Knyihár-Csillik E, Csillik B, Oestreicher A B
Department of Anatomy, Albert Szent-Gyorgyi Medical University, Szeged, Hungary.
J Neurosci Res. 1992 May;32(1):93-109. doi: 10.1002/jnr.490320112.
Crush or transection of a peripheral nerve is known to induce transganglionic degenerative atrophy (TDA) in the segmentally related, ipsilateral Rolando substance of the spinal cord. When the lost peripheral connectivity is reestablished, the consecutive regenerative synaptoneogenesis results in restoration of the circuitry in the formerly deteriorated upper dorsal horn. Enhanced expression of the growth-associated protein (GAP43) B-50 occurs during neuronal differentiation, axon outgrowth, and peripheral nerve regeneration. This study documents changes in immunocytochemical distribution of B-50 in the regions of the lumbar spinal cord which are segmentally related to the axotomized sciatic nerve. At the light microscopic level, a weak B-50 immunoreactivity (BIR) is present in the neuropil of the upper dorsal horn of control animals. After unilateral transection and ligation of the sciatic nerve, BIR increased in the ipsilateral upper dorsal horn at 17 days postinjury, but decreased again after 24 days with respect to the contralateral side. Differences between effects of crush and transection were prominent in combined crush-cut experiments as well (i.e., after unilateral crush and contralateral transection and ligation of the sciatic nerve). Electron microscopic studies show that in the uninjured and injured spinal cord, BIR is detected in axons and axon terminals, but not all are stained. After transection of the sciatic nerve, BIR is found in afflicted primary sensory axon terminals, including those contacting substantia gelatinosa neurons and in axon terminals undergoing glial phagocytosis. The localization of BIR seen after crushing the sciatic nerve is similar. However, at 24 days after crush, BIR is detected also in axonal growth cones. In the ventral horn of control animals, synaptic boutons impinging upon motor neurons exhibited weak BIR. At 17 days after unilateral transection of the sciatic nerve, the pericellular BIR surrounding motor neurons is decreased at the ipsilateral with respect to the contralateral side, whereas 24 days after crush injury it increased considerably. Our results show that peripheral nerve injury inducing TDA also affects BIR distribution in the spinal gray matter. Successful regeneration of the peripheral nerve after crush lesion is associated with enhanced expression of B-50 in growth cones of sprouting central axons. The neuroplastic response of B-50 is in line with a function of B-50 in axonal sprouting and reactive synaptogenesis.
已知外周神经的挤压或横断会在脊髓节段相关的同侧罗兰多物质中诱导跨神经节变性萎缩（TDA）。当失去的外周连接重新建立时，连续的再生性突触形成会导致先前受损的上背角神经回路的恢复。生长相关蛋白（GAP43）B - 50在神经元分化、轴突生长和外周神经再生过程中表达增强。本研究记录了与坐骨神经轴突切断节段相关的腰脊髓区域中B - 50免疫细胞化学分布的变化。在光学显微镜水平，对照动物上背角的神经毡中存在微弱的B - 50免疫反应性（BIR）。单侧坐骨神经横断和结扎后，损伤后17天同侧上背角的BIR增加，但与对侧相比，24天后又下降。在联合挤压 - 切断实验中（即单侧挤压和对侧坐骨神经横断及结扎后），挤压和横断的影响差异也很显著。电子显微镜研究表明，在未受伤和受伤的脊髓中，BIR在轴突和轴突终末中被检测到，但并非所有都被染色。坐骨神经横断后，在受累的初级感觉轴突终末中发现BIR，包括那些与胶状质神经元接触的轴突终末以及正在经历胶质细胞吞噬作用的轴突终末。坐骨神经挤压后所见的BIR定位相似。然而，在挤压后24天，在轴突生长锥中也检测到BIR。在对照动物的腹角，撞击运动神经元的突触小体表现出微弱的BIR。单侧坐骨神经横断后17天，运动神经元周围的细胞周BIR在同侧相对于对侧减少，而在挤压损伤后24天它显著增加。我们的结果表明，诱导TDA的外周神经损伤也会影响脊髓灰质中BIR的分布。挤压损伤后外周神经的成功再生与发芽的中枢轴突生长锥中B - 50的表达增强有关。B - 50的神经可塑性反应与B - 50在轴突发芽和反应性突触形成中的功能一致。
