Decreased beta2*-nicotinic acetylcholine receptor availability after chronic ethanol exposure in nonhuman primates

Abstract

Ethanol associated behaviors have been linked to the β2- subunit containing nicotinic acetylcholine receptors (β2*- nAChR); however, there is conflicting evidence on ethanol-induced changes in nAChR expression during and after chronic ethanol consumption. In this study, five male animals orally self-administered ethanol for 18 ± 1 weeks. Animals were scanned with [123I]5-IA-85380 and SPECT prior to ethanol self-administration, and at 24 h and 5-13 wks withdrawal. β2 *-nAChR availability was not significantly different from baseline at 24 h withdrawal, but was significantly decreased compared to baseline at 5-13 wks withdrawal throughout the cortex and in the thalamus, but not the midbrain. The percent decrease in β2*-nAChR availability from baseline to 5-13 wks withdrawal in the parietal cortex was negatively correlated with total grams of ethanol consumed in lifetime and in the midbrain was negatively correlated with average daily ethanol consumption (g/kg). Prolonged withdrawal from chronic ethanol consumption is associated with a decrease in β2*-nAChR availability. The decrease in β2*-nAChR availability is influenced by alcohol consumption, suggesting the chronicity and severity of alcohol consumption may underlie persistent changes in β2*-nAChR availability. © 2010 Wiley-Liss, Inc.