RGD Reference Report - Effect of dextromethorphan, a NMDA antagonist, on DNA repair in rat photochemical thrombotic cerebral ischemia. - Rat Genome Database
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Effect of dextromethorphan, a NMDA antagonist, on DNA repair in rat photochemical thrombotic cerebral ischemia.

Authors: Yin, KJ  Sun, FY 
Citation: Yin KJ and Sun FY, Brain Res. 1999 Jan 2;815(1):29-35.
RGD ID: 10401103
Pubmed: (View Article at PubMed) PMID:9974119

Photochemical thrombotic ischemia model was used to study the possible roles of excision repair cross-complementing group 6 (ERCC6), a DNA repair gene, in the neuroprotection of dextromethorphan (DM), a NMDA antagonist, in ischemic brain injury. The results showed that no obvious ERCC6 mRNA expression was found in the perifocal area of irradiated cerebral cortex before 24 h postischemia. Then, the number of ERCC6 mRNA positive cells gradually enhanced, and attained a peak value at 72 h after light irradiation, which followed a declined tendency at 7-day postlesion. These results suggest that DNA repair gene ERCC6 mRNA expression in the perifocal area may be involved in the pathophysiological processes following the photochemical thrombotic cerebral ischemia. By the administration of DM, we observed that it can significantly upregulate the expression of ERCC6 mRNA in the perifocal area at 48 h after ischemic event. The neuroprotective mechanisms of DM may be related to the upregulation of DNA repair gene ERCC6 mRNA.

Annotation

Disease Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Ercc6  (ERCC excision repair 6, chromatin remodeling factor)

Genes (Mus musculus)
Ercc6  (excision repair cross-complementing rodent repair deficiency, complementation group 6)

Genes (Homo sapiens)
ERCC6  (ERCC excision repair 6, chromatin remodeling factor)


Additional Information