Booker, Sam A.
[Author];
Loreth, Desirée
[Author];
Gee, Annabelle L.
[Author];
Watanabe, Masahiko
[Author];
Kind, Peter C.
[Author];
Wyllie, David J.A
[Author];
Kulik, Akos
[Author];
Vida, Imre
[Author]
Postsynaptic GABA B Rs inhibit L-type calcium channels and abolish long-term potentiation in hippocampal somatostatin interneurons
Extent:
1 Online-Ressource (9 Seiten); Illustrationen, Diagramme; Supplemental information
Language:
English
DOI:
10.1016/j.celrep.2017.12.021
Identifier:
Origination:
Footnote:
Description:
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