synapses, and loss of synaptic contacts, at the very least, cannot explain the loss of neurons in all cases; 2) Consistent with the observations in the retina, the Pcdhgdel/del;Bax−/− and Pcdhgtcko/tcko;Bax−/− compound mutants showed preservation of stretch reflex circuits and major synaptic inputs onto motor neurons, indicating that these severe synaptic defects observed are secondary to interneuron loss; 3) Neural circuitries and synaptic functions are restored to a substantial extent in Pcdhgtcko/tcko;Bax−/− mutants, as shown by the rescue of neonatal lethality. If the synaptic defects are primary, they should remain when neuronal apoptosis is blocked by Bax deficiency (Buss et al., 2006). This is most likely the case in Pcdhgdel/del;Bax−/− mutants, which could not be rescued.
