Postsynaptic GABA B Rs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons.

Inhibition provided by local GABAergic interneurons (INs) activates ionotropic GABAA and metabotropic GABAB receptors (GABAB Rs). Despite GABAB Rs 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 GABAB R on their somato-dendritic surface, they fail to produce significant postsynaptic inhibitory currents. Instead, GABAB Rs selectively inhibit dendritic CaV 1.2 (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 GABAB Rs can contribute to disinhibition and control the efficacy of extrinsic inputs to hippocampal networks.