Postsynaptic GABABRs Inhibit L-Type Calcium Channels and Abolish Long-Term Potentiation in Hippocampal Somatostatin Interneurons
32 Pages Posted: 5 Apr 2018 Publication Status: Published
More...Abstract
Inhibition provided by a diverse set of local GABAergic interneurons (INs) activates both ionotropic GABAA and metabotropic GABAB receptors. Despite the fact that GABAB receptors represent a major source of inhibition onto INs, 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 receptors and G-protein coupled inward-rectifying K (Kir3) channels on their somato-dendritic surface, they fail to produce significant postsynaptic inhibitory currents. Instead, GABAB receptors selectively inhibit dendritic CaV1.2 (L- type) Ca2 channels on dendrites of SOM-INs, leading to attenuation of calcium influx and loss of long-term potentiation at excitatory input synapses onto these INs. These data provide a novel mechanism by which GABABRs can contribute to disinhibition and control of efficacy of CA3 and entorhinal cortex synaptic inputs in hippocampal networks.
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