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RESEARCH PRODUCT

Emotional memory impairment produced by binge drinking in mice is counteracted by the anti-inflammatory indomethacin

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Abstract The Binge Drinking (BD) pattern of alcohol consumption, prevalent in adolescents and young adults, has been associated with memory impairment. In addition, evidence shows that alcohol abuse causes neuroinflammation, which may contribute to the brain damage produced by alcohol and explain its cognitive consequences. In this study, we evaluated the effectiveness of the anti-inflammatory indomethacin in counteracting the memory impairment produced by alcohol (ethanol) in adolescent mice of both sexes. Animals were randomly assigned to one of four groups for each sex: SS (saline + saline), SA (saline + alcohol), SI (saline + indomethacin) and AI (alcohol + indomethacin). They were injected acutely (Experiment 1) or chronically intermittent (Experiment 2) with saline, ethanol (3 g/kg) and indomethacin (10 mg/kg). All subjects were evaluated in an inhibitory avoidance task 96 h after treatment. With acute administration, SA groups showed significantly lower Test latencies than SS groups, while AI groups had similar latencies to controls. The chronic-intermittent administration of alcohol, an animal model of BD, produced significant emotional memory impairment -blocking learning in males- which was counteracted by indomethacin, as the AI groups had similar latencies to the SS groups. No significant differences were observed in locomotor activity or analgesia. In conclusion, alcohol BD (one or several episodes) impairs emotional memory in mice. This impairment is not secondary to the effects of alcohol BD on locomotor activity or pain sensitivity, and it is counteracted by indomethacin. Therefore, the memory impairment produced by alcohol BD seems to be mediated, in part, by neuroinflammatory processes. These findings open a window for new treatments for alcohol use disorders.