Alcohol Dependence Modulates Amygdalar mTORC2 and PKC Expression in a Rodent Model

Multiple alcohol use disorder (AUD)-related behavioral alterations are governed by protein kinase C epsilon (PKC & epsilon;), particularly in the amygdala. Protein kinase C (PKC) is readily phosphorylated at Ser729 before activation by the mTORC2 protein complex. In keeping with this, the current study was conducted to assess the variations in mTORC2 and PKC & epsilon; during different ethanol exposure stages. The following groups of rats were employed: control, acute, chronic, ethanol withdrawal (EW), and EW + ethanol (EtOH). Ethanol-containing and non-ethanol-containing modified liquid diets (MLDs) were administered for 27 days. On day 28, either saline or ethanol (2.5 g/kg, 20% v/v) was intraperitoneally administered, followed by bilateral amygdala extraction. PKC & epsilon; mRNA levels were noticeably increased in the amygdala of the EW + EtOH and EW groups. Following chronic ethanol consumption, the stress-activated map kinase-interacting protein 1 (Sin1) gene expression was markedly decreased. In the EW, EW + EtOH, and chronic ethanol groups, there was a profound increase in the protein expression of mTOR, Sin1, PKC & epsilon;, and phosphorylated PKC & epsilon; (Ser729). The PKC & epsilon; gene and protein expressions showed a statistically significant moderate association, according to a correlation analysis. Our results suggest that an elevated PKC & epsilon; protein expression in the amygdala during EW and EW + EtOH occurred at the transcriptional level. However, an elevation in the PKC & epsilon; protein expression, but not its mRNA, after chronic ethanol intake warrants further investigation to fully understand the signaling pathways during different episodes of AUD.