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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.