Biphasic action of vigabatrin on cortical epileptic after-discharges in rats
Jazyk angličtina Země Německo Médium print-electronic
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
- MeSH
- elektrický šok metody MeSH
- elektroencefalografie metody MeSH
- epilepsie chemicky indukované patofyziologie prevence a kontrola MeSH
- krysa rodu Rattus MeSH
- mozková kůra účinky léků fyziologie MeSH
- potkani Wistar MeSH
- vigabatrin terapeutické užití toxicita MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- vigabatrin MeSH
The time course of the anticonvulsant effect of vigabatrin against cortically induced epileptic after-discharges (ADs) was studied in freely moving rats with implanted electrodes. Adult rats (n=30) were exposed to five stimulation sessions each consisting of six stimulation series at 20-min intervals. The first session was a control one, then two groups of animals (n=10 each) were given vigabatrin (600 or 1,200 mg/kg i.p.), the control animals received physiological saline. Stimulation sessions were repeated 1, 24, 48, and 96 hours after the injection. Control animals exhibited an increased transition from the spike-and-wave type of AD to the second, "limbic" type and an increased intensity of movements accompanying stimulation. ADs in the second and subsequent sessions were, however, shorter than in the first session. Vigabatrin facilitated the transition to the second type of AD 1 h after administration but suppressed this transition as well as decreased the number of stimulations eliciting ADs 48 h later. AD duration and the severity of clonic seizures accompanying spike-and-wave ADs were influenced similarly. The effects of the lower dose of vigabatrin were more marked than those of the higher dose. The biphasic action of vigabatrin in our model might be due either to uneven changes of GABA concentration in different brain structures or to an additional mechanism of action. Our results in a cortical model of seizure demonstrate that the sequence of pro- and anticonvulsant actions of vigabatrin is not restricted to seizures of limbic origin and might represent a general phenomenon.
Zobrazit více v PubMed
Eur J Pharmacol. 1977 Oct 15;45(4):319-28 PubMed
Epilepsy Res. 2001 May;44(2-3):109-17 PubMed
Epilepsia. 1991 Mar-Apr;32(2):242-9 PubMed
Physiol Res. 2002;51(4):363-70 PubMed
J Neural Transm. 1985;63(2):157-67 PubMed
Epilepsy Res Suppl. 1991;3:23-8 PubMed
Exp Neurol. 1969 Nov;25(3):295-330 PubMed
Epilepsy Res. 1999 Nov;37(2):95-108 PubMed
Brain Res. 1986 Nov 29;398(2):370-4 PubMed
Epilepsy Res. 2002 Mar;49(1):35-43 PubMed
Exp Neurol. 1987 Feb;95(2):391-402 PubMed
Exp Neurol. 1986 Sep;93(3):546-56 PubMed
Epilepsia. 1993 Nov-Dec;34(6):1123-9 PubMed
Brain Res. 1979 May 11;167(2):297-305 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1994 Mar;349(3):270-8 PubMed
Electroencephalogr Clin Neurophysiol. 1972 Mar;32(3):281-94 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1980;315(2):119-28 PubMed
Epilepsy Res Suppl. 1991;3:161-8 PubMed
Eur J Pharmacol. 1989 Apr 12;163(1):1-14 PubMed
Annu Rev Pharmacol Toxicol. 1978;18:269-89 PubMed
J Neurochem. 1981 Apr;36(4):1521-7 PubMed
J Neural Transm. 1988;72(3):213-33 PubMed
Epilepsy Res Suppl. 1996;12:75-8 PubMed
J Neurochem. 1990 Dec;55(6):1870-4 PubMed
Electroencephalogr Clin Neurophysiol. 1972 Mar;32(3):269-79 PubMed
J Neurochem. 1989 Dec;53(6):1737-50 PubMed
J Neurochem. 1985 Sep;45(3):879-89 PubMed
Br J Clin Pharmacol. 1989;27 Suppl 1:3S-11S PubMed
Epilepsia. 1994 Mar-Apr;35(2):431-6 PubMed
Brain Res. 1994 Jul 18;651(1-2):85-91 PubMed
Exp Neurol. 1981 Dec;74(3):829-36 PubMed
Neurosci Lett. 2001 Oct 12;312(1):37-40 PubMed
Epilepsia. 1996 Apr;37(4):336-41 PubMed
Drugs. 1998 Mar;55(3):437-60 PubMed