Hu B, Steriade M, Deschênes M
Département de Physiologie, Faculté de Médecine, Université Laval, Québec, Canada.
Neuroscience. 1989;31(1):25-35. doi: 10.1016/0306-4522(89)90028-6.
The cellular mechanisms underlying the genesis of thalamic ponto-geniculo-occipital waves were studied in reserpinized cats under urethane anaesthesia. Simultaneous field potential and intracellular recordings were performed in the lateral geniculate nucleus after acute lesions of retinal and visual cortical inputs. In most relay cells, reserpine-induced ponto-geniculo-occipital waves were associated with a transient depolarization that was often interrupted by a unitary inhibitory postsynaptic potential. The depolarization grew in size with membrane hyperpolarization and was accompanied by an increase in membrane conductance. The inhibitory postsynaptic potential is likely to have resulted from the activation of intrageniculate interneurons since perigeniculate cells were always inhibited during the occurrence of ponto-geniculo-occipital waves. Under reserpine, thalamic ponto-geniculo-occipital waves could also be triggered by peribrachial or auditory stimulation. These evoked ponto-geniculo-occipital waves were associated with intracellular events identical to those occurring spontaneously after reserpine administration. In addition, thalamic spindle oscillations were readily blocked by the occurrence of spontaneous or evoked ponto-geniculo-occipital waves. On the basis of the present results and those already published in the literature, the conclusion is reached that lateral geniculate ponto-geniculo-occipital waves result from a nicotinic activation of relay cells and from a parallel muscarinic inhibition of perigeniculate cells by peribrachial afferents. The functional significance of the ponto-geniculo-occipital activity is discussed on the basis of the antagonistic action of these signals on thalamic oscillations. It is proposed that these signals are the central correlates of orienting reactions elicited by sensory stimuli during waking (the so-called eye movement potentials) and by internally generated drives during paradoxical sleep.
在乌拉坦麻醉下的利血平化猫中,研究了丘脑桥脑 - 膝状体 - 枕叶波产生的细胞机制。在视网膜和视觉皮层输入急性损伤后,在外侧膝状核进行了同步场电位和细胞内记录。在大多数中继细胞中,利血平诱导的桥脑 - 膝状体 - 枕叶波与短暂去极化相关,这种去极化常被单一抑制性突触后电位中断。去极化大小随膜超极化而增加,并伴有膜电导增加。抑制性突触后电位可能是由膝状体内中间神经元的激活引起的,因为在桥脑 - 膝状体 - 枕叶波出现期间,膝状体周围细胞总是被抑制。在利血平作用下,丘脑桥脑 - 膝状体 - 枕叶波也可由臂周或听觉刺激触发。这些诱发的桥脑 - 膝状体 - 枕叶波与给药后自发出现的细胞内事件相同。此外,自发或诱发的桥脑 - 膝状体 - 枕叶波的出现很容易阻断丘脑纺锤体振荡。根据目前的结果以及文献中已发表的结果,得出结论:外侧膝状体桥脑 - 膝状体 - 枕叶波是由中继细胞的烟碱样激活以及臂周传入纤维对膝状体周围细胞的平行毒蕈碱样抑制引起的。基于这些信号对丘脑振荡的拮抗作用,讨论了桥脑 - 膝状体 - 枕叶活动的功能意义。有人提出,这些信号是清醒时感觉刺激(所谓的眼动电位)和异相睡眠期间内源性驱动引起的定向反应的中枢相关物。