Rodgers R J
Neuropharmacology. 1982 Dec;21(12):1291-4. doi: 10.1016/0028-3908(82)90135-6.
Two opiate antagonists, naloxone and diprenorphine, were used to examine the proposed involvement of endogenous opioid mechanisms in the modulation of shock-induced defensive behaviour patterns in rats. Naloxone was found to exert a biphasic influence on defensive fighting, with small dose (0.1 mg/kg) facilitation and large dose (10 mg/kg) inhibition. This compound also induced a dose-dependent inhibitory effect on shock-elicited threat whilst facilitated escape/avoidance behaviour was observed with the largest doses only. None of these influences could be attributed to alterations in electric shock thresholds. In contrast to the effects of naloxone, diprenorphine (0.1-10 mg/kg) was largely ineffective in modifying shock-induced defensive behaviour. These data suggest that endogenous opioid mechanisms may not be involved in the effects of naloxone on defensive fighting and cast some doubt upon the general hypothesis of the involvement of endorphins in the regulation of innate defence patterns.
使用两种阿片类拮抗剂纳洛酮和二丙诺啡,来检验内源性阿片机制是否参与调节大鼠休克诱导的防御行为模式。发现纳洛酮对防御性争斗有双相影响,小剂量(0.1毫克/千克)促进,大剂量(10毫克/千克)抑制。该化合物对休克诱发的威胁也有剂量依赖性抑制作用,而仅在最大剂量时观察到对逃避/回避行为有促进作用。这些影响均不能归因于电击阈值的改变。与纳洛酮的作用相反,二丙诺啡(0.1 - 10毫克/千克)在改变休克诱导的防御行为方面基本无效。这些数据表明内源性阿片机制可能不参与纳洛酮对防御性争斗的作用,并对内啡肽参与先天防御模式调节的一般假说提出了一些质疑。