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. 2017 Jun 14;42(10):1991–1999. doi: 10.1038/npp.2017.96

Figure 3.

Figure 3

Effects of cocaine exposure and rolipram pretreatments on the AMPAR/NMDAR ratio in VTA dopamine neurons. (a) Representative AMPAR- and NMDAR-mediated evoked EPSCs recorded from VTA dopamine neurons. Compared with vehicle, rolipram pretreatments increased the AMPAR/NMDAR ratio in slices from saline-injected mice (***p<0.001, n=11) and did not further increase the AMPAR/NMDAR ratio in slices from cocaine-injected mice (p=0.871, n=11-12). (b) Acute rolipram perfusion caused a significantly greater increase in the amplitude of evoked EPSCs in slices from saline-injected mice than that in cocaine-injected mice (p=0.024, n=6–7). The effect of rolipram in slices from saline- or cocaine-injected mice was blocked by the PKA inhibitor H89 (saline, p<0.001, n=7; cocaine, p=0.011, n=6).