FIGURE 5.

Adult galantamine treatment restored the adolescent intermittent ethanol (AIE)-induced loss and somal shrinkage of cholinergic neurons in the adult basal forebrain. (A) Modified unbiased stereological assessment revealed an 18% (±4%) reduction of choline acetyltransferase immunoreactive (ChAT + IR) neurons in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone from P57 to P73 did not affect ChAT + IR in CONs, but restored the AIE-induced loss of ChAT + IR neurons in adulthood, relative to vehicle-treated AIE subjects. (B) Modified unbiased stereological assessment revealed a 23% (±3%) reduction of tropomyosin receptor kinase A immunoreactive (TrkA + IR) neurons in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone did not affect TrkA + IR in CONs, but restored the AIE-induced loss of TrkA + IR neurons in adulthood, relative to vehicle-treated AIE subjects. (C) Modified unbiased stereological assessment revealed a 30% (±6%) reduction of p75 neurotrophin receptor immunoreactive (p75^NTR + IR) neurons in the adult (P73) basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone did not affect p75^NTR + IR in CONs, but restored the AIE-induced loss of p75^NTR + IR neurons in adulthood, relative to vehicle-treated AIE subjects. (D) Analysis of ChAT + neuron somal size revealed an 18% (±2%) reduction in somal size of the residual ChAT + neurons in the adult basal forebrain of AIE-treated subjects, relative to CONs. Adult galantamine treatment alone did not affect ChAT + somal size, but restored the AIE-induced somal shrinkage of ChAT + cholinergic neurons in the adult basal forebrain, relative to vehicle-treated AIE subjects. Data are presented as mean ± SEM (n = 8/group). ^∗p < 0.05, ^∗∗p < 0.01.