Postsynaptic GABABRs inhibit L-type calcium channels and abolish long-term potentiation in hippocampal somatostatin interneurons

Booker, S. A., Loreth, D., Gee, A. L., Watanabe, M., Kind, P. C., Wyllie, D. J.A., Kulik, Á. and Vida, I. (2018) Postsynaptic GABABRs inhibit L-type calcium channels and abolish long-term potentiation in hippocampal somatostatin interneurons. Cell Reports, 22(1), pp. 36-43. (doi:10.1016/j.celrep.2017.12.021) (PMID:29298431)

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Abstract

Inhibition provided by local GABAergic interneurons (INs) activates ionotropic GABAA and metabotropic GABAB receptors (GABABRs). Despite GABABRs representing a major source of inhibition, little is known of their function in distinct IN subtypes. Here, we show that, while the archetypal dendritic-inhibitory somatostatin-expressing INs (SOM-INs) possess high levels of GABABR on their somato-dendritic surface, they fail to produce significant postsynaptic inhibitory currents. Instead, GABABRs selectively inhibit dendritic CaV1.2 (L-type) Ca2+ channels on SOM-IN dendrites, leading to reduced calcium influx and loss of long-term potentiation at excitatory input synapses onto these INs. These data provide a mechanism by which GABABRs can contribute to disinhibition and control the efficacy of extrinsic inputs to hippocampal networks.

Item Type:Articles
Keywords:Cav1.2 channels, GABA(B) receptors, GABAergic interneurons, dendrites, electron microscopy, feedback inhibition, hippocampus, multi-photon imaging, synaptic plasticity, whole-cell recording.
Status:Published
Refereed:Yes
Glasgow Author(s) Enlighten ID:Vida, Dr Imre
Authors: Booker, S. A., Loreth, D., Gee, A. L., Watanabe, M., Kind, P. C., Wyllie, D. J.A., Kulik, Á., and Vida, I.
College/School:College of Medical Veterinary and Life Sciences > Institute of Neuroscience and Psychology
College of Medical Veterinary and Life Sciences > School of Life Sciences
Journal Name:Cell Reports
Publisher:Elsevier (Cell Press)
ISSN:2211-1247
ISSN (Online):2211-1247
Copyright Holders:Copyright © 2017 The Authors
First Published:First published in Cell Reports 22(1): 36-43
Publisher Policy:Reproduced under a Creative Commons License

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