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. Author manuscript; available in PMC: 2017 Dec 1.
Published in final edited form as: Alcohol Clin Exp Res. 2016 Oct 31;40(12):2537–2547. doi: 10.1111/acer.13258

Figure 2.

Figure 2

GluA1 phosphorylation in the prefrontal cortex. Alcohol (1 g/kg, 15 minute pretreatment) robustly increases PKA-mediated GluA1 phosphorylation in the dmPFC, although this effect is largely absent in animals with a prior history of nicotine exposure (A). In contrast, alcohol failed to alter PKC/CaMKII-mediated GluA1 phosphorylation in the dmPFC (B). Alcohol modestly increased pGluA1S845 in the vmPFC, and this effect was not modified by prior nicotine exposure (C). This alteration in alcohol-mediated PKA signaling also did not extend to PKC/CaMKII phosphorylation of GluA1 subunits (D). Representative pGluA1S845 and total GluA1 immunoblots are indicated in (E). N=6/group. Pound signs indicate a main group effect of alcohol treatment (##p<0.01, ###p<0.001). Asterisks indicate increased GluA1S845 phosphorylation following alcohol challenge as determined by Tukey’s post hoc test (***p<0.001) or a significant attenuation of this effect in the context of nicotine pre-exposure (*p<0.05).