Abstract
Acute exposure (20 min) to loud noise (100 dB) decreased sodium-dependent high-affinity choline uptake activities in the frontal cortex and hippocampus of the rat. These effects were blocked by intracerebroventricular (i.c.v.) administration of the cotricotropin-releasing factor (CRF) antagonist α-helical-CRF 9–41 (α-HCRF) immediately before noise exposure. Intracerebroventricular injection of CRF (1 μg) also decreased high-affinity choline uptake in the frontal cortex and the hippocampus of the rat, and these effects of CRF could be blocked by pretreating the animal with the narcotic antagonist naltrexone (1 mg/kg, i.p.). These results indicate that the effects of noise on central cholinergic systems are mediated by CRF and suggest a stressor-CRF-endogenous opioid-acetylcholine sequence of effects in the brain.
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