McElhaney M R, Chandler L J, Streit W J
Department of Comparative and Experimental Pathology, College of Veterinary Medicine, University of Florida, Gainesville 32610.
Neurosci Lett. 1994 Oct 10;180(1):67-70. doi: 10.1016/0304-3940(94)90915-6.
The purpose of this study was to identify cellular sources of nitric oxide (NO) after injury to rat facial motor neurons using NADPH-diaphorase histochemistry. We employed intraneural injections of either saline or toxic ricin, followed by nerve crush, in order to produce regeneration or degeneration of facial motor neurons (FMNs), respectively. Reactive astrocytes responding to ricin-induced degeneration of FMNs showed increased NADPH-diaphorase activity while reactive astrocytes responding to axotomy (saline injection) did not. Reactive microglial cells were found not to express NADPH-diaphorase in either one of these two paradigms. We conclude that irreversible neuron injury resulting in neurodegeneration causes increased production of NO by reactive astrocytes.
本研究的目的是利用还原型辅酶Ⅱ黄递酶组织化学法，确定大鼠面部运动神经元损伤后一氧化氮（NO）的细胞来源。我们分别通过神经内注射生理盐水或毒性蓖麻毒素，随后进行神经挤压，以分别诱导面部运动神经元（FMNs）的再生或变性。对蓖麻毒素诱导的FMNs变性做出反应的反应性星形胶质细胞显示出还原型辅酶Ⅱ黄递酶活性增加，而对轴突切断（注射生理盐水）做出反应的反应性星形胶质细胞则没有。在这两种模式中的任何一种中，均未发现反应性小胶质细胞表达还原型辅酶Ⅱ黄递酶。我们得出结论，导致神经变性的不可逆神经元损伤会使反应性星形胶质细胞增加NO的产生。
