Neuronal nitric oxide synthase immunopositivity in motoneurons of the rabbit's spinal cord after transient ischemia/reperfusion injury

被引:6
作者
A. Schreiberová [1 ]
M. Lacková [2 ]
D. Kolesár [1 ]
N. Lukáčová [1 ]
J. Maršala [1 ]
机构
[1] Institute of Neurobiology, Slovak Academy of Sciences, 040 01, Košice
关键词
Ischemia/reperfusion; Motoneurons; Neuronal nitric oxide synthase; Rabbit; Ventral horn;
D O I
10.1007/s10571-006-9087-z
中图分类号
学科分类号
摘要
1. Motoneurons in the spinal cord are especially vulnerable to ischemic injury and selectively destroyed after transient ischemia. To evaluate the role of nitric oxide (NO) in the pathophysiology of the spinal cord ischemia, the expression of neuronal nitric oxide synthase (nNOS) in the motoneurons of the lumbosacral spinal cord was examined in the rabbit model of transient abdominal aorta occlusion. 2. The aim of the present study was to find if there is any consensus between the duration of transient abdominal aorta occlusion, nNOS positivity of the motoneurons and neurological hind limb impairment. 3. According to the degree of neurological damage (i.e., from the group with almost no sign of damage to a group with fully developed paraplegia), the experimental animals were divided into three groups. The respective spinal cord segments of each experimental group were compared to the control group. 4. Spinal cord ischemia (15 min) was induced by Fogarty arterial embolectomy catheter occlusion of abdominal aorta with a reperfusion period of 7 days. On seventh day, the sections of lumbosacral segments were immunohistochemically treated and L1-L7, and S1-S2 segment sections were monitored using light microscopy. © 2006 Springer Science+Business Media, Inc.
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页码:1483 / 1494
页数:11
相关论文
共 44 条
[31]  
Saito S., Kidd G.J., Trapp B.D., Dawson T.M., Bredt D.S., Wilson D.A., Traystman R.J., Snyder S.H., Hanley D.F., Rat spinal cord neurons contain nitric oxide synthase, Neuroscience, 59, pp. 447-456, (1994)
[32]  
Sakurai M., Aoki M., Abe K., Sadahiro M., Tabayashi K., Selective motor neuron death and heat shock protein induction after spinal cord ischemia in rabbits, J. Thorac. Cardiovasc. Surg., 113, pp. 159-164, (1997)
[33]  
Shigeno T., Yamasaki Y., Kato G., Kausaka K., Mima T., Takakura K., Graham D.I., Furukawa S., Reduction of delayed neuronal death by inhibition of protein synthesis, Neurosci. Lett., 120, pp. 117-119, (1990)
[34]  
Sims N.R., Zaidan E., Biochemical changes associated with selective neuronal death following short-term cerebral ischaemia, Int. J. Biochem. Cell. Biol., 27, pp. 531-550, (1995)
[35]  
Stefano G.B., Goumon Y., Bilfinger T.V., Welters I.D., Cadet P., Basal nitric oxide limits immune, nervous and cardiovascular excitation: Human endothelia express a mu opiate receptor, Prog. Neurobiol., 60, pp. 513-530, (2000)
[36]  
Suzuki K., Kazui T., Terada H., Umemura K., Ikeda Y., Bashar A.H., Yamashita K., Washiyma N., Suzuki T., Ohkura K., Yasuike J., Experimental study on the protective effects of edaravone against ischemic spinal cord injury, J. Thorac. Cardiovasc. Surg., 130, pp. 1586-1592, (2005)
[37]  
Vannucchi M.G., Corsani L., Gianfriddo M., Pedata F., Faussone-Pellegrini M.S., Expression of neuronal and inducible nitric oxide synthase in neuronal and glial cells after transient occlusion of the middle cerebral artery, Neuroscience, 136, pp. 1015-1026, (2005)
[38]  
Vizzard M.A., Erdman S.L., Forstermann U., De Groat W.C., Differential distribution of nitric oxide synthase in neural pathways to the urogenital organs (urethra, penis, urinary bladder) of the rat, Brain Res., 646, pp. 279-291, (1994)
[39]  
Watanabe M., Sakurai M., Abe K., Aoki M., Sadahiro M., Tabayashi K., Okamoto K., Shoji M., Itoyama Y., Inductions of Cu/Zn superoxide dismutase- and nitric oxide synthase-like immunoreactivities in rabbit spinal cord after transient ischemia, Brain Res., 732, pp. 69-74, (1996)
[40]  
Wood J., Garthwaite J., Models of diffusional spread of nitric oxide: Implications for neural nitric oxide signalling and its pharmacological properties, Neuropharmacology, 33, pp. 1235-1244, (1994)