Administration of levetiracetam after prolonged status epilepticus does not protect from mitochondrial dysfunction in a rodent model.
Neuronal death and dysfunction occur after status epilepticus (SE), and is associated with mitochondrial enzyme damage. We previously showed, using the rat perforant pathway stimulation model, that levetiracetam administration (LEV; 1000 mg/kg intraperitoneal) during established SE reduces seizure severity and prevents mitochondrial dysfunction. We now show that administration of the same dose of LEV after 5h SE, does not protect from mitochondrial dysfunction.
Gibbs
J E
JE
Epilepsy Group, Centre for Clinical Neurosciences, St. George's University of London, Cranmer Terrace, Tooting, London SW17 0RE, United Kingdom.
Cock
H R
HR
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004558:Electric Stimulation; D004569:Electroencephalography / Q000187:drug effects*; D000077287:Levetiracetam; D008928:Mitochondria / Q000187:drug effects* / Q000473:pathology; D018696:Neuroprotective Agents / Q000627:therapeutic use; D010889:Piracetam / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology; D013997:Time Factors
D000927:Anticonvulsants; D018696:Neuroprotective Agents; D000077287:Levetiracetam; D010889:Piracetam