Increase of diazepam binding inhibitor mRNA levels in the brains of chronically ethanol-treated and -withdrawn mice.
Increase of diazepam binding inhibitor mRNA levels in the brains of chronically ethanol-treated and -withdrawn mice.
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长期乙醇治疗和戒断小鼠大脑中地西泮结合抑制剂 mRNA 水平增加。
DOI：
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发表时间：
1995
影响因子：
3.5
通讯作者：
K. Kuriyama
中科院分区：
文献类型：
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作者：
M. Katsura;S. Ohkuma;A. Tsujimura;K. Kuriyama
虽然在乙醇（EtOH）依赖性和戒断动物中观察到的行为反应的分子机制尚不清楚，但有几条证据表明，EtOH的某些药理作用是通过增强γ-氨基丁酸（GABA）能传递介导的。在本研究中，急性和慢性乙醇处理的影响，地西泮结合抑制剂（DBI）mRNA的表达在小鼠脑和苯二氮卓类（BDZ）受体的功能参与乙醇诱导的DBI mRNA表达的改变进行了检查。与未处理的小鼠相比，EtOH处理的小鼠（对照的130%）和EtOH撤回的小鼠（对照的220%）的脑DBI mRNA的表达显著增加，而DBI mRNA水平在单次给予EtOH（3 g/kg i. p.）后没有改变。在小鼠大脑皮层中的DBI mRNA表达的增加后，乙醇撤出减少超过14天，尽管在2天内的撤药迹象消失后，乙醇撤出。同时给予氟硝西泮（10 mg/kg i. p.）用EtOH完全消除EtOH诱导的DBI mRNA表达的增加。另一方面，β-肌动蛋白mRNA的水平不受类似的EtOH处理的影响。这些结果表明，脑DBI mRNA表达的变化，由长期乙醇处理可能参与酒精依赖的建立，这种变化也可能是由BDZ受体调节。
Although the molecular mechanisms underlying behavioral responses observed in ethanol (EtOH)-dependent and -withdrawn animals are poorly understood, several lines of evidence have suggested that some of the pharmacological actions of EtOH are mediated via the potentiation of gamma-aminobutyric acid (GABA)ergic transmission. In the present study, the effects of acute and chronic EtOH treatment on the expression of diazepam binding inhibitor (DBI) mRNA in the mouse brain and the functional involvement of the benzodiazepine (BDZ) receptor in EtOH-induced alteration of the DBI mRNA expression were examined. The expression of cerebral DBI mRNA significantly increased in EtOH-treated (130% of control) and EtOH-withdrawn (220% of control) mice in comparison with untreated mice, whereas the DBI mRNA level was not altered after a single administration of EtOH (3 g/kg i.p.). The increase in the DBI mRNA expression in the mouse cerebral cortex after EtOH withdrawal diminished over 14 days despite the disappearance of withdrawal signs within 2 days after the withdrawal of EtOH. Simultaneous administration of flunitrazepam (10 mg/kg i.p.) with EtOH completely abolished the EtOH-induced increase in DBI mRNA expression. On the other hand, the level of beta-actin mRNA was not affected by similar EtOH treatment. These results indicate that changes in the expression of cerebral DBI mRNA induced by long-term EtOH treatment may be involved in the establishment of alcohol dependence, and such changes may be also regulated by BDZ receptors.