Wood A L, Healey P A, Menéndez J A, Verne S L, Atrens D M
Department of Psychology, University of Sydney, NSW, Australia.
Life Sci. 1989;45(16):1467-73. doi: 10.1016/0024-3205(89)90037-4.
The ability of the putative ethanol antagonist RO 15-4513 to antagonize ethanol - induced hypoactivity, hypothermia and hyperglycemia was investigated in rats. Although RO 15-4513 produced hypoactivity by itself, it attenuated ethanol - induced hypoactivity. This antagonism suggests that ethanol - induced hypoactivity is mediated by the GABA-benzodiazepine receptor complex which is thought to be the site of action of RO 15-4513. In contrast, although RO 15-4513 produced hypothermia by itself, it had no significant effect on ethanol - induced hypothermia. This suggests that the hypothermic effect of ethanol is not mediated by the GABA-benzodiazepine receptor complex. The fact that RO 15-4513, ethanol and the vehicle all produced hyperglycemia suggests a common stress effect and does not permit any firm conclusions to be drawn as to the interaction between ethanol and RO 15-4513 in modulating glycemic responses. These data indicate that the ethanol antagonism of RO 15-4513 is primarily confined to ethanol's behavioural effects and that ethanol's behavioural and physiological effects are mediated by neurochemically distinct mechanisms.
在大鼠中研究了假定的乙醇拮抗剂RO 15 - 4513拮抗乙醇诱导的活动减退、体温过低和高血糖的能力。尽管RO 15 - 4513自身会引起活动减退，但它能减轻乙醇诱导的活动减退。这种拮抗作用表明，乙醇诱导的活动减退是由γ-氨基丁酸-苯二氮䓬受体复合物介导的，而该复合物被认为是RO 15 - 4513的作用位点。相比之下，尽管RO 15 - 4513自身会引起体温过低，但它对乙醇诱导的体温过低没有显著影响。这表明乙醇的体温过低效应不是由γ-氨基丁酸-苯二氮䓬受体复合物介导的。RO 15 - 4513、乙醇和溶媒均会引起高血糖这一事实表明存在共同的应激效应，并且无法就乙醇和RO 15 - 4513在调节血糖反应中的相互作用得出任何确凿结论。这些数据表明，RO 15 - 4513对乙醇的拮抗作用主要局限于乙醇的行为效应，并且乙醇的行为和生理效应是由神经化学上不同机制介导的。
