Previous studies showed that deletion of the Pcdhg cluster leads to extensive apoptosis and eventual loss of specific subpopulations of spinal interneurons (Prasad et al., 2008; Wang et al., 2002b; Weiner et al., 2005). To determine whether these changes also occur in TCKO mutants, we labeled cells undergoing apoptosis with anti-cleaved caspase-3 in P0 spinal cords. As expected, the number of apoptotic profiles is markedly increased in the spinal cord of both Pcdhgtcko/tcko and Pcdhgdel/del mutants (Figures 2A–A”). Concurrently, the spinal cords of both mutants exhibit similar levels of astrogliosis and microglia activation (Figures S2A), which typically accompany neuronal cell death. To compare the extent of neuronal cell loss in different Pcdhg mutant lines, we quantified the surviving NeuN+ neurons in different spinal regions at P0. The spinal cords of Pcdhgtcko/tcko and Pcdhgdel/del mutants have a similarly reduced cross sectional area compared to those of the wild type littermates, particularly in the ventral horn (LVI-VIII) and in the deep dorsal horn (LIV-V). Superficial dorsal horn (LI-III) and motor pools (LIX), however, appear relatively normal (Figures 2B–B” and S2B). Consistently, the
