Fig. 8.

Neuroprotective effect of PKC-induced synaptic remodeling. Neurons were cultured at low density in the presence (gray bars) or absence (black bars) of APV and were treated with TPA for 45 min or untreated, as indicated. Neurons were then assayed for excitotoxicity by washout of the APV and TPA, exposure to high-K⁺ buffer, and determination of viability by Trypan blue exclusion. a, Neurons cultured chronically with APV exhibited greater toxicity than neurons cultured without APV (t test;p < 0.01), correlating with a higher level of synaptic NMDAR, as reported previously (Crump et al., 2001). This enhanced toxicity of the chronic APV group was mediated by NMDAR, as indicated by sensitivity to APV during the toxicity assay.b, TPA treatment of the APV group partially protected the neurons from excitotoxicity (p < 0.01) by an amount corresponding to the NMDAR-mediated component. TPA was not protective in the no-APV group with the much lower levels of synaptic NMDAR, suggesting that the protective effect of TPA was attributable to the dispersion of synaptic NMDAR in the chronic APV group.