EFFECTS OF PRENATAL ETHANOL EXPOSURE ON ALCOHOL INTAKE AND MET-ENKEPHALIN EXPRESSION IN BRAIN REGIONS RELATED WITH REINFORCEMENT

ABATE P; HERNANDEZ FONSECA K.; REYES GUZMAN A.C.; BARBOSA LUNA I.G.; MÉNDEZ UBACH M.

Valencia

Congreso; 15th ESBRA Congress AND LASBRA; 2015

European Society for Biomedical Research on Alcoholism and Latin American Society for Biomedical Research on Alcoholism

The endogenous opioid system is involved in ethanol reinforcement.Ethanol-induced changes in opioidergic transmission have not beenextensively studied during infancy (postnatal days ?PDs- 14 and15).We investigated the effect of prenatal ethanol exposure on alcoholintake in rat pups. After behavioral tests, Methionine-enkephalin(Met-enk) was measured in the ventral tegmental area [VTA], nucleusaccumbens [NAcc], prefrontal cortex [PFC], substantia nigra [SN],caudate-putamen [CP], amygdala, hypothalamus and hippocampus.Pregnant rats were treated with ethanol (0 or 2 g/kg) during gestationaldays (GDs) 17?20. At PDs 14-15, preweanlingswere evaluated in anethanol intake test. Met-enk content in brain regions of infants prenatally exposed to ethanol was quantitated by radioimmunoassay.Infantile ethanol consumption was facilitated by prenatal experiencewith the drug. Infantile Met-enk content in PFC and NAcc was increasedas a consequence of prenatal exposure to ethanol. Conversely,Met-enk levels in the VTA were reduced by prenatal ethanol manipulation.Prenatal ethanol also increased peptide levels in the medialposteriorCP, hippocampus and hypothalamus. These findings showthat prenatal ethanol exposure stimulates consumption of the drugin infant rats, and induces changes in Met-enk levels in regions ofthe mesocorticolimbic and nigrostriatal systems, hypothalamusand hippocampus. Our results support the role of mesocorticolimbicenkephalins in ethanol reinforcement in infancy, as has been reportedin adults. This work was supported by grants from CONICETArgentina(PA) and CONACyT, 82728-Mexico (MM).