Orexin and its receptors were shown to be involved into mechanisms of pathological craving to alcohol. This paper demonstrates that the orexin receptor type 1 (OX1R) mRNA level significantly decreased in the prefrontal cortex of rats chronically (during 6 months) consuming ethanol compared with intact control. The same results were observed on day 1 and day 7 of alcohol withdrawal after chronic alcoholization. On the contrary, in the hippocampus, the OX1R mRNA level increased on day 1 and day 7 of alcohol withdrawal. In the ventral tegmental area, the OX1R mRNA level did not change on the day 1 and day 7 of alcohol withdrawal compared with the groups of chronic alcoholization and intact control. These findings point out involvement of the prefrontal cortex and hippocampus first of all in mechanisms mediating chronic alcohol intoxication. The ventral tegmental area is described as a typical dopaminergic structure providing the executive mechanism of emotion reactions connected with alcohol abuse in particular. It is possibe, that the modulating action of orexins on dopaminergic neurons in this structure does not provide a significant effect on control of emotion reactions in alcoholism.
Oreksin i ego retseptory vovlecheny v mekhanizmy patologicheskogo vlecheniia k alkogoliu. V dannoĭ rabote pokazano, chto uroven' mRNK OX1R dostoverno snizhaetsia v prefrontal'noĭ kore u gruppy khronicheski alkogolizirovannykh (6 mes) krys v sravnenii s intaktnoĭ gruppoĭ kontrolia, takzhe nabliudetsia snizhennaia ékspressiia gena OX1R na pervyĭ i sed'moĭ dni otmeny étanola. V gippokampe, naprotiv, nabliudaetsia uvelichenie urovnia mRNK OX1R na pervyĭ i sed'moĭ dni abstinentsii. V ventral'noĭ oblasti pokryshki uroven' mRNK OX1R na pervyĭ i sed'moĭ dni po otnosheniiu k gruppe khronicheskoĭ alkogolizatsii i k gruppe intaktnykh zhivotnykh ne izmenialsia. Éto ukazyvaet na vovlechennost' prefrontal'noĭ kory i gippokampa v mekhanizmy, oposreduiushchie khronicheskuiu alkogol'nuiu intoksikatsiiu.
Keywords: OX1R; alcoholism; neuropeptides; orexin.