Sherman J E, Kalin N H
Psychiatry Service, William S. Middleton Memorial Veterans Hospital, Madison, WI 53705.
Pharmacol Biochem Behav. 1988 Aug;30(4):801-7. doi: 10.1016/0091-3057(88)90103-7.
Freezing is an adaptive response often induced by stressful, fear-eliciting stimuli. Three experiments with rats investigated the effects of intracerebroventricular (ICV) administration of corticotropin-releasing hormone (CRH) on freezing behavior and pain sensitivity. Experiments 1 and 3 demonstrated that ICV-CRH (300 ng) enhanced shock-elicited freezing. In Experiment 1, ICV-CRH also enhanced recovery from shock-elicited freezing, suggesting that the peptide has a biphasic effect. Experiments 2 and 3 established that CRH-induced freezing was not caused by heightened pain sensitivity. Interestingly, in Experiment 2, hot-plate exposure produced increased freezing that was attenuated by ICV-CRH. Thus, the direction of the ICV-CRH effect on freezing was found to depend on the nature of the stressor. These results suggest that endogenous CRH systems modulate stress-induced freezing.
冻结是一种通常由应激性、引发恐惧的刺激所诱导的适应性反应。对大鼠进行的三项实验研究了脑室内(ICV)注射促肾上腺皮质激素释放激素(CRH)对冻结行为和疼痛敏感性的影响。实验1和实验3表明,脑室内注射300纳克CRH可增强电击诱发的冻结。在实验1中,脑室内注射CRH还能增强电击诱发的冻结的恢复,这表明该肽具有双相效应。实验2和实验3证实,CRH诱导的冻结并非由疼痛敏感性提高所致。有趣的是,在实验2中,热板暴露导致冻结增加,而脑室内注射CRH可使其减弱。因此,发现脑室内注射CRH对冻结的影响方向取决于应激源的性质。这些结果表明,内源性CRH系统调节应激诱导的冻结。