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. Author manuscript; available in PMC: 2011 Apr 15.
Published in final edited form as: J Neurosci. 2009 May 20;29(20):6535–6544. doi: 10.1523/JNEUROSCI.4773-08.2009

Figure 4.

Figure 4

PKA contribution to the initial CRF-induced potentiation of NMDAR EPSCs appears only after chronic cocaine. Data without inhibitors are the same as in Figure 1. A, B, Intracellular application of the PKA inhibitor PKI (20 μM) did not affect CRF-induced NMDAR EPSC potentiation at the initial time period in saline-treated mice. C, D, Intracellular application of the PKC inhibitor BIS (1 μM) reduced the CRF-induced NMDAR EPSC potentiation at the initial time period in saline-treated mice. E–H, Intracellular PKI (E, F) and BIS (G, H) decreased the augmented NMDAR EPSC potentiation by CRF in cocaine-treated mice at both time points. I, J, Coapplication of PKI and BIS completely blocked the enhanced CRF effect after chronic cocaine. ***p <0.001, comparing CRF effect with and without inhibitors (two-way ANOVA with Bonferroni’s post test).