INHIBITION OF SPINAL NOCICEPTIVE INFORMATION BY STIMULATION IN MIDBRAIN OF THE CAT IS BLOCKED BY LIDOCAINE MICROINJECTED IN NUCLEUS RAPHE MAGNUS AND MEDULLARY RETICULAR-FORMATION
INHIBITION OF SPINAL NOCICEPTIVE INFORMATION BY STIMULATION IN MIDBRAIN OF THE CAT IS BLOCKED BY LIDOCAINE MICROINJECTED IN NUCLEUS RAPHE MAGNUS AND MEDULLARY RETICULAR-FORMATION
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DOI：
10.1152/jn.1983.50.6.1446
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发表时间：
1983-01-01
影响因子：
2.5
通讯作者：
ZIMMERMANN, M
中科院分区：
文献类型：
--
作者：
GEBHART, GF;SANDKUHLER, J;ZIMMERMANN, M
在麻醉、瘫痪猫中，通过定量评价在内侧和/或外侧延髓微量注射利多卡因产生的可逆性阻滞的效果，研究了脑干中脊髓伤害性信息下行抑制控制的组织。刺激中缝大核（NRMS）产生的脊髓神经元抑制进行了比较，在延髓网状结构（MRFS）的刺激2 mm外侧产生的相同的背角神经元的抑制。当在这些延髓部位微量注射利多卡因阻断抑制作用时，评价刺激中脑导水管周围灰质（PAGS）和网状结构外侧4 mm处（LRFS）产生的脊髓神经元抑制作用，并与微量注射利多卡因前产生的抑制作用进行比较。所研究的所有32个脊髓背角神经元均响应于对于A-α，三角洲-和C-纤维对施加到皮肤上的机械刺激有反应，27个还对有害辐射加热（50 ° C）有反应。C，10 s）的皮肤的脚或脚趾垫（5 U有感受野在毛茸茸的皮肤后肢）。NRMS或MRFS均能抑制各单位的伤害性热诱发反应。所研究的脊髓单位对皮肤的分级有害加热的响应在所采用的整个温度范围（42 ℃-45 ℃）内是单调线性函数。50.degree. C）。MRFS将该刺激反应函数（SRF）向右移动，显著提高反应阈值，平均2.2 °。C对皮肤的有害加热，而不显著影响SRF的斜率。在中缝大核（NRM）或延髓网状结构（MRF）中微量注射利多卡因（10 μ g/1 μ l）不影响热诱发反应或增加背角神经元的自发活动。NRM内微量注射利多卡因可阻断刺激NRM产生的脊髓抑制作用，但不影响MRFS产生的脊髓抑制作用，也不影响PAGS或LRFS产生的神经元抑制作用。在MRF中微量注射利多卡因可阻断MRFS的抑制作用，而不影响NRMS、PAGS或LRFS的疗效。只有当微量注射利多卡因并同时阻断内侧和外侧延髓时，PAGS或LRFS产生的脊髓抑制才会受到影响。这些数据与PAGS产生的镇痛和下行抑制依赖于NRM中的延髓中继的观点相矛盾。
The organization in the brain stem of descending inhibitory control of spinal nociceptive information was studied in anesthetized, paralyzed cats by quantitatively evaluating the effects of reversible blocks produced by lidocaine microinjected in the medial and/or lateral medulla. Spinal neuronal inhibition produced by stimulation in the nucleus raphe magnus (NRMS) was compared to the inhibition of the same dorsal horn neurons produced by stimulation 2 mm lateral in the medullary reticular formation (MRFS). When the inhibition was blocked by lidocaine microinjected in those medullary sites, the efficacy of spinal neuronal inhibition produced by stimulation in the midbrain periaqueductal gray (PAGS) and 4 mm lateral in the reticular formation (LRFS) was evaluated and compared with the inhibition produced before microinjection of lidocaine. All 32 spinal dorsal horn neurons studied responded to hindlimb cutaneous nerve stimulation at strengths supramaximal for activation of A-.alpha.,.delta.- and C-fibers, to mechanical stimuli applied to the skin, and 27 also responded to noxious radiant heating (50.degree. C, 10 s) of the skin of the foot- or toepads (5 U had receptive fields in the hairy skin of the hindlimb). The noxious heat-evoked responses of all units studied were inhibited by NRMS or MRFS. The responses of the spinal units studied to graded noxious heating of the skin was a monotonic linear function throughout the temperature range employed (42.degree.-50.degree. C). MRFS shifted this stimulus response function (SRF) to the right, raising significantly the threshold of response a mean 2.2.degree. C to noxious heating of the skin without significantly affecting the slope of the SRF. Lidocaine (10 .mu.g in 1 .mu.l) microinjected in either the nucleus raphe magnus (NRM) or medullary reticular formation (MRF) did not affect the heat-evoked responses or increase the spontaneous activity of dorsal horn neurons. Lidocaine microinjected in the NRM blocked the spinal inhibition produced by stimulation in the NRM but did not affect the efficacy of spinal inhibition produced by MRFS nor affect neuronal inhibition produced by PAGS or LRFS. Lidocaine microinjected in the MRF blocked the inhibitory effects of MRFS without affecting the efficacy of NRMS, PAGS, or LRFS. The spinal inhibition produced by PAGS or LRFS was affected only when lidocaine was microinjected and simultaneously blocked both the medial and lateral medulla. The data contradict the view that the analgesia and descending inhibition produced by PAGS is dependent on a bulbar relay in the NRM.