Thyroxine administration prevents matrilineal intergenerational consequences of in utero ethanol exposure in rats.

ABSTRACT: The neurodevelopmental fetal alcohol spectrum disorder (FASD) is characterized by cognitive and behavioral deficits in the offspring. Conferring the deficits to the next generation would increase overall FASD disease burden and prevention of this transmission could be highly significant. Prior studies showed the reversal of these behavioral deficits by low dose thyroxine (T4) supplementation to the ethanol-consuming mothers. Here we aim to identify whether prenatal ethanol (PE) exposure impairs hippocampus-dependent learning and memory in the second-generation (F2) progeny, and whether T4 administration to the ethanol-consuming dam can prevent it. Sprague-Dawley (S) dams received control diets (ad libitum and nutritional control) or ethanol containing liquid diet with and without simultane

SUBMITTER: Tunc-Ozcan E 

PROVIDER: S-EPMC4902747 | biostudies-literature | 2016 Jun

REPOSITORIES: biostudies-literature