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

机译:在大鼠中涉及弥散性有害抑制控制的脑结构研究:延髓腹侧延髓。

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摘要

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)
机译:1.先前的电生理学,药理学和解剖学证据表明,延髓腹侧延髓(RVM)可能参与弥散性有害抑制控制(DNIC)的pin上棘部分。为了检验该假设,进行了两个实验系列,在这些实验系列中,在对照假手术大鼠和具有RVM损伤的大鼠以及具有这种作用的邻近候选者,即网状巨大网状细胞核(Gi)中比较了DNIC。 2.在第一个实验系列中,在麻醉的动物中,通过向RVM或Gi中注射喹啉酸(0.3-0.8微升360 nmol /微升溶液)来诱发病变。在对照动物(n = 10)中,仅注射了媒介物(人工脑脊液)。每个电生理实验后进行组织学病变重建。考虑三组动物:在第一组(n = 5)中,病变位于RVM的中心,包括三分之二的裂核(NRM)和邻近的网状区域;在第二组(n = 5)中,病灶扩展到额叶更多,并累及NRM的鼻尖。在第三组(n = 5)中,病灶向外侧和背侧扩展,包括网状核(giA),网状旁核(LPGi)和Gi。在每种情况下,病变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,通过流过阴极电流(5 mA,8 s),在麻醉的动物中诱导出NRM的整个后尾神经范围的电解损伤(n = 5)。在对照动物(n = 5)中,电极降低但未施加电流。 4.损伤后1周,麻醉动物,使其瘫痪,人工通气,并记录三叉尾尾核中的会聚神经元。当将经皮电刺激应用于它们的感受野时,这些神经元会由于A和C纤维的激活而产生响应。将每个爪浸入50摄氏度的水浴中触发DNIC。在不同的动物组中比较了收敛神经元的一般特性和这些异位有害刺激产生的C纤维诱发的反应的抑制作用。 5.在对照组和患病动物中,感受野的大小,自发活动,C纤维诱发反应的阈值和对C纤维活化的反应没有差异。在不同时期的动物中,在适应期之后和之后的44s中,C纤维诱发的反应的抑制百分比也非常相似。(摘要截短了400字)

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