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c-FOS PROTEIN AND NADPH-DIAPHORASE DETECTION IN RAT MIDBRAEV AND SPINAL CORD AFTER CONTUSION INJURY

机译:创伤后大鼠中脑和脊髓中c-FOS蛋白和NADPH的透支检测

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Spinal cord injury appears to involve neuroplastic remodeling or cell death that is the result of intense neuronal cells response to lesion. The damage may occur near the site of lesion, as well as in proximal brain areas. Thus, neurons located in brain centers and functionally connected to the damaged areas may present constitutive changes after spinal cord damage. Experimental studies and clinical observations show that spinal cord trauma may be amplified by secondary neuronal damage. However, little is known about the molecular mechanism that initiates and maintains this neuronal reaction. We have started an investigation of neural changes induced by acute spinal cord injury. We assessed the degree of functional neurologic impairment that follows spinal cord injury by behavioral tests and histological methods. In lesioned areas and throughout the central nervous system expression of the transcription factor protein c-Fos was investigated by immunocytochemistry. The localization of c-Fos may indicate, in addition to neuronal activation, spatial and temporal patterns related to the type of stimulus and to the long-term variation in neuronal physiology. In parallel, to identify spinal neurons that synthesize Nitric Oxide, cells and fibers histochemically stained for NADPH diaphorase (a nitric oxide synthase), were studied. Fos expression was detected in NADPH-diaphorase positive cells at intermedio lateral column, central canal, dorsal horn, including nucleus trigeminalis caudalis, two hours after contusion by weight drop. It was found that NADPH-diaphorase is induced in spinal motoneurons, neurons that are normally NADPH-diaphorase negative; however, no Fos protein expression was detected in these cells. The results suggest that central nervous system areas close or proximal to the lesion site, are activated after contusion by weight drop. In addition they show that Fos protein expression and changes on NADPH-diaphorase activity after spinal cord contusion are not necessarily dependent on each other.
机译:脊髓损伤似乎涉及神经塑性重塑或细胞死亡,这是强烈的神经元细胞对病变的反应所致。损伤可能发生在病变部位附近以及大脑近端区域。因此,位于大脑中心并在功能上连接到受损区域的神经元在脊髓受损后可能会发生组成性变化。实验研究和临床观察表明,继发性神经元损伤可能会加剧脊髓损伤。然而,关于启动和维持这种神经元反应的分子机制知之甚少。我们已经开始研究由急性脊髓损伤引起的神经变化。我们通过行为测试和组织学方法评估了脊髓损伤后功能神经功能缺损的程度。在病变区域和整个中枢神经系统中,通过免疫细胞化学研究了转录因子蛋白c-Fos的表达。除了神经元激活外,c-Fos的定位还可能指示与刺激类型和神经元生理学的长期变化有关的时空格局。平行地,为了鉴定合成一氧化氮的脊髓神经元,对组织化学染色了NADPH心肌黄递酶(一氧化氮合酶)的细胞和纤维进行了研究。减重挫伤后2小时,在中间外侧柱,中央管,背角,包括三叉神经尾核的NADPH-心肌黄酶阳性细胞中检测到Fos表达。已发现NADPH-黄递酶在脊髓运动神经元中被诱导,神经元通常为NADPH-黄递酶阴性。然而,在这些细胞中未检测到Fos蛋白表达。结果表明,挫伤后,体重减轻可激活靠近或靠近病变部位的中枢神经系统区域。另外,它们表明脊髓挫伤后Fos蛋白的表达和NADPH-心肌黄递酶活性的变化不一定相互依赖。

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