1. Adolescent binge ethanol exposure reduces cholinergic marker expression in the whole mouse brain.
Adolescent binge ethanol exposure reduces cholinergic marker expression in the whole mouse brain. Adolescent mice received either water (CON) or ethanol (EtOH; 5.0 g/kg, i.g.) once per day for 10 consecutive days from P28 to P37. Alcohol treatment ended on P37. Shown in (A–D) are expression levels (mRNA) 1 day after the last AIE dose of ethanol and 50 days after the last dose in AIE animals (Coleman et al., 2011). Changes in controls represent maturation from adolescence to adulthood. (A) mRNA levels of ChAT, the acetylcholine-synthesizing enzyme, were reduced by 55% in adolescent mouse whole brain samples 24 hours after the conclusion of EtOH exposure (P38) as well as by 58% in adulthood (P88) compared with CON. (B) Comparison of ChAT immunohistochemistry revealed an 8% reduction of ChAT–immunopositive cells in the posterior basal forebrain of EtOH-treated adult mice, relative to CON. (C) mRNA expression of muscarinic acetylcholine receptor subtypes R1 and R5 was reduced 24 hours after the conclusion of EtOH exposure by 62% and 54%, respectively, which persisted into adulthood (R1: ↓45%; R5: ↓50%). (D) Similarly, mRNA expression of nicotinic acetylcholine receptor subtypes α4 and α7 was reduced by 30% and 56% at the conclusion of EtOH exposure, respectively, that persisted into adulthood (α4: ↓48%; α7: ↓54%). These data reveal that adolescent binge ethanol exposure leads to long-term alterations in the cholinergic system that might contribute to cognitive dysfunction in adulthood. Data are presented as mean ± S.E.M. *p < 0.05, relative to CON, and are adapted from Coleman et al. (2011).
Fulton T. Crews et al. Pharmacol Rev 2016;68:
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