As described for the Pcdhgdel/del;Bax−/− mutants (Prasad et al., 2008; Weiner et al., 2005), the morphology of spinal cord sections of Pcdhgtcko/tcko;Bax−/− is indistinguishable from that of the Pcdhg+/+;Bax−/− animals, showing no signs of astrogliosis or microglia activation, and the arborization patterns of IaPA terminals appear largely indistinguishable from those of the controls (Figure S5A). Counts of both VGAT+ and VGLUT1+ inputs onto motor neurons were normal in the Bax−/− genetic background, while VGLUT2+ and VAChT+ synapses remain unchanged (Figure S5B). Therefore, the decreased number of VGAT+ contacts, as well as the increased number of VGLUT1+ contacts and IaPA terminals found in both Pcdhgtcko/tcko and Pcdhgdel/del mutants at P0, are both secondary to the cell death of spinal interneurons. These results are reminiscent of findings in the Pcdhg deficient retina in the Bax−/− genetic background, where retinal architecture, cell numbers, and synaptic densities are restored in the absence of neuronal apoptosis (Lefebvre et al., 2008).
