Postsynaptic GABABRs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons

Sam A Booker, Desiree Loreth, Annabelle L Gee, Masahiko Watanabe, Peter C Kind, David J A Wyllie, Ákos Kulik, Imre Vida

Research output: Contribution to journalArticlepeer-review

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.

Original languageEnglish
Pages (from-to)36-43
Number of pages8
JournalCell Reports
Volume22
Issue number1
DOIs
Publication statusPublished - 2 Jan 2018

Keywords

  • Journal Article

Fingerprint

Dive into the research topics of 'Postsynaptic GABA<sub>B</sub>Rs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons'. Together they form a unique fingerprint.

Cite this