Effects of 3-aminopyridine-induced seizures on platelet eicosanoid synthesis
We investigated the influence of recurrent epileptic seizures on the arachidonic acid (AA) cascade in platelets and brain microvessels, using [C-14]AA as a tracer substrate and chromatographic determination. The recurrent epileptic seizures of male Wistar rats were induced every second day with 3-am...
Elmentve itt :
| Szerzők: | |
|---|---|
| Dokumentumtípus: | Cikk |
| Megjelent: |
2008
|
| Sorozat: | PHARMACOLOGICAL REPORTS
60 No. 3 |
| mtmt: | 1168144 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/9967 |
| LEADER | 02705nab a2200289 i 4500 | ||
|---|---|---|---|
| 001 | publ9967 | ||
| 005 | 20200127135520.0 | ||
| 008 | 161119s2008 hu o 0|| zxx d | ||
| 022 | |a 1734-1140 | ||
| 024 | 7 | |a 1168144 |2 mtmt | |
| 040 | |a SZTE Publicatio Repozitórium |b hun | ||
| 041 | |a zxx | ||
| 100 | 1 | |a Csányi Gábor | |
| 245 | 1 | 0 | |a Effects of 3-aminopyridine-induced seizures on platelet eicosanoid synthesis |h [elektronikus dokumentum] / |c Csányi Gábor |
| 260 | |c 2008 | ||
| 300 | |a 345-352 | ||
| 490 | 0 | |a PHARMACOLOGICAL REPORTS |v 60 No. 3 | |
| 520 | 3 | |a We investigated the influence of recurrent epileptic seizures on the arachidonic acid (AA) cascade in platelets and brain microvessels, using [C-14]AA as a tracer substrate and chromatographic determination. The recurrent epileptic seizures of male Wistar rats were induced every second day with 3-aminopyridine (3-AP, 25 mg/kg ip) for two weeks. In the chronic 3-AP model, the earlier epileptic insults resulted in a decreased incidence of limbic seizures and higher survival rate at later administration of 3-AP. After 3-AP treatment, the formation of lipoxygenase products was unchanged, but the total amount of cyclooxygenase (COX) metabolites was decreased both in platelets and brain microvessels:- The reduction in COX-mediated eicosanoid synthesis after recurrent seizures was due to the decreased synthesis of vasodilator and vasoconstrictor COX metabolites. In platelets, the 3-AP-treatment reduced the synthesis of vasodilator prostacyclin (PGI(2)), prostaglandin E-2 (PGE(2)) and 12-L-hydroxy5,8, 10-heptadecatrienoic acid (12-HHT), while the synthesis of prostaglandin D-2 (PGD(2)) remained unchanged. In isolated brain capillaries, the PGD2, PGE2 and 12-HHT synthesis was decreased after recurrent seizures. As for the vasoconstrictor COX metabolites, both platelets and brain microvessels synthesized significantly lesser amount of prostaglandin F-2 alpha, (PGF(2 alpha)) and thromboxane A(2) (TxA(2)) upon 3-AP administration. Our results indicate that platelets and isolated brain capillaries synthesize significantly lesser amount of COX metabolites after chronic 3-AP treatment. The decreased conversion of AA into different COX products may play a role in the neuroprotective/preconditional adaptation of the brain against subsequent seizures. | |
| 700 | 0 | 1 | |a Kis Béla |e aut |
| 700 | 0 | 1 | |a Gecse Árpád |e aut |
| 700 | 0 | 1 | |a Telegdy Gyula |e aut |
| 700 | 0 | 1 | |a Szupera Zoltán |e aut |
| 700 | 0 | 1 | |a Vécsei László |e aut |
| 700 | 0 | 1 | |a Szente Magdolna |e aut |
| 700 | 0 | 1 | |a Leprán István |e aut |
| 700 | 0 | 1 | |a Mezei Zsófia |e aut |
| 856 | 4 | 0 | |u http://publicatio.bibl.u-szeged.hu/9967/1/Csanyi_G._effects_of_3_aminopyr._u.pdf |z Dokumentum-elérés |