کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4312913 | 1612994 | 2013 | 6 صفحه PDF | دانلود رایگان |
Recent studies suggest that the brain histaminergic system and especially the H3 receptors are involved in the regulation of alcohol consumption and alcohol-induced behaviors. Part of this effect might be due to a modulation of ethanol-induced sedation by central histamine. The aim of the present study was to investigate the effects of several histaminergic drugs on ethanol-induced sedation using the loss of righting reflex experimental protocol in female Swiss mice. A pretreatment with l-histidine, the histamine precursor, significantly reduced ethanol-induced sedation, suggesting that brain histamine protects against the sedative effects of ethanol. In a second set of experiments, several H3 receptor agonists (immepip or imetit) and inverse agonists/antagonists (thioperamide, A331440, or BF2.649) were tested. Surprisingly, both H3 receptor agonists and antagonists potentiated the sedative effects of ethanol. This paradoxical effect might be due to the subtle regulatory actions related to the H3 heteroreceptor function.
► The effects of histaminergic drugs were tested on the sedative effects of ethanol in mice.
► Ethanol-induced sedation was tested with the loss of righting reflex procedure.
► The histamine precursor, l-histidine, decreased the sedative effects of ethanol.
► H3 receptors agonists and inverse agonists potentiated the sedative effects of ethanol.
► The H3 heteroreceptor function probably contributes to these effects.
Journal: Behavioural Brain Research - Volume 238, 1 February 2013, Pages 113–118