NA+, K+-ATPase activity in the brain of the rats with kainic acid-induced seizures: influence of lamotrigine.
OBJECTIVE
Kainic acid (KA) is used as an experimental agent which produces convulsions and neurotoxic lesions. Lamotrigine (LTG) is an antiepileptic drug, a glutamate release inhibitor, with action at the neuronal voltage-gated sodium channel. The aim of the present study was to investigate the Na+-K+-ATPase activity in the hippocampus and cortex of rats with KA-induced convulsions. Further, this study was also designed to investigate the influence of the LTG pre-treatment on the mentioned hippocampal and cortex changes.


METHODS
The study was carried out on Hannover-Wistar rats. Na+, K+-ATPase activity from hippocampal and temporal cortex tissue was determined two hours after a single subcutaneous KA (8 mg/kg) injection as well as on the third or the fifth experimental day. LTG (30 mg/kg i.p.) was used one hour before KA application and during the next two or four consecutive days. All animals of KA and KA+LTG groups were observed during the first 2 hours after KA application and their behavior was noted. Only animals with characteristically KA-induced behavioral changes observed were used in the study. KA typical behavioral changes were confirmed with electroencephalography.


RESULTS
After KA application, Na+, K+-ATPase activity was significantly inhibited. Na+-K+-ATPase activity inhibition in the hippocampus of the LTG pretreated rats on the fifth experimental day was statistically less pronounced than in KA treated rats. The LTG pretreatment showed also a protective effect on the Na+-K+-ATPase activity in the rats' brain cortex.


CONCLUSIONS
KA systemic application induced Na+, K+- ATPase activity inhibition in the rat hippocampus and cortex and LTG pre-treatment showed a partially protective effect on the enzyme activity.
Vitezić
Dinko
D
University of Rijeka School of Medicine, Rijeka, Croatia. vdinko@medri.hr
Pelcić
Jasenka Mrsić
JM
Zupan
Gordana
G
Vitezić
Miomira
M
Ljubicić
Dulijano
D
Simonić
Ante
A
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D001522:Behavior, Animal / Q000187:drug effects; D001921:Brain / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D002540:Cerebral Cortex / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D004195:Disease Models, Animal; D004569:Electroencephalography / Q000706:statistics & numerical data; D006624:Hippocampus / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D007608:Kainic Acid / Q000494:pharmacology*; D000077213:Lamotrigine; D051381:Rats; D017208:Rats, Wistar; D012640:Seizures / Q000139:chemically induced / Q000201:enzymology / Q000378:metabolism*; D015222:Sodium Channels / Q000187:drug effects / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors* / Q000187:drug effects / Q000378:metabolism*; D014227:Triazines / Q000494:pharmacology*
D000927:Anticonvulsants; D015222:Sodium Channels; D014227:Triazines; D000254:Sodium-Potassium-Exchanging ATPase; D007608:Kainic Acid; D000077213:Lamotrigine