Differential vulnerability to motor deficits in second replicate HAS and LAS rats following neonatal alcohol exposure.

Children exposed prenatally to alcohol suffer from a variety of behavioral alterations. However, variation exists in the pattern and severity of these alcohol-related neurodevelopmental disorders. We examined the influence of alcohol sensitivity in the etiology of fetal alcohol effects by studying rat lines selectively bred for extremes in alcohol-induced sleep time: high-alcohol-sensitive (HAS) and low-alcohol-sensitive (LAS) rats. Using subjects from the first replicate, we previously reported that HAS rats exposed to alcohol during development were more vulnerable to ethanol-induced hyperactivity and motor deficits compared to LAS rats. To determine if these effects were, in fact, related to the trait for which these subjects were selected, the present study examined the consequences of developmental alcohol exposure in second replicate HAS and LAS rats. Second replicate HAS and LAS rats, as well as Sprague-Dawley rats, were exposed to 6.0 g/kg/day ethanol on Postnatal Days (PD) 4-9, a period of brain development equivalent to the third trimester, via an artificial rearing procedure. Artificially and normally reared controls were included. Activity was measured on PD 18-21 and parallel bar motor coordination on PD 30-32. Ethanol exposure produced hyperactivity in all genetic groups, and there were no differences among HAS and LAS rats. In contrast, consistent with findings from the first replicate, ethanol-exposed HAS rats were more impaired on the motor coordination task compared with LAS rats. These data suggest that genetically mediated responses to alcohol may relate to behavioral vulnerability to motor deficits following developmental alcohol exposure. They also provide evidence that genetic factors play a role in fetal alcohol effects and suggest that phenotypic markers may indicate individuals at high risk for some fetal alcohol effects.