Sastre J P, Sakai K, Jouvet M
Brain Res. 1981 Dec 14;229(1):147-61. doi: 10.1016/0006-8993(81)90752-6.
We have compared the effects of electrolytic and kainic acid lesions of the pontine gigantocellular tegmental field (FTG) upon paradoxical sleep (PS). Following bilateral electrolytic destruction of the ventrolateral part of the FTG, there was an almost total suppression of PS which lasted at least for 5 weeks. Muscular atonia was absent and ponto-geniculo-occipital (PGO) activity was reduced by 80% in the few remaining episodes of PS. Contrary to to these effects, total neuronal cell loss of the FTG induced by bilateral kainic acid injection was not followed by a significant quantitative and qualitative alteration of PS. These results indicate that the neurons located within the FTG are not critical for the generation of both phasic and tonic components of PS. Elimination of this state of sleep after electrolytic destruction of the ventrolateral pontine reticular formation can be explained by interruption of fibers connecting the region of the locus coeruleus complex and the bulbar reticular formation.
我们比较了脑桥巨细胞被盖区(FTG)的电解损伤和 kainic 酸损伤对异相睡眠(PS)的影响。在 FTG 腹外侧部分进行双侧电解破坏后,PS 几乎完全被抑制,这种抑制至少持续 5 周。在仅存的少数 PS 发作中,肌肉弛缓消失,脑桥-膝状体-枕叶(PGO)活动减少了 80%。与这些效应相反,双侧注射 kainic 酸诱导的 FTG 神经元完全丧失后,PS 并未出现显著的数量和质量改变。这些结果表明,位于 FTG 内的神经元对于 PS 的相位和紧张性成分的产生并非至关重要。电解破坏腹侧脑桥网状结构后这种睡眠状态的消除可通过连接蓝斑复合体区域和延髓网状结构的纤维中断来解释。