Vasar E E, Riago L K, Allikmets L Kh
Zh Vyssh Nerv Deiat Im I P Pavlova. 1983 Sep-Oct;33(5):864-9.
In experiments of male Wistar rats, it was established that a long-term apomorphine treatment caused changes in density of benzodiazepine receptors in forebrain structures opposite to those elicited by acute administration. The changes in benzodiazepine binding correlated with decrease of antiaggressive effect of diazepam and Ro 15-1788 after long-term apomorphine administration. The action of apomorphine on the benzodiazepine receptors was not direct, as apomorphine did not change the benzodiazepine agonist-antagonist interaction, and naloxone, opiate blocator, was a more powerful antagonist of antiaggressive action of diazepam than Ro 15-1788. The involvement of the two types of benzodiazepine receptors in the regulation of aggressive behavior is suggested, the first being apparently linked with GABA and opiate receptors and the other one--with the serotoninergic system. Ro 15-1788 was able to antagonize the effects of diazepam on the first but not on the second type of benzodiazepine receptors.
在雄性Wistar大鼠实验中发现，长期给予阿扑吗啡治疗会导致前脑结构中苯二氮䓬受体密度发生变化，这种变化与急性给药所引发的变化相反。长期给予阿扑吗啡后，苯二氮䓬结合的变化与地西泮和Ro 15 - 1788抗攻击作用的降低相关。阿扑吗啡对苯二氮䓬受体的作用并非直接作用，因为阿扑吗啡不会改变苯二氮䓬激动剂 - 拮抗剂的相互作用，并且阿片受体阻断剂纳洛酮比Ro 15 - 1788更能有效拮抗地西泮的抗攻击作用。这表明两种类型的苯二氮䓬受体参与攻击行为的调节，第一种显然与GABA和阿片受体有关，另一种与5 - 羟色胺能系统有关。Ro 15 - 1788能够拮抗地西泮对第一种而非第二种类型苯二氮䓬受体的作用。
