The role of NO resulted from neuronal nitric oxide synthase in the metabotropic glutamate receptor2/3 mediated-brain ischemic tolerance / 中国应用生理学杂志
Chinese Journal of Applied Physiology
; (6): 182-185, 2009.
Article
ي Zh
| WPRIM
| ID: wpr-356302
المكتبة المسؤولة:
WPRO
ABSTRACT
<p><b>AIM</b>To explore the role of nitric oxide (NO) resulted from nNOS in the mGluR2/3 mediated-brain ischemic tolerance induced by cerebral ischemic preconditioning (CIP), the present study is undertaken to observe the influences of alpha-methyl-(4-tetrazolyl-phenyl) glycine (MTPG), an antagonist of mGluR2/3, on the expression of nNOS during the induction of the brain ischemic tolerance based on confirming the blocking effect of MTPG on the induction of the tolerance.</p><p><b>METHODS</b>Thirty-six Sprague-Dawley rats, whose vertebral arteries were permanently occluded, were randomly divided into sham, CIP, ischemic insult, CIP+ ischemic insult, MTPG+ CIP and MTPG+ CIP+ ischemic insult groups. Thionin staining and immunohistochemistry were used for neuropathological evaluation and assay of nNOS expression in the hippocampal CA1 subregion of the rats.</p><p><b>RESULTS</b>The expression of nNOS showed moderate and extreme up-regulation in the CIP and ischemia groups, respectively, compared to the sham group. The preceded CIP blocked in certain extent the extreme up-regulation of nNOS induced by brain ischemia in CIP + ischemia group. Administration of MTPG via lateral cerebral ventricle 20 min before CIP blocked the up-regulation of nNOS induced by CIP, but had no influence on the pyramidal neuronal survival. While in the MTPG+ CIP+ ischemic insult group, the expression of nNOS was stronger than that in the MTPG + CIP group, and the up-regulation was accompanied with obvious delayed neuronal death. Discussion concerned illustrated that the relative intensive up-regulation of nNOS in this group might be attributed to brain ischemia other than MTPG.</p><p><b>CONCLUSION</b>NO resulted from nNOS participated the induction of mGluR2/3 mediated-brain ischemic tolerance as a downstream molecule of activation of mGluR2/3 during CIP.</p>
النص الكامل:
1
الفهرس:
WPRIM
الموضوع الرئيسي:
Pharmacology
/
Physiology
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Tetrazoles
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Random Allocation
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Brain Ischemia
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Rats, Sprague-Dawley
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Receptors, Metabotropic Glutamate
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Ischemic Preconditioning
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Alanine
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Nitric Oxide Synthase Type I
المحددات:
Animals
اللغة:
Zh
مجلة:
Chinese Journal of Applied Physiology
السنة:
2009
نوع:
Article