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Intrinsic control of cerobro-vascular tone-role of central nor-advenergic system

中枢去甲肾上腺系统脑血管张力作用的内在控制

基本信息

批准号：
03670690
负责人：
MAEDA Minoru
金额：
$ 1.28万
依托单位：
Juntendo University School of Medicine
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1991
资助国家：
日本
起止时间：
1991 至 1993
项目状态：
已结题

项目摘要

We have investigated the role of the central dorsal and rentral noradrenergic systems (Locus Coeruleus Complex, LC, Medullary Reticular Formation, MRF) and the cholinoceptive pontine area (CPA) in control of cerebral vasomotor tone. The experiments were performed on 30 chloralose-anesthetized cats with or without Kaolin induced hydrocephalus.[I] Microinjection of glutamate or carbochol into the LC or the MRF induced decrease of ICP in association with a slight rise of BP.On the other hand microinjection of carbachol or Ach into the CPA produced "plateau wave" like ICP-variations.[II] Tonic discharges of the LC neuron were gradually suppressed at 10 to 30 sec. prior to the onset of plateau waves, almost completely silenced during the plateau phase. Tonic MRF-neuron discharges were gradually suppressed about 30 sec. before onset o fplateau wave like ICP-variations and sharply suppressed during the plateau phase. Recovery began 10 to 30 sec. before the ICP decrease. On the other hand, the firing rate of the CPA-neuron was increased in phase with the plateau waves.[III] Electrophysiological studies show that the CPA neurons suppress both the LC and MRF-neurons which make up the central noradrenergic system. Activation of the CPA neurons should suppress activity in the central noradrenergic system. The increase in CBV then occurrs in response to dilatation of cerebral vessels.These results suggest that activity within the CPA, LC and MRF contributes to ICP changes and is the endogenous neuronal origin of plateau waves occurring in some conditions such as Kaolin induced hydrocephalus.

我们研究了中央背侧和房侧去甲肾上腺素能系统（蓝斑复合体，LC，髓质网状结构，MRF）和胆碱感受桥脑区（CPA）在控制脑血管舒缩张力中的作用。实验在 30 只氯醛糖麻醉的猫上进行，有或没有高岭土诱导的脑积水。[I] 将谷氨酸或卡巴胆碱微量注射到 LC 或 MRF 中，会导致 ICP 降低，并伴有血压的轻微升高。另一方面，将卡巴胆碱或乙酰胆碱微量注射到 CPA 中会产生“平台波”，如 ICP-变化。[II] LC 神经元的强直放电在 10 至 30 秒时逐渐受到抑制。在高原波出现之前，在高原阶段几乎完全沉寂。强直性 MRF 神经元放电在约 30 秒内逐渐受到抑制。类似 ICP 变化的平台波出现之前，在平台期期间急剧受到抑制。 10 到 30 秒后开始恢复。在ICP下降之前。另一方面，CPA 神经元的放电率与平台波同相增加。[III] 电生理学研究表明，CPA 神经元抑制构成中枢去甲肾上腺素能系统的 LC 和 MRF 神经元。 CPA 神经元的激活应抑制中枢去甲肾上腺素能系统的活动。然后，CBV 的增加响应脑血管的扩张而发生。这些结果表明，CPA、LC 和 MRF 内的活动导致 ICP 变化，并且是在某些情况下（例如高岭土诱发的脑积水）发生平台波的内源性神经元起源。