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豚鼠膝关节固定后腰骶部运动神经元中NADPH-黄递酶和一氧化氮合酶的表达

Expression of NADPH-diaphorase and nitric oxide synthase in lumbosacral motoneurons after knee joint immobilisation in the guinea pig.

作者信息

He X H, Tay S S, Ling E A

机构信息

Department of Anatomy, Faculty of Medicine, National University of Singapore, Singapore.

出版信息

J Anat. 1997 Nov;191 ( Pt 4)(Pt 4):603-10. doi: 10.1046/j.1469-7580.1997.19140603.x.

Abstract

The expression of nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) and nitric oxide synthase (NOS) in spinal ventral horn neurons was studied in the guinea pig after right knee joint immobilisation (RKJI). At 1 wk after RKJI, neurons in the ipsilateral ventral horn from L4 to S1 segments showed a moderate reactivity for NADPH-d staining. At 2 wk, NADPH-d labelled neurons were also observed in the contralateral ventral horn. Ipsilateral NOS immunoreactive cells were not detectable until wk 2. The intensity of NADPH-d and NOS labelled neurons in the bilateral ventral horns was sustained, peaking at the 4th wk after RKJI. In guinea pigs subjected to 4 wk of RKJI and subsequently released from the immobilisation for 2 and 4 wk, NADPH-d and NOS reactivity in ventral horn neurons diminished. The expression of NADPH-d positive neurons differed from that of NOS labelled neurons in terms of time interval, cell number and staining intensity, the latter being later, fewer and weaker. It is suggested that the induction and upregulation of NADPH-d and NOS are attributable to reduced activity of muscles acting on the knee joint after RKJI; the changes are reversible. It is speculated that increased levels of NO production are involved in protective mechanisms against possible neuronal degeneration as a consequence of target dysfunction.

摘要

在豚鼠右膝关节固定(RKJI)后,研究了脊髓腹角神经元中烟酰胺腺嘌呤二核苷酸磷酸黄递酶(NADPH-d)和一氧化氮合酶(NOS)的表达。RKJI后1周,L4至S1节段同侧腹角的神经元对NADPH-d染色呈中度反应。2周时,在对侧腹角也观察到NADPH-d标记的神经元。直到第2周才检测到同侧NOS免疫反应性细胞。双侧腹角中NADPH-d和NOS标记神经元的强度持续存在,在RKJI后第4周达到峰值。在接受4周RKJI并随后解除固定2周和4周的豚鼠中,腹角神经元中的NADPH-d和NOS反应性减弱。NADPH-d阳性神经元的表达在时间间隔、细胞数量和染色强度方面与NOS标记的神经元不同,后者出现较晚、数量较少且较弱。提示RKJI后作用于膝关节的肌肉活动减少可导致NADPH-d和NOS的诱导和上调;这些变化是可逆的。推测NO产生水平的增加参与了针对因靶功能障碍可能导致的神经元变性的保护机制。

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