iNOS contribution to the NMDA-induced excitotoxic lesion in the rat striatum
| Autor: | Isabelle Margaill, Laurent Lecanu, C. Verrecchia, Roger G. Boulu, Michel Plotkine |
|---|---|
| Rok vydání: | 1998 |
| Předmět: |
Pharmacology
medicine.medical_specialty Microdialysis biology Glutamate receptor Brain damage Nitric oxide Nitric oxide synthase Lesion chemistry.chemical_compound Endocrinology nervous system chemistry Anesthesia Internal medicine biology.protein medicine NMDA receptor medicine.symptom Dexamethasone medicine.drug |
| Zdroj: | British Journal of Pharmacology. 125:584-590 |
| ISSN: | 0007-1188 |
| DOI: | 10.1038/sj.bjp.0702119 |
| Popis: | 1 The aim of this study was to assess whether an excitotoxic insult induced by NMDA may induce an iNOS activity which contributes to the lesion in the rat striatum. 2 For this purpose, rats were perfused with 10 mM NMDA through a microdialysis probe implanted in the left striatum. Microdialysate nitrite content, striatal Ca-independent nitric oxide synthase activity and lesion volume were measured 48 h after NMDA exposure in rats treated with dexamethasone (DXM) (3 mg kg−1×4) or aminoguanidine (AG) (100 mg kg−1×4). 3 A significant increase in microdialysate nitrite content and in the Ca-independent NOS activity was observed 48 h after NMDA infusion. Both these increases were reduced by DXM and AG. The NMDA-induced striatal lesion was also reduced by both treatments. 4 Our results demonstrate that NMDA excitotoxic injury induces a delayed, sustained activation of a Ca-independent NOS activity. This activity is blocked by DXM and AG, strongly suggesting the involvement of iNOS. The fact that AG and DXM reduce the NMDA-elicited lesion suggests that iNOS contributes to the brain damage induced by excitotoxic insult. British Journal of Pharmacology (1998) 125, 584–590; doi:10.1038/sj.bjp.0702119 |
| Databáze: | OpenAIRE |
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