Multiple
alcohol use disorder (AUD)-related behavioral alterations are governed by
protein kinase C epsilon (PKCε), 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 PKCε 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. PKCε
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, PKCε, and phosphorylated PKCε (Ser729). The PKCε gene and
protein expressions showed a statistically significant moderate association, according to a correlation analysis. Our results suggest that an elevated PKCε
protein expression in the amygdala during EW and EW + EtOH occurred at the transcriptional level. However, an elevation in the PKCε
protein expression, but not its
mRNA, after chronic
ethanol intake warrants further investigation to fully understand the signaling pathways during different episodes of AUD.