1. Vigabatrin protects against kainic acid-induced neuronal damage in the rat hippocampus
- Author
-
Jarkko Tuunanen, Ari Toppinen, Paavo Riekkinen, Toivo Halonen, Tiina Kotti, and Riitta Miettinen
- Subjects
Male ,Kainic acid ,Silver Staining ,Central nervous system ,Status epilepticus ,Pharmacology ,Neuroprotection ,Hippocampus ,Vigabatrin ,gamma-Aminobutyric acid ,Epilepsy ,chemistry.chemical_compound ,Status Epilepticus ,medicine ,Excitatory Amino Acid Agonists ,Hippocampus (mythology) ,Animals ,Rats, Wistar ,gamma-Aminobutyric Acid ,Neurons ,Kainic Acid ,Behavior, Animal ,business.industry ,Histocytochemistry ,General Neuroscience ,medicine.disease ,Rats ,medicine.anatomical_structure ,nervous system ,chemistry ,Anesthesia ,Anticonvulsants ,medicine.symptom ,business ,medicine.drug - Abstract
We studied the neuroprotective effect of vigabatrin (gamma-vinyl GABA, VGB) in the rat hippocampus after status epilepticus (SE) induced by kainic acid (KA). Rats were treated with VGB (500 or 1000 mg/kg, i.p.) 24 h before KA injection (9 mg/kg, i.p.). The lower dose of VGB had no effect on the generation or severity of convulsions. However, VGB decreased neuronal damage in the CA3a (P < 0.05) and CA1 (P < 0.01) subfields of the hippocampus. The higher dose of VGB attenuated the severity of convulsions (P < 0.05) but had no effect on the development or generalization of convulsions. This finding may have clinical implications in the prevention of neuronal damage induced by drug refractory seizures or SE.
- Published
- 1995