Postnatal binge ethanol exposure affects habituation of the cardiac orienting response to an olfactory stimulus in preweanling rats.

Abstract

Prenatal exposure to alcohol can result in intellectual impairments, reduced habituation and distractibility, visual-spatial deficits, and problems in attention. Dysfunction in attention, including habituation of responses to nonsignal stimuli, can have devastating consequences for cognitive development. This research examined whether binge exposure to ethanol on postnatal days (PD) 4 to 9 would affect cardiac orienting or response habituation to an olfactory stimulus in preweanling rats. Ethanol-exposed subjects were given ethanol 5.25 g/kg/day on PD4 to 9. Controls were either sham intubated or unhandled during this time. To assess baseline and phasic cardiac function, PD16 subjects were tested under differential pharmacological blockade of the sympathetic or parasympathetic nervous systems by administration of the peripherally acting antagonists atenolol or atropine methyl nitrate. In a second experiment, separate groups of subjects were tested for habituation of the cardiac orienting response to an olfactory stimulus. Results indicate that postnatal ethanol had no observable effect on the functional development of autonomic control over heart rate. Similarly, ethanol exposure had no effect on the form or magnitude of the cardiac orienting response. However, neonatal ethanol exposure did result in a deficit in orienting response habituation; ethanol-exposed subjects continued to respond to the stimulus with a large-magnitude bradycardia after control subjects exhibited complete response habituation. In addition, ethanol-exposed subjects had longer orienting response latencies than controls. The results indicate that this animal model has the potential to contribute to investigations designed to understand basic forms of memory impairments observed in humans with a history of prenatal alcohol exposure. The postnatal binge ethanol model of fetal alcohol effects produces deficits in nonassociative memory that are similar to those observed in human infants exposed prenatally to ethanol. Deficits in response habituation have important implications for cognitive development.