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. In key areas of the mammalian brain, such as the hippocampus or the basolateral
amygdala, the clustering of the scaffolding protein Gephyrin and of γ-aminobutyric acid type
A receptors at inhibitory neuronal synapses is critically dependent upon the brain-specific
guanine nucleotide exchange factor Collybistin (Cb). Accordingly, it was discovered recently …