Hippocampal-dependent Pavlovian conditioning in adult rats exposed to binge-like doses of ethanol as neonates

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Abstract

HIGHLIGHTS

★ Early ethanol exposure damages the brain, including the cerebellum and hippocampus. ★ Hippocampal function assessed via trace eyeblink conditioning. ★ Trace eyeblink conditioning was unimpaired by early ethanol exposure. ★ Hippocampal function assessed via contextual gating of eyeblink conditioned response. ★ Contextual control of conditioned response was unimpaired by early ethanol exposure. ★ Results best explained by ethanol-induced cerebellar damage.

Binge-like postnatal ethanol exposure produces significant damage throughout the brain in rats, including the cerebellum and hippocampus. In the current study, cue- and context-mediated Pavlovian conditioning were assessed in adult rats exposed to moderately low (3E; 3 g/kg/day) or high (5E; 5 g/kg/day) doses of ethanol across postnatal days 4–9. Ethanol-exposed and control groups were presented with 8 sessions of trace eyeblink conditioning followed by another 8 sessions of delay eyeblink conditioning, with an altered context presented over the last two sessions. Both forms of conditioning rely on the brainstem and cerebellum, while the more difficult trace conditioning also requires the hippocampus. The hippocampus is also needed to gate or modulate expression of the eyeblink conditioned response (CR) based on contextual cues. Results indicate that the ethanol-exposed rats were not significantly impaired in trace EBC relative to control subjects. In terms of CR topography, peak amplitude was significantly reduced by both doses of alcohol, whereas onset latency but not peak latency was significantly lengthened in the 5E rats across the latter half of delay EBC in the original training context. Neither dosage resulted in significant impairment in the contextual gating of the behavioral response, as revealed by similar decreases in CR production across all four treatment groups following introduction of the novel context. Results suggest ethanol-induced brainstem-cerebellar damage can account for the present results, independent of the putative disruption in hippocampal development and function proposed to occur following postnatal ethanol exposure.

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