Figure 3

Pretreatment of NMDA alters the regulation of mGluR5 modulators on the potentiation of NMDA activation and prevention of NMDA blockade. The hippocampal slices were initially exposed to NMDA with ketamine (a, 10 μM), D-APV (b, 50 μM), or ifenprodil (c, 5 μM). After washout, the NMDA was re-exposed to the mGluR5 modulator, DFB (10 μM), CHPG (50 μM), or CDPPB (10 μM) was co-applied with NMDA, followed by a co-application of NMDA, the mGluR5 modulator, and ketamine, D-APV, or ifenprodil. Summary data showing the average amplitude of field potentials induced by NMDA with and without ketamine, D-APV, or ifenprodil as well as in the co-application of mGluR5 modulators, DFB (10 μM), CHPG (50 μM), or CDPPB (10 μM). All values are expressed as the mean ± S.E.M. (n = 5-7). Data were statistically analyzed by one-way ANOVA followed by a Student-Newman-Keuls post-hoc test. ^#p < 0.05 as compared with the NMDA groups. *p < 0.05 as compared with the NMDA plus ketamine or D-APV groups.