Prenatal ethanol increases ethanol intake throughout adolescence, alters ethanol- and LiCl mediated aversive learning; and affects mu, but not delta or kappa, opioid receptor mRNA expression .

FABIO, MC; MACCHIONE, AF; NIZHNIKOV, ME; PAUTASSI, RM

EUROPEAN JOURNAL OF NEUROSCIENCE

WILEY-BLACKWELL PUBLISHING, INC

Lugar: Londres; Año: 2015 vol. 41 p. 1569 - 1579

0953-816X

Animal models of prenatal ethanol exposure (PEE) have indicated a facilitatory effect of PEE on adolescent ethanol intake, but few studies have assessed the effects of moderate PEE throughout adolescence. The mechanisms underlying this facilitatory effect remain largely unknown. The present study analyzed ethanol intake in male and female Wistar rats with or without PEE (2.0 g/kg, gestational days 17-20) from postnatal days 37 to 62. The results revealed greater ethanol consumption in PEE animals than in controls, which persisted throughout adolescence. By the end of testing, ethanol ingestion in PEE animals neared 6.0 g/kg. PEE was associated with alterations in the extinction of aversive taste learning and insensitivity to ethanol-induced aversion. PEE and control animals were further analyzed for levels of , , and  opioid receptor mRNA in the infralimbic cortex, nucleus accumbens shell, and ventral tegmental area. Similar levels of mRNA were observed across most areas and opioid receptors, but  receptor mRNA in the ventral tegmental area was significantly increased by PEE. Unlike previous studies that assessed the effects of PEE on ethanol intake close to birth, or in only a few sessions during adolescence, the present study observed a facilitatory effect of PEE that lasted throughout adolescence. PEE was associated with insensitivity to the aversive effect of ethanol, and increased levels of  opioid receptor transcripts. PEE is a prominent vulnerability factor that likely favors the engagement of adolescents in risky trajectories of ethanol use.