Cell Reports
Volume 22, Issue 1, 2 January 2018, Pages 36-43
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Postsynaptic GABABRs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons

https://doi.org/10.1016/j.celrep.2017.12.021Get rights and content
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Highlights

  • GABAB receptors do not activate Kir3-currents in CA1 somatostatin interneurons

  • In somatostatin interneurons, GABAB receptors inhibit dendritic L-type Ca2+ channels

  • CaV1.2 channels co-cluster with GABAB1 on somatostatin interneuron dendrites

  • GABAB activation abolishes long-term potentiation in somatostatin interneurons

Summary

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.

Keywords

GABAergic interneurons
feedback inhibition
GABAB receptors
dendrites
Cav1.2 channels
synaptic plasticity
hippocampus
electron microscopy
whole-cell recording
multi-photon imaging

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