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大鼠中参与弥漫性伤害性抑制控制的脑结构研究:延髓头端腹内侧区。

Studies of brain structures involved in diffuse noxious inhibitory controls in the rat: the rostral ventromedial medulla.

作者信息

Bouhassira D, Bing Z, Le Bars D

机构信息

INSERM, U-161, Paris, France.

出版信息

J Physiol. 1993 Apr;463:667-87. doi: 10.1113/jphysiol.1993.sp019616.

Abstract
  1. Previous electrophysiological, pharmacological and anatomical evidence had suggested a possible participation of rostral ventromedial medulla (RVM) in the supraspinal part of the loop underlying diffuse noxious inhibitory controls (DNICs). In order to test this hypothesis, two experimental series were performed during which DNICs were compared in control sham-operated rats and rats with lesions of the RVM and of an adjacent candidate for such a role, the nucleus gigantocellularis reticularis (Gi). 2. In the first experimental series, lesions were induced, in anaesthetized animals, by injections of quinolinic acid (0.3-0.8 microliter of a 360 nmol/microliter solution) into the RVM or Gi. In the control animals (n = 10), the vehicle alone (artificial cerebrospinal fluid) was injected. Histological lesion reconstructions were performed after each electrophysiological experiment. Three groups of animals were considered: in the first group (n = 5), the lesion was centered on the RVM, including the two caudal thirds of nucleus raphe magnus (NRM) and adjacent reticular areas; in the second group (n = 5), the lesions extended more rostrally and involved the rostral pole of NRM; in the third group (n = 5), the lesion extended more laterally and dorsally and included nucleus reticularis gigantocellularis pars alpha (GiA), nucleus reticularis paragigantocellularis lateralis (LPGi) and the Gi. In each case, all the neuronal cell bodies within the lesioned area were destroyed. 3. In the second experimental series, electrolytic lesions of the total rostrocaudal extent of the NRM (n = 5) were induced, in anesthetized animals, by passing cathodal current (5 mA, 8 s). In the control animals (n = 5), the electrode was lowered but current was not applied. 4. One week after lesioning, the animals were anaesthetized, paralysed, artificially ventilated and recordings were made from convergent neurones in trigeminal nucleus caudalis. These neurones gave responses due to activation of A and C fibres when percutaneous electrical stimuli were applied to their receptive fields. DNICs were triggered by immersion of each paw in a 50 degrees C water-bath. Both the general properties of the convergent neurones and the inhibitions of the C fibre-evoked responses produced by these heterotopic noxious stimuli were compared in the different groups of animals. 5. The sizes of receptive field, spontaneous activities, thresholds for C fibre-evoked responses and responses to C fibre activation were not different in the control and lesioned animals. The percentage inhibitions of the C fibre-evoked responses both during and in the 44s following the conditioning periods were also very similar in the different groups of animals.(ABSTRACT TRUNCATED AT 400 WORDS)
摘要
  1. 先前的电生理、药理学及解剖学证据表明,延髓头端腹内侧区(RVM)可能参与了弥漫性伤害性抑制控制(DNICs)环路的脊髓上部分。为验证这一假说,进行了两个实验系列,在此期间,对假手术对照组大鼠以及RVM和相邻的可能起此作用的巨细胞网状核(Gi)损伤的大鼠的DNICs进行了比较。2. 在第一个实验系列中,在麻醉动物中,通过向RVM或Gi注射喹啉酸(360 nmol/微升溶液0.3 - 0.8微升)诱导损伤。在对照动物(n = 10)中,仅注射溶媒(人工脑脊液)。每次电生理实验后进行组织学损伤重建。考虑了三组动物:第一组(n = 5),损伤以RVM为中心,包括中缝大核(NRM)的后三分之二及相邻网状区域;第二组(n = 5),损伤向更靠前的方向扩展,累及NRM的头端;第三组(n = 5),损伤向更外侧和背侧扩展,包括巨细胞网状核α部(GiA)、外侧旁巨细胞网状核(LPGi)和Gi。在每种情况下,损伤区域内的所有神经元细胞体均被破坏。3. 在第二个实验系列中,在麻醉动物中,通过施加阴极电流(5 mA,8 s)诱导NRM全长(n = 5)的电解损伤。在对照动物(n = 5)中,电极下移但不施加电流。4. 损伤一周后,将动物麻醉、麻痹、人工通气,并从三叉神经尾核的会聚神经元进行记录。当经皮电刺激施加于其感受野时,这些神经元因A和C纤维的激活而产生反应。通过将每只爪子浸入50℃水浴触发DNICs。在不同组动物中比较了会聚神经元的一般特性以及这些异位伤害性刺激对C纤维诱发反应的抑制作用。5. 对照动物和损伤动物的感受野大小、自发活动、C纤维诱发反应阈值及对C纤维激活的反应并无差异。在不同组动物中,条件刺激期间及之后44秒内C纤维诱发反应的抑制百分比也非常相似。(摘要截选至400字)
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b1fc/1175365/f4fc0f5c799d/jphysiol00419-0663-a.jpg

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