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猫中压力感受器向孤束核的传入:下丘脑的调节作用。

Baroreceptor inputs to the nucleus tractus solitarius in the cat: modulation by the hypothalamus.

作者信息

Mifflin S W, Spyer K M, Withington-Wray D J

机构信息

Department of Physiology, Royal Free Hospital School of Medicine, London.

出版信息

J Physiol. 1988 May;399:369-87. doi: 10.1113/jphysiol.1988.sp017086.

Abstract
  1. The effects of stimulation within the hypothalamic defence area (HDA) on the activity of neurones in the nucleus of the solitary tract (NTS) have been investigated in vivo. 2. HDA stimulation exerted marked influences on NTS neurones. Approximately two-thirds of units receiving a carotid sinus nerve (SN) input were inhibited by HDA stimulation. All units shown to receive an excitatory input from carotid sinus baroreceptors were inhibited by HDA stimulation. 3. The specificity of the HDA stimulation was investigated by generalized hypothalamic stimulation. In these experiments the number of units activated by SN stimulation that were inhibited was reduced considerably. A much smaller percentage (27%) of baroreceptive units were inhibited from hypothalamic stimulation outside the defence area. 4. Intracellular recordings revealed that HDA stimulation evoked a long-lasting hyperpolarization of membrane potential that resulted from postsynaptic inhibition (rather than disfacilitation). The HDA-evoked IPSP 'shunted' the SN-evoked EPSP when the SN stimulus was timed to occur during the initial peak hyperpolarizing phase of the HDA-evoked IPSP. 5. HDA stimulation disinhibited cells receiving an inhibitory input from the carotid sinus baroreceptors. 6. The effects of HDA stimulation were not limited to cells receiving SN afferent information or to cells within the NTS. 7. Our results explain, at the intracellular level, the mechanism for the central suppression of the baroreceptor reflex that forms an integral part of the defence response in the cat.
摘要
  1. 已在活体中研究了下丘脑防御区(HDA)内的刺激对孤束核(NTS)神经元活动的影响。2. HDA刺激对NTS神经元产生了显著影响。接受颈动脉窦神经(SN)输入的单位中约三分之二受到HDA刺激的抑制。所有显示接受来自颈动脉窦压力感受器兴奋性输入的单位都受到HDA刺激的抑制。3. 通过全身性下丘脑刺激研究了HDA刺激的特异性。在这些实验中,被SN刺激激活后又受到抑制的单位数量大幅减少。来自防御区外下丘脑刺激所抑制的压力感受性单位的比例要小得多(27%)。4. 细胞内记录显示,HDA刺激引起膜电位的持久超极化,这是由突触后抑制(而非去易化)导致的。当SN刺激在HDA诱发的IPSP初始超极化峰值阶段定时发生时,HDA诱发的IPSP会“分流”SN诱发的EPSP。5. HDA刺激解除了接受来自颈动脉窦压力感受器抑制性输入的细胞的抑制。6. HDA刺激的作用不仅限于接受SN传入信息的细胞或NTS内的细胞。7. 我们的结果在细胞水平上解释了压力感受器反射中枢抑制的机制,该机制是猫防御反应的一个组成部分。

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