title: Different effect of hippocampal granule cell destruction on amygdaloid kindling in Sprague-Dawley and Wistar rats.
abstract: The hippocampal granule cells receive major inputs via the perforant path from other limbic structures such as the amygdala (AM). In this study, we examined Sprague-Dawley (SD) and Wistar rats, the effect of bilateral destructions of the hippocampal granule cells on the process of AM kindling and kindled AM seizures after completion of kindling. The granule cells were selectively and completely destroyed bilaterally by intra-hippocampal injections of colchicine. The left AM was used as the primary kindling site and the right AM as the secondary site. In SD rats, prior destruction of the granule cells caused a marked delay in the seizure development of both the primary AM kindling and subsequent secondary AM kindling. However, once AM kindling was established in SD rats, the destruction of granule cells was totally ineffective in preventing kindled seizures. In Wistar rats, unlike SD rats, prior destruction of the granule cells failed to change the rate of kindling at the primary and secondary sites. However, Wistar rats showed a transient and marked regression of kindled seizures when the granule cells were destroyed after the completion of AM kindling. In both strains, granule cell destruction had no effect on the re-establishment of kindled seizures at the time of primary-site re-test. These findings suggest that hippocampal granule cells of SD and Wistar rats play different roles in AM kindling.
authors.affiliation: Department of Neuropsychiatry, Fukushima Medical College, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Tsunoda
authors.forename: N
authors.initials: N
authors.lastname: Mori
authors.forename: M
authors.initials: M
authors.lastname: Osonoe
authors.forename: K
authors.initials: K
authors.lastname: Ariga
authors.forename: H
authors.initials: H
authors.lastname: Saitoh
authors.forename: H
authors.initials: H
authors.lastname: Kittaka
authors.forename: S
authors.initials: S
authors.lastname: Ogata
mesh_terms: D000679:Amygdala / Q000166:cytology / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D003078:Colchicine; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D007696:Kindling, Neurologic; D008297:Male; D009474:Neurons / Q000502:physiology*; D009498:Neurotoxins; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012640:Seizures / Q000503:physiopathology
chemical_list: D009498:Neurotoxins; D003078:Colchicine