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pubmed:abstractText |
Binge-like exposure to ethanol early in development results in neurotoxic impairments throughout the brain, including the cerebellum and brainstem. Rats exposed to ethanol, during a period of time commensurate with the human third trimester, also show deficits in classical eyeblink conditioning (EBC), a cerebellar-dependent associative learning procedure. The relationship between ethanol-mediated EBC deficits and the intensity of the unconditioned stimulus (US) was explored in the current study. Neonatal rats were intubated and infused with ethanol (EtOH rats), sham-intubated and given no ethanol (SI rats), or reared as unhandled controls (UC rats). As adults, all rats underwent 10 days of 350 ms delay eyeblink conditioning with a tone conditioned stimulus (CS) and one of three co-terminating periorbital shock US. The frequency and topography of the conditioned eyeblink response (CR) were impaired in EtOH rats relative to UC rats. EtOH rats produced fewer CRs, with longer onset latencies, at all US intensities. In contrast, CR amplitude was impaired in EtOH rats at the highest US intensity only. Following conditioning, the unconditioned eyeblink response (UR) was analyzed in subsets of rats from each treatment group at five US intensities. Early ethanol exposure did not impair UR peak amplitude. The deficits in CR production are proposed to result from ethanol-mediated damage within specific regions of the EBC neural circuit.
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