| Summary: | Withdrawal from long-term ethanol consumption results in overexcitation of glutamatergic neurotransmission
in the amygdala, which induces an anxiety-like syndrome. Most alcoholics that suffer from
such symptoms frequently depend on habitual drinking as self-medication to alleviate their symptoms.
Metabotropic glutamate receptor subtype 5 (mGlu5) and protein kinase C (PKC) epsilon have been reported
to mediate acute and chronic effects of ethanol. This study explores the changes in mGlu5 and
PKC epsilon in the amygdala following acute administration of ethanol during ethanol withdrawal (EW)
induced anxiety. Male Wistar rats were fed a modified liquid diet containing low-fat cow milk, sucrose,
and maltodextrin, with a gradual introduction of 2.4%, 4.8% and 7.2% ethanol for 20 days. Six hours into
EW, the rats were intraperitoneally injected with normal saline and ethanol (2.5 g/kg, 20% v/v), and
exposed to open-field and elevated plus maze tests. Then, amygdala tissue was dissected from the rat
brain for Western blot and gene expression studies. EW-induced anxiety was accompanied by a significant
increase in mGlu5, total PKC epsilon, and phosphorylated PKC epsilon protein levels, and also of
mRNA of mGlu5 (GRM5) in the amygdala. Acute administration of ethanol significantly attenuated EWinduced
anxiety as well as an EW-induced increase in GRM5. The acute challenge of ethanol to EW rats
had little effect on the phosphorylated and total protein levels of PKC epsilon in the amygdala. Our results
demonstrate that amygdala PKC epsilon may not be directly involved in the development of anxiety
following EW.
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