The α3 subunit of GABA_A receptors promotes formation of inhibitory synapses in the absence of collybistin.

ABSTRACT: Signaling at nerve cell synapses is a key determinant of proper brain function, and synaptic defects-or synaptopathies-are at the basis of many neurological and psychiatric disorders. Collybistin (CB), a brain-specific guanine nucleotide exchange factor, is essential for the formation of γ-aminobutyric acidergic (GABAergic) postsynapses in defined regions of the mammalian forebrain, including the hippocampus and basolateral amygdala. This process depends on a direct interaction of CB with the scaffolding protein gephyrin, which leads to the redistribution of gephyrin into submembranous clusters at nascent inhibitory synapses. Strikingly, synaptic clustering of gephyrin and GABA_A type A receptors (GABA_ARs) in several brain regions, including the cerebral cortex and cer

SUBMITTER: Wagner S 

PROVIDER: S-EPMC8141935 | biostudies-literature | 2021 Jan-Jun

REPOSITORIES: biostudies-literature