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Nitric Oxide (NO) and Convulsions Induced by Pentylenetetrazol
Author(s) -
JELENKOVIĆ ANKICA,
JOVANOVIĆ MARINA,
NINKOVIĆ MILICA,
MAKSIMOVIĆ M.,
BOKONJIĆ D.,
BOŠKOVIĆ B.
Publication year - 2002
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2002.tb04075.x
Subject(s) - pentylenetetrazol , nitric oxide , epileptogenesis , medicine , anesthesia , anticonvulsant , tonic (physiology) , incidence (geometry) , nitric oxide synthase , epilepsy , convulsion , pharmacology , physics , psychiatry , optics
A bstract : Data about the role of nitric oxide (NO) in epileptogenesis are contradictory. It is found to exert both proconvulsant and anticonvulsant effects. In an attempt to elucidate the role of NO in seizures, male Wistar rats were treated intraperitoneally by pentylenetetrazol (PTZ) (60, 80, and 100 mg/kg) and by a nitric oxide synthase antagonist, N ‐omega‐nitro‐l‐arginine‐methyl‐ester ( l ‐NAME) (10, 40, and 70 mg/kg), applied before PTZ. The time to onset and incidence of forelimb dystonia (FLD), generalized clonic convulsions (GCC), clonic‐tonic convulsions (CTC), and mortality were recorded. The most successful convulsive response and mortality prevention were found in PTZ (80 mg/kg)‐treated groups, where l ‐NAME (70 mg/kg) decreased the incidence by 29, 50, 67 ( p = 0.052 ), and 50%, respectively, and significantly prolonged the time to onset, except that for mortality. Unexpectedly, l ‐NAME (40 mg/kg) increased incidence of GCC and mortality by 16%, similar to l ‐NAME (10 mg/kg) in PTZ (60 mg/kg)‐treated groups, where GCC, CTC, and mortality increased by 14, 14, and 28%, respectively. Convulsive latency was prolonged in some PTZ (100 mg/kg) + l ‐NAME (40 and 70 mg/kg)‐treated groups. In the experimental model and protocol used, it is concluded that (1) the effects of NO are l ‐NAME‐ and PTZ‐dose dependent; (2) clonic‐tonic convulsions are more strongly influenced by NO than limbic, probably because of PTZ limbic structure overstimulation; (3) l ‐NAME decreases the incidence of CTC and prolongs FLD, GCC, and CTC times to onset, indicating that NO acts as a proconvulsant; and (3) increased GCC, CTC, and mortality that suggests an anticonvulsant effect of NO needs further investigation.