Stover J D, Schwab C A, Matthews M A
Department of Anatomy, Louisiana State University Medical Center, New Orleans 70119.
Somatosens Mot Res. 1992;9(2):107-30. doi: 10.3109/08990229209144766.
Electrophysiological studies (Sessle, 1987, 1991) suggest that trigeminal deafferenting injuries can cause an "unmasking" of existing but normally suppressed convergent inputs to the spinal trigeminal nucleus, including many that arise from the cervical spinal cord. However, the spatial arrangement of this projection has not been examined, particularly with reference to nociceptive components that might become involved in pathological changes leading to chronic pain. Therefore, the purpose of this study was to apply selective interruptions of the trigeminal and/or cervical primary afferent inputs to the spinal trigeminal subnucleus caudalis (Vc) in the cat, followed by (1) demonstration and quantification of axonal degeneration in the spinal trigeminal tract to determine the extent of trigeminal-cervical primary afferent overlap; and (2) an analysis of lesion-induced alterations in the distribution of calcitonin gene-related peptide immunoreactivity (CGRP-IR) in laminae I and II of Vc, since recent evidence strongly suggests that CGRP is involved in pathophysiological elevations of central nervous system neuronal excitability. Degenerating fibers were found throughout the spinal tract following a trigeminal rhizotomy or tractotomy, with the largest numbers adjacent to the rostral two-thirds of Vc, but with a significant number extending caudally to at least the level of C2. CGRP-IR was reduced or eliminated from the rostral one-third and periobex region of Vc, except for a dorsomedial zone that was minimally affected. Retention of CGRP-IR was greater at more caudal levels. Following a combined trigmeninal and cervical tractotomy, fiber degeneration was massive throughout the spinal tract, yet a population of small myelinated fibers persisted at 60 days after surgery. Concomitantly, CGRP-IR was profoundly reduced throughout Vc, except for a small dorsomedial zone of retention, which became more extensive caudally. A cervical tractotomy resulted in moderate numbers of degenerating fibers adjacent to the caudal one-third of Vc, and this number declined rostrally; however, degenerating fibers could be seen at the level of the obex. CGRP-IR was reduced in the dorsomedial and ventrolateral zones of Vc, particularly in its caudal one-third. Electron-microscopic analysis revealed a population of CGRP-IR boutons, most of which were of the simple axodendritic type with asymmetrical contacts. A few examples of axoaxonic contacts were observed. Loss of labeled boutons observed with the electron microscope was consistent with light-microscopic quantitative results. Those boutons that were retained were variable in size and displayed simple axodendritic contacts.(ABSTRACT TRUNCATED AT 400 WORDS)
电生理研究(塞斯尔,1987年,1991年)表明,三叉神经传入纤维切断损伤可导致脊髓三叉神经核中现有的但通常被抑制的汇聚性输入“脱抑制”,其中许多输入源自颈脊髓。然而,这种投射的空间排列尚未得到研究,特别是涉及可能参与导致慢性疼痛的病理变化的伤害性成分。因此,本研究的目的是对猫的三叉神经和/或颈初级传入纤维输入到三叉神经尾侧亚核(Vc)进行选择性切断,然后(1)显示并量化三叉神经脊髓束中的轴突退变,以确定三叉神经 - 颈初级传入纤维的重叠程度;(2)分析损伤引起的Vc层I和层II中降钙素基因相关肽免疫反应性(CGRP-IR)分布的改变,因为最近的证据强烈表明CGRP参与中枢神经系统神经元兴奋性的病理生理升高。在三叉神经根切断术或束切断术后,在整个脊髓束中发现了退变纤维,数量最多的位于Vc头侧三分之二附近,但有相当数量的纤维向尾侧延伸至至少C2水平。Vc头侧三分之一和闩周区域的CGRP-IR减少或消失,除了一个受影响最小的背内侧区。在更靠尾侧的水平,CGRP-IR的保留更多。在三叉神经和颈联合束切断术后,整个脊髓束中的纤维退变大量存在,但一群有髓小纤维在术后60天仍持续存在。与此同时,除了一个小的背内侧保留区且该区域在尾侧变得更广泛外,整个Vc中的CGRP-IR显著减少。颈束切断术导致Vc尾侧三分之一附近有中等数量的退变纤维,且该数量向头侧递减;然而,在闩水平可见退变纤维。Vc的背内侧和腹外侧区的CGRP-IR减少,特别是在其尾侧三分之一。电子显微镜分析显示一群CGRP-IR终扣,其中大多数是简单的轴 - 树突型,具有不对称性接触。观察到一些轴 - 轴突接触的例子。电子显微镜下观察到的标记终扣的丢失与光学显微镜定量结果一致。保留的终扣大小不一,并显示出简单的轴 - 树突接触。(摘要截断于400字)