THE SYNAPTIC BASIS OF SLEEP CYCLE CONTROL

为了发现睡眠周期中的突触机制， 负责控制快速眼动（REM）的各个方面 或去睡眠（D）阶段，我建议做细胞内 记录在脑桥内侧网状结构（mPRF）神经元， 自然发生的睡眠-觉醒周期在未麻醉，unrugged猫。 将进行神经元的生理鉴定和表征 通过将细胞内记录与两种电图 睡眠周期的数据（即，EEG、EMG、EOG记录），并与 微刺激诱发的突触后电位和逆行电位 激活位于中脑，延髓和 对侧脑桥网状结构和蓝斑， 中缝背核 形态特征鉴定 与特定生理特性相关的神经元将被制成 通过HRP注射到神经元细胞内记录， 自然睡眠猫。这些研究将解决几个问题， 对了解大脑如何控制其活动的重要性 睡眠-觉醒周期中的兴奋性： mPRF表明该区域参与产生一些 D的现象，也许是国家本身的启动，如果是这样，什么 这些变化的机制是什么？ 我们初步发现的D特异性 紧张性膜去极化改变，膜输入减少 抵抗力和增加的兴奋性适用于所有细胞类型和区域， PRF？ 这些改变的一种机制是通过 蓝斑和中缝背核的生物胺细胞？ 最近发现的一个背吻侧区对mPRF的抑制输入是否 神经元在PGO波的产生和其他D 现象？ mPRF最内侧部分的细胞是否启动PGO 波浪？ 这些问题的答案对精神病学有着广泛的意义， 大脑状态调节机制的知识是这方面的基础 领域，但在自然行为的脊椎动物中很少有研究。 现在众所周知的D睡眠异常和 内源性抑郁症表明， 在情感障碍和D. 这些研究也与睡眠障碍的研究有关，特别是 嗜睡症，并在精神病学中使用梦的状态作为一个模型， 精神病

To discover the synaptic mechanisms operating during the sleep cycle and responsible for control of various aspects of the rapid eye movement (REM) or desynchronized (D) phase of sleep, I propose to do intracellular recordings in medial pontine reticular formation (mPRF) neurons during naturally occurring sleep-waking cycles in unanesthetized, undrugged cats. Physiological identification and characterization of neurons will be made by correlation of the intracellular recordings with both electrographic data of the sleep cycle (i.e., EEG, EMG, EOG records) and with the effects of microstimulation-induced post-synaptic potentials and antidromic activation from sites located in the mesencephalic, bulbar and contralateral pontine reticular formation and in the locus coerulus and dorsal raphe nucleus. Identification of morphological characteristics of neurons associated with particular physiological properties will be made through HRP injections into neurons intracellularly recorded in the naturally sleeping cat. These studies will address several questions of fundamental importance to knowledge of how the brain controls its excitability during the sleep-wake cycle: Are there D-specific changes in the mPRF suggestive of an involvement of this region in generation of some D phenomena and perhaps of initiation of the state itself, and, if so, what are the mechanisms of these changes? Do our initial findings of D-specific changes of tonic membrane depolarization, decreased membrane input resistance, and increased excitability apply to all cell types and areas in PRF? Is one mechanism for these alterations disinhibition by biogenic-amine containing cells in the locus coeruleus and dorsal raphe? Does a recently discovered dorso-rostral zone of inhibitory input to mPRF neurons play an important role in PGO wave generation and other D phenomena? Do cells in the most medial portion of mPRF initiate PGO waves? Answers to these questions have broad implications for psychiatry, where knowledge of mechanisms of brain state regulation is basic for this field, but where there are few studies in naturally behaving vertebrates. The now well-known correlation between D sleep abnormalities and endogeneous depression suggests a specific link between aspects of pysiological control mechanisms important in affective disorder and in D. These studies are also relevant to the study of sleep disorders, especially narcolepsy, and to the use in psychiatry of the dream state as a model for psychosis.