Nitric oxide and convulsions in 4-aminopyridine-treated mice
| Autor: | Marian Wielosz, Stanisław J. Czuczwar, Zdzisław Kleinrok, Dorota Żółkowska, Małgorzata Młynarczyk, Piotr Tutka |
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| Rok vydání: | 2002 |
| Předmět: |
Male
Molsidomine Arginine Pharmacology Nitric Oxide Nitroarginine Nitric oxide Lethal Dose 50 Mice chemistry.chemical_compound Seizures Convulsion medicine Animals Channel blocker 4-Aminopyridine Enzyme Inhibitors Injections Intraventricular Behavior Animal biology Nitric oxide synthase chemistry Enzyme inhibitor Anesthesia biology.protein Nitric Oxide Synthase medicine.symptom Injections Intraperitoneal medicine.drug |
| Zdroj: | European Journal of Pharmacology. 437:47-53 |
| ISSN: | 0014-2999 |
| Popis: | We studied whether N G -nitro- l -arginine (NNA), an inhibitor of nitric oxide (NO) synthase as well as l -arginine and molsidomine, two agents elevating NO, influenced convulsions caused by 4-aminopyridine, a K + channel blocker in mice. NNA, in a dose known to decrease level of NO (40 mg kg −1 ), enhanced the seizure susceptibility to intraperitoneal (i.p.) and intracerebroventricular (i.c.v.) 4-aminopyridine. l -arginine (500 mg kg −1 ) and molsidomine (20 mg kg −1 ) alone did not influence 4-aminopyridine-induced seizure activity. Surprisingly, the proconvulsant effect of NNA upon clonic and tonic seizures was potentiated by molsidomine (20 mg kg −1 ). No influence of l -arginine on the proconvulsant effect of NNA was found. Taking into account the proconvulsant effect of NNA, an involvement of NO-mediated events in the mechanism of convulsive activity of 4-aminopyridine might be postulated. However, the ineffectiveness of l -arginine and molsidomine to suppress the convulsive activity of 4-aminopyridine as well as a paradoxical potentiation of the proconvulsant effect of NNA by molsidomine seem to exclude the impact of NO pathway on 4-aminopyridine-induced convulsions in mice. Our data suggest that the proconvulsant effect of NNA in this seizure model is caused by other, not related to NO, mechanisms. |
| Databáze: | OpenAIRE |
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