诱导型一氧化氮信号通路在代谢型谷氨酸受体2/3介导的脑缺血耐受中的作用

AIM: To explore the role of NO/ inducible nitric oxide synthase (iNOS) in the metabotromi glutamate receptor 2/3C (mGluR2/3) mediated-brain ischemic tolerance induced by cerebral ischemic preconditioning (CIP), and to observe the influences of α-methyl- (4-tetrazolyl- phenyl) glycine (MTPG), an antagonist of mGluR2/3, on the expression of iNOS during the induction of brain ischemic tolerance. METHODS: Thirty-six Sprague-Dawley rats were subjected to four vessel occluding global brain ischemic model. Thionin staining and immunohistochemistry were used for neuropathological evaluation and assay of iNOS expression in the hippocampal CA1 subregion of the rats. RESULTS: In the sham group, weak expression of iNOS was detected. The expression of iNOS in the CIP and CIP+ischemic insult groups were increased significantly compared with that in the sham group. Administration of MTPG via lateral cerebral ventricle 20 min before CIP blocked the up-regulation of iNOS induced by CIP, but had no influence on the pyramidal neuron survival. However, in the MTPG+CIP+ischemic insult group, the expression of iNOS was extremely intensive compared to that in CIP and MTPG+CIP groups. Importantly, this up-regulation was accompanied with obvious delayed neuronal death. CONCLUSION: NO/iNOS pathway plays an important role in the process of mGluR2/3 mediated-brain ischemic tolerance induced by CIP.

Role of inducible nitric oxide synthase in the metabotropic glutamate receptor2/3 mediated-brain ischemic tolerance

AIM: To explore the role of NO/ inducible nitric oxide synthase (iNOS) in the metabotromi glutamate receptor 2/3C (mGluR2/3) mediated-brain ischemic tolerance induced by cerebral ischemic preconditioning (CIP), and to observe the influences of α-methyl- (4-tetrazolyl- phenyl) glycine (MTPG), an antagonist of mGluR2/3, on the expression of iNOS during the induction of brain ischemic tolerance. METHODS: Thirty-six Sprague-Dawley rats were subjected to four vessel occluding global brain ischemic model. Thionin staining and immunohistochemistry were used for neuropathological evaluation and assay of iNOS expression in the hippocampal CA1 subregion of the rats. RESULTS: In the sham group, weak expression of iNOS was detected. The expression of iNOS in the CIP and CIP+ischemic insult groups were increased significantly compared with that in the sham group. Administration of MTPG via lateral cerebral ventricle 20 min before CIP blocked the up-regulation of iNOS induced by CIP, but had no influence on the pyramidal neuron survival. However, in the MTPG+CIP+ischemic insult group, the expression of iNOS was extremely intensive compared to that in CIP and MTPG+CIP groups. Importantly, this up-regulation was accompanied with obvious delayed neuronal death. CONCLUSION: NO/iNOS pathway plays an important role in the process of mGluR2/3 mediated-brain ischemic tolerance induced by CIP.