Decreased Beta(2)*-nicotinic acetylcholine receptor availability after chronic ethanol exposure in nonhuman primates

Abstract

Ethanol associated behaviors have been linked to the beta(2)-subunit containing nicotinic acetylcholine receptors (beta(2)*-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 [(123)I]5-IA-85380 and SPECT prior to ethanol self-administration, and at 24 h and 5-13 wks withdrawal. beta(2)*-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 beta(2)*-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 beta(2)*-nAChR availability. The decrease in beta(2)*-nAChR availability is influenced by alcohol consumption, suggesting the chronicity and severity of alcohol consumption may underlie persistent changes in beta(2)*-nAChR availability.

Figure 1

β₂*-nAChR availability (BP_ND) in 5 animals at baseline, e.g., prior to this ethanol exposure, at 24 h and 5–13 wks abstinence in the average cortex (average of frontal, parietal, cingulate, temporal and occipital), midbrain, and thalamus. Each symbol represents an individual data point and the lines represent the mean. * indicates significantly different from baseline at p<0.05.