VOLUNTARY ETHANOL INTAKE INCREASES EXTRACELLULAR ACETYLCHOLINE LEVELS IN THE VENTRAL TEGMENTAL AREA IN THE RAT


    loading  Checking for direct PDF access through Ovid

Abstract

AimsConcurrent use of ethanol and nicotine (tobacco) is often seen in human beings. In previous animal experiments, we have demonstrated that nicotinic acetylcholine receptors, especially α-conotoxin MII and mecamylamine sensitive receptors located in the ventral tegmental area may be involved in the stimulatory, dopamine enhancing, and rewarding effects of ethanol in rodents. Ethanol may exert these effects via direct interaction with nicotinic acetylcholine receptors and/or indirectly via enhancement of extracellular acetylcholine levels in the ventral tegmental area. The present experiments investigated a possible indirect effect of ethanol in stimulating the mesoaccumbal dopamine system.MethodsNeurochemical effects of voluntary ethanol intake on extracellular ventral tegmental acetylcholine and accumbal dopamine levels were measured by means of in vivo microdialysis with a two-probe approach in freely moving rats.ResultsObtained data indicate that voluntary ethanol intake (∼0.7 g/kg/h) leads to an increase of extracellular acetylcholine levels in the ventral tegmental area, and an almost time-locked increase of dopamine levels in the nucleus accumbens. A positive correlation between the ventral tegmental acetylcholine levels and ethanol intake as well as preference was also observed.ConclusionThe present results suggest that voluntary ethanol intake enhances extracellular ventral tegmental acetylcholine that may interact with nicotinic acetylcholine receptors, possibly α-conotoxin MII sensitive receptors, localized in the ventral tegmental area that subsequently may stimulate dopamine overflow in the nucleus accumbens.

    loading  Loading Related Articles