title: Vigabatrin and carbamazepine have different efficacies in the prevention of status epilepticus induced neuronal damage in the hippocampus and amygdala.
abstract: The present study compares the efficacy of carbamazepine (20 mg/kg/day) and vigabatrin (250 mg/kg/day) in preventing hippocampal and amygdaloid damage in the perforant pathway stimulation model of status epilepticus in the rat. One group of rats received a combination of the drugs. Drug treatments were started one week before the stimulation and continued for two weeks thereafter. Gallyas silver impregnation and somatostatin immunohistochemistry were used to detect neuronal damage. All drug treatments were equally effective in decreasing the number and severity of seizures during electrical stimulation. In the vigabatrin group, the damage to the hilar somatostatin-immunoreactive (SOM-ir) neurons and hippocampal CA3c pyramidal cells was less severe than in the vehicle (SOM-ir, P < 0.01; CA3c, P < 0.05) and carbamazepine (SOM-ir, P < 0.01; CA3c, P < 0.05) groups. In the carbamazepine and combination groups, the severity of neuronal damage in the hippocampus did not differ from that in vehicle-treated animals. The amygdaloid neurons were not protected by any of the treatments. Our results show that even though vigabatrin and carbamazepine treatments had similar anticonvulsant efficacy during the perforant pathway stimulation, only vigabatrin but not carbamazepine decreased seizure-induced neuronal damage. Vigabatrin decreased neuronal damage in the hippocampus but not in the amygdala. These results demonstrate that different brain regions and neuronal networks may be protected unequally by different anticonvulsants.
authors.affiliation: A.I. Virtanen Institute, University of Kuopio, Finland. apitkane@messi.uku.fi
authors.forename: A
authors.initials: A
authors.lastname: Pitkänen
authors.forename: J
authors.initials: J
authors.lastname: Tuunanen
authors.forename: T
authors.initials: T
authors.lastname: Halonen
mesh_terms: D000679:Amygdala / Q000473:pathology*; D000818:Animals; D000927:Anticonvulsants / Q000627:therapeutic use*; D002220:Carbamazepine / Q000627:therapeutic use*; D004558:Electric Stimulation; D006624:Hippocampus / Q000473:pathology*; D007150:Immunohistochemistry; D008297:Male; D009434:Neural Pathways / Q000187:drug effects / Q000502:physiology; D009474:Neurons / Q000187:drug effects / Q000502:physiology / Q000648:ultrastructure; D018696:Neuroprotective Agents / Q000627:therapeutic use*; D017966:Pyramidal Cells / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D016622:Silver Staining; D013004:Somatostatin / Q000378:metabolism; D013226:Status Epilepticus / Q000150:complications* / Q000473:pathology*; D020888:Vigabatrin; D005680:gamma-Aminobutyric Acid / Q000031:analogs & derivatives* / Q000627:therapeutic use
chemical_list: D000927:Anticonvulsants; D018696:Neuroprotective Agents; D002220:Carbamazepine; D013004:Somatostatin; D005680:gamma-Aminobutyric Acid; D020888:Vigabatrin