Denlinger S L, Patarca R, Hobson J A
Laboratory of Neurophysiology, Harvard Medical School, Boston, MA 02115.
Brain Res. 1988 Nov 8;473(1):116-26. doi: 10.1016/0006-8993(88)90322-8.
The cholinergic agonist carbachol and the beta-adrenergic antagonist propranolol were microinjected at the same pontine sites and their effects on polygraphic rapid eye movement (REM) sleep, especially pontogeniculo-occipital (PGO) waves, were measured. While both propranolol and carbachol enhanced PGO wave activity and polygraphic REM sleep, the carbachol-correlated enhancement was more impressive. The increases in REM sleep signs elicited by carbachol were 5-fold over baseline and lasted throughout the 4-h recording period. Propranolol elicited 2.5-fold increases that were significant in the first 2 h only. Yet, the increase in PGO wave activity evoked by propranolol was equal to that of carbachol during non-REM sleep and wakefulness. The results indicate that while propranolol is less potent in activating the distributed neuronal network responsible for REM sleep generation, it selectively facilities that part of the network responsible for PGO waves.
将胆碱能激动剂卡巴胆碱和β-肾上腺素能拮抗剂普萘洛尔微量注射到相同的脑桥部位,并测量它们对多导快速眼动(REM)睡眠,尤其是脑桥-膝状体-枕叶(PGO)波的影响。虽然普萘洛尔和卡巴胆碱均增强了PGO波活动和多导REM睡眠,但与卡巴胆碱相关的增强更为显著。卡巴胆碱引起的REM睡眠征象增加比基线高5倍,并在整个4小时记录期内持续存在。普萘洛尔引起的增加为2.5倍,仅在前2小时显著。然而,在非REM睡眠和清醒期间,普萘洛尔引起的PGO波活动增加与卡巴胆碱相当。结果表明,虽然普萘洛尔在激活负责REM睡眠产生的分布式神经网络方面效力较低,但它选择性地促进了负责PGO波的那部分网络。