Transient degradation of myelin basic protein in the rat hippocampus following acute carbon monoxide poisoning

被引：22

作者：

Watanabe, Satoru ^{[1
]}

Matsuo, Hirotaka ^{[2
]}

Kobayashi, Yasushi ^{[3
]}

Satoh, Yasushi ^{[4
]}

Fujita, Masanori ^{[1
]}

Nakayama, Akiyoshi ^{[2
,5
]}

Aizawa, Yoshifusa ^{[6
]}

Shinomiya, Nariyoshi ^{[2
]}

Suzuki, Shinya ^{[1
]}

机构：

[1] Natl Def Med Coll, Res Inst, Div Environm Med, Tokorozawa, Saitama 3598513, Japan

[2] Natl Def Med Coll, Dept Integrat Physiol & Bionano Med, Tokorozawa, Saitama 3598513, Japan

[3] Natl Def Med Coll, Dept Anat & Neurobiol, Tokorozawa, Saitama 3598513, Japan

[4] Natl Def Med Coll, Dept Anesthesiol, Tokorozawa, Saitama 3598513, Japan

[5] Japan Air Self Def Force, Med Evaluat Sect, Div 3, Aeromed Lab, Sayama, Saitama 3501394, Japan

[6] Niigata Univ, Grad Sch Med & Dent Sci, Div Cardiol, Niigata 9518510, Japan

来源：

NEUROSCIENCE RESEARCH | 2010年 / 68卷 / 03期

关键词：

CO poisoning; Delayed neurological deterioration; Immunohistochemistry; Morris water maze; Memory impairment; Animal model; MAZE TASK; OXYGEN; TRANSPORTER; AFFINITY; INJURY; BLOOD; MICE;

D O I：

10.1016/j.neures.2010.07.2029

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

The neurotoxicity of carbon monoxide (CO) poisoning is a significant clinical problem, but its mechanisms remain unclear. Previous studies of CO-exposed rats showed spatial memory disturbances and degradation of myelin basic protein (MBP) in the brain; however, regional localization of the degradation was not analyzed. In the present study, we histologically determined the foci of CO effects in the hippocampus. Wistar rats were exposed to CO for 60 min (1000 ppm for 40 min + 3000 ppm for 20 min) and returned into room air. For histological evaluation, the animals were sacrificed 90 min, 1,7 and 14 days after CO exposure and the brain tissue was analyzed with hematoxylin-eosin (HE), Nissl and Gallyas myelin staining as well as immunohistochemistry for MBP and phosphorylated or nonphosphorylated neurofilament. No histological changes were observed on HE, Nissl or Gallyas staining. In contrast, we detected MBP reduction at 90 min after CO exposure in the dentate gyrus and CA3, and the recovery of MBP was observed after 14 days. The immunoreactivity of neurofilament also changed after CO exposure. Nevertheless, water maze test showed no significant effects of CO exposure on spatial memory. Our findings demonstrate that CO poisoning causes transient degradation of MBP and axonal injury in the hippocampus even though the animals showed no neurological disturbances. (C) 2010 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.

引用

页码：232 / 240

页数：9

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