Anticonvulsant action of 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline in immature rats: comparison with the effects on motor performance
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
9190844
Knihovny.cz E-zdroje
- MeSH
- antikonvulziva farmakologie MeSH
- chinoxaliny farmakologie MeSH
- krysa rodu Rattus MeSH
- mozková kůra účinky léků MeSH
- novorozená zvířata MeSH
- plnění a analýza úkolů MeSH
- pohybová aktivita účinky léků MeSH
- potkani Wistar MeSH
- vztah mezi dávkou a účinkem léčiva MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 2,3-dioxo-6-nitro-7-sulfamoylbenzo(f)quinoxaline MeSH Prohlížeč
- antikonvulziva MeSH
- chinoxaliny MeSH
Anticonvulsant action of 2,3-dihydroxy-6-nitro-7-sulfamoylbenzo(f)quinoxaline (NBQX), a competitive antagonist at non-N-methyl-D-aspartate receptors for excitatory amino acids, was studied in a model of cortical epileptic afterdischarges (ADs) in 12-, 18- and 25-day-old rat pups with implanted electrodes. Electrical stimulation of sensorimotor cortex was repeated four times with 20-min intervals, NBQX (in doses of 10, 30, 60 or 90 mg/kg i.p.) or solvent (dimethyl sulfoxide, 1 ml/kg i.p.) were injected 10 min after the first afterdischarge. Dimethyl sulfoxide did not change the phenomena recorded; NBQX shortened ADs or at least blocked progressive prolongation observed under control conditions. Intensity of movements accompanying stimulation decreased after NBQX, and clonic movements accompanying ADs were suppressed in a dose-dependent manner. The highest dose of NBQX disabled the animals; therefore, the action of this drug on motor skills was studied in another group of animals. Even the dose of 30 mg/kg NBQX interfered with motor performance in 12- and 18-day-old rat pups, 25-day-old rat pups were more resistant to this action. NBQX exhibited only moderate antiepileptic action (suppression of progressive lengthening of ADs) at doses where unwanted side effects were absent.