masahiko","last_name":"Watanabe","full_name":"Watanabe, Masahiko"},{"last_name":"Fukazawa","full_name":"Fukazawa, Yugo","first_name":"Yugo"},{"id":"499F3ABC-F248-11E8-B48F-1D18A9856A87","first_name":"Ryuichi","last_name":"Shigemoto","full_name":"Ryuichi Shigemoto","orcid":"0000-0001-8761-9444"},{"last_name":"Maylie","full_name":"Maylie, James G","first_name":"James"},{"full_name":"Adelman, John P","last_name":"Adelman","first_name":"John"},{"last_name":"Luján","full_name":"Luján, Rafael","first_name":"Rafael"}],"title":" Developmental profile of SK2 channel expression and function in CA1 neurons","date_updated":"2021-01-12T06:57:57Z","citation":{"short":"C. Ballesteros Merino, M. Lin, W. Wu, C. Ferrándiz Huertas, M. Cabañero, M. Watanabe, Y. Fukazawa, R. Shigemoto, J. Maylie, J. Adelman, R. Luján, Hippocampus 22 (2012) 1467–1480.","ieee":"C. Ballesteros Merino et al., “ Developmental profile of SK2 channel expression and function in CA1 neurons,” Hippocampus, vol. 22, no. 6. Wiley-Blackwell, pp. 1467–1480, 2012.","apa":"Ballesteros Merino, C., Lin, M., Wu, W., Ferrándiz Huertas, C., Cabañero, M., Watanabe, M., … Luján, R. (2012). Developmental profile of SK2 channel expression and function in CA1 neurons. Hippocampus. Wiley-Blackwell. https://doi.org/10.1002/hipo.20986","ama":"Ballesteros Merino C, Lin M, Wu W, et al. Developmental profile of SK2 channel expression and function in CA1 neurons. Hippocampus. 2012;22(6):1467-1480. doi:10.1002/hipo.20986","mla":"Ballesteros Merino, Carmen, et al. “ Developmental Profile of SK2 Channel Expression and Function in CA1 Neurons.” Hippocampus, vol. 22, no. 6, Wiley-Blackwell, 2012, pp. 1467–80, doi:10.1002/hipo.20986.","ista":"Ballesteros Merino C, Lin M, Wu W, Ferrándiz Huertas C, Cabañero M, Watanabe M, Fukazawa Y, Shigemoto R, Maylie J, Adelman J, Luján R. 2012. Developmental profile of SK2 channel expression and function in CA1 neurons. Hippocampus. 22(6), 1467–1480.","chicago":"Ballesteros Merino, Carmen, Michael Lin, Wendy Wu, Clotilde Ferrándiz Huertas, María Cabañero, Masahiko Watanabe, Yugo Fukazawa, et al. “ Developmental Profile of SK2 Channel Expression and Function in CA1 Neurons.” Hippocampus. Wiley-Blackwell, 2012. https://doi.org/10.1002/hipo.20986."},"extern":1,"type":"journal_article","status":"public","_id":"2515"}]