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Cortical function critically depends on inhibitory/excitatory balance. Cortical inhibitory interneurons (cINs) are born in the ventral forebrain and migrate into cortex, where their numbers are adjusted by programmed cell death. Here, we show that loss of clustered gamma protocadherins ( Pcdhg ), but not of genes in the alpha or beta clusters, increased dramatically cIN BAX-dependent cell death in mice. Surprisingly, electrophysiological and morphological properties of  Pcdhg -deficient and wild-type cINs during the period of cIN cell death were indistinguishable. Co-transplantation of wild-type with  Pcdhg -deficient interneuron precursors further reduced mutant cIN survival, but the proportion of mutant and wild-type cells undergoing cell death was not affected by their density. Transplantation also allowed us to test for the contribution of  Pcdhg  isoforms to the regulation of cIN cell death. We conclude that  Pcdhg , specifically  Pcdhgc3 ,  Pcdhgc4 , and  Pcdhgc5 , play a critical role in regulating cIN survival during the endogenous period of programmed cIN death.

Clustered gamma-protocadherins regulate cortical interneuron programmed cell death