The vulnerability of nitrergic neurons to transient spinal cord ischemia: a quantitative immunohistochemical and histochemical study
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  • 作者:Andrea Schreiberová (1) schreiberova@saske.sk
    Alexandra Kisucká (1)
    ?udmila Hricová (1)
    Andrea Kucharíková (1)
    Jaroslav Pavel (1)
    Nade?da Luká?ová (1)
  • 关键词:Neuronal nitric oxide synthase – NADPH ; diaphoraseLumbar and sacral spinal cord – Rabbit – Ischemia/reperfusion – Paraplegia
  • 刊名:Journal of Molecular Histology
  • 出版年:2012
  • 出版时间:April 2012
  • 年:2012
  • 卷:43
  • 期:2
  • 页码:203-213
  • 全文大小:1,001.4 KB
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  • 作者单位:1. Institute of Neurobiology, Slovak Academy of Sciences, ?oltésovej 4, 040 01 Ko?ice, Slovak Republic
  • 刊物类别:Biomedical and Life Sciences
  • 刊物主题:Life Sciences
    Cell Biology
    Biomedicine
    Developmental Biology
  • 出版者:Springer Netherlands
  • ISSN:1567-2387
文摘
Spinal cord ischemia belongs to serious and relatively frequent diseases of CNS. The aim of the present study was to find out the vulnerability of nitrergic neurons to 15 min transient spinal cord ischemia followed by 1 and 2 weeks of reperfusion. We studied neuronal nitric oxide synthase (nNOS) and nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d) in structural elements of lumbosacral spinal cord along its rostrocaudal axis. In addition, a neurological deficit of experimental animals was evaluated. Spinal cord ischemia, performed on the rabbit, was induced by abdominal aorta occlusion using Fogarty catheter introduced into the right femoral artery for a period of 15 min. After surgical intervention the animals survived for 7 and 14 days. nNOS-immunoreactivity (nNOS-IR) was measured by immunohistochemical and NADPHd-positivity by histochemical method, and both immunohistochemical and histochemical stainings were quantified by densitometric analyses. Neurological deficit was evaluated according Zivin′s criteria. The number of nNOS-IR and/or NADPH-d positive neurons and the density of neuropil were markedly increased in superficial dorsal horn (laminae I–III) after 15 min ischemia and 7 days of reperfusion. However, ischemia followed by longer time of survival (14 days) returned the number of nNOS-IR and NADPH-d positive neurons to control. In the pericentral region (lamina X) containing interneurons and crossing fibers of spinal tracts, than in lamina VII and in dorsomedial part of the ventral horn (lamina VIII) we recorded a decreased number of nNOS-IR and NADPH-d positive neurons after both ischemia/reperfusion periods. In the medial portion of lamina VII and dorsomedial part of the ventral horn (lamina VIII) we observed many necrotic loci. This area was the most sensitive to ischemia/reperfusion injury. Fifteen minute ischemia caused a marked deterioration of neurological function of hind limbs, often developing into paraplegia. A quantitative immunohistochemical and histochemical study have shown a strong vulnerability of nitrergic neurons in intermediate zone to transient spinal cord ischemia.

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