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Synapse. 2010 Sep;64(9):729-32. doi: 10.1002/syn.20795.

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

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Department of Psychiatry, Yale University School of Medicine and the VACHS, New Haven, CT 06516, USA.


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.

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