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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Analysis of the NMDA in Focal Cerebral Ischemia in Rats

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Author(s):
Tirapelli, D. P. C. [1] ; Carlotti Jr, C. G. [2] ; Leite, J. P. [3] ; Lizarte, F. S. N. [2] ; Tirapelli, L. F. [2] ; Colli, B. O. [2]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Ribeirao Preto Fac Med, Dept Surg & Anat, BR-14049900 Ribeirao Preto, SP - Brazil
[2] Carlotti Jr, Jr., C. G., Univ Sao Paulo, Ribeirao Preto Fac Med, Dept Surg & Anat, BR-14049900 Ribeirao Preto, SP - Brazil
[3] Univ Sao Paulo, Ribeirao Preto Fac Med, Dept Internal Med, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 3
Document type: Journal article
Source: INTERNATIONAL JOURNAL OF MORPHOLOGY; v. 30, n. 3, p. 979-985, 2012.
Web of Science Citations: 1
Abstract

NMDAR (N-methyl-D-aspartate receptor) is one subtype of ionotrophic glutamate receptor which is extensively distributed in the central nervous system (CNS). In the mammalian CNS, NMDAR serves prominent roles in the pathophysiologic process of cerebral ischemia. This study aimed to investigate the pattern of expression of protein and gene of the excitatory neurotransmitter NMDAR in experimental focal cerebral ischemia and the hole of neuroprotection with hypothermia and ketoprofen. 120 rats were randomly divided into 6 groups (20 animals each): control - no surgery; sham - simulation of surgery; ischemic - focal ischemia for 1 hour, without reperfusion; ischemic + intraischemic hypothermia; ischemic + previous intravenous ketoprofen, and ischemic + hypothermia and ketoprofen. Ten animals from each experimental group were used to establish the volume of infarct. Transient focal cerebral ischemia was obtained in rats by occlusion of the middle cerebral artery with an intraluminal suture. The infarct volume was measured using morphometric analysis of infarct areas defined by triphenyl tetrazolium chloride and the patterns of expression of the protein and gene NMDA were evaluated by immunohistochemistry and quantitative real-time PCR, respectively. Increases in the protein and gene NMDA receptor in the ischemics areas were observed and these increases were reduced by hypothermia and ketoprofen. The increase in the NMDA receptor protein and gene expression observed in the ischemic animals was reduced by neuroprotection (hypothermia and ketoprofen). The NMDA receptor increases in the ischemic area suggests that the NMDA mediated neuroexcitotoxicity plays an important role in cell death and that the neuroprotective effect of both, hypothermia and ketoprofen is directly involved with the NMDA. (AU)

FAPESP's process: 05/00381-8 - Gene expression apoptosis after focal brain ischemia in rats and neutoprotective effect of hypotermia and ketoprofen
Grantee:Benedicto Oscar Colli
Support Opportunities: Regular Research Grants