CHRONIC ETHANOL INGESTION PRODUCES CHOLINERGIC HYPOFUNCTION IN RAT-BRAIN

Citation
Ea. Floyd et al., CHRONIC ETHANOL INGESTION PRODUCES CHOLINERGIC HYPOFUNCTION IN RAT-BRAIN, Alcohol, 14(1), 1997, pp. 93-98
Citations number
28
Categorie Soggetti
Substance Abuse","Pharmacology & Pharmacy",Toxicology
Journal title
ISSN journal
07418329
Volume
14
Issue
1
Year of publication
1997
Pages
93 - 98
Database
ISI
SICI code
0741-8329(1997)14:1<93:CEIPCH>2.0.ZU;2-S
Abstract
Alterations in cholinergic function due to prolonged ethanol exposure (up to 9 months) were assessed by choline acetyl transferase (ChAT) ac tivity and high-affinity choline uptake (HAChU) in three brain regions of the Long-Evans rat: frontal cortex, parietal cortex, and region of the nucleus basalis of Meynert (NbM). No statistically significant ch anges were found in ChAT activity in the 3-month group; however, ChAT activity was decreased in both the frontal cortex (-32%) and NbM regio n (-22%) after 6 months of ethanol exposure. ChAT activity in the pari etal cortex was increased 30% after 6 months. Nine months of exposure significantly decreased ChAT activity in all three brain regions. No s ignificant differences were observed in high-affinity choline uptake a fter 3 months of ethanol exposure. However, after 6 months of ethanol exposure HAChU was decreased to 51% of control values in the frontal c ortex. There was a simultaneous increase in HAChU to 43% and 178% of c ontrol values in the NbM and parietal cortex, respectively. However, c holine uptake was significantly decreased in the frontal cortex and Nb M region after 9 months of exposure. The results indicate a neurotoxic effect of prolonged intake of ethanol on the basal forebrain choliner gic projection system, which may cause impairment of cholinergic inner vation of target areas of the basal nucleus complex. Copyright (C) 199 7 Elsevier Science Inc.