Abstract
This review summarizes the data showing the possible involvement of an endogenous ligand for benzodiazepine (BDZ) receptors, diazepam binding inhibitor (DBI), in the development of alcohol dependence. The expression of cerebral DBI mRNA significantly increased in EtOH-inhaled and EtOH-withdrawn mice in comparison with that in EtOH-untreated mice, whereas the DBI mRNA level was not altered after a single administration of EtOH. After EtOH-withdrawal, this increase in the DBI mRNA expression in the mouse cerebral cortex diminished over 14 days despite the disappearance of withdrawal signs within 2 days after the withdrawal of EtOH. Simultaneous administration of flunitrazepam, a BDZ receptor agonist, with EtOH completely abolished the EtOH-induced increase in DBI mRNA expression. These results lead to the assumption that the changes in the expression of cerebral DBI mRNA induced by continuous EtOH treatment may be involved in the establishment of alcohol dependence, and such changes may be also regulated by BDZ receptors.
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