TY - JOUR
T1 - A behavioral and immunohistochemical study on the development of perirhinal cortical kindling
T2 - A comparison with other types of limbic kindling
AU - Sato, Toshiki
AU - Yamada, Norihito
AU - Morimoto, Kiyoshi
AU - Uemura, Shuji
AU - Kuroda, Shigetoshi
N1 - Funding Information:
This study was supported by a Grant-in-Aid-for Scientific Research (07671070) from the Ministry of Education, Science, Sports and Culture, Japan.
PY - 1998/11/16
Y1 - 1998/11/16
N2 - We have previously reported that the perirhinal cortex (PRC) plays an important role in the generalization of kindled seizures. In the present study, we kindled the rat PRC and made a comparison with amygdala (AM) and dorsal hippocampal (dHIPP) kindling. In order to produce a functional map of the seizure generalization pathway from these limbic foci, we also stained for Fos protein in sections of the PRC-, AM- and dHIPP-kindled brains using an immunohistochemistry technique. In the generalized seizures of PRC kindling the duration of afterdischarges (ADs) and the latency to forelimb clonus were significantly shorter than those of AM kindling or dHIPP kindling. Typically, the PRC-kindled rats demonstrated moving arrest or exploratory behavior for about 10 days, and then a characteristic 'rapid backward moving' behavior for 1 day, followed by the sudden appearance of generalized motor seizures. Fos protein induction after a single stimulation of the PRC is more widely observed than after a single stimulation of the AM, in that the PRC stimulation produced Fos protein expression in the temporal and parietal neocortices. Following AM and PRC kindling, the Fos-positive areas were asymmetrically propagated from the ipsilateral to the contralateral hemisphere. The contralateral PRC was primarily activated at the generalization of epileptic activity in the contralateral hemisphere. In contrast, the Fos protein distribution of the dHIPP-kindled rats was restricted to the bilateral hippocampi during the early stages, followed by the symmetrical propagation from the limbic system to the neocortex during the generalized seizures. These results indicate that the PRC plays a characteristic role in the seizure generalization of kindling.
AB - We have previously reported that the perirhinal cortex (PRC) plays an important role in the generalization of kindled seizures. In the present study, we kindled the rat PRC and made a comparison with amygdala (AM) and dorsal hippocampal (dHIPP) kindling. In order to produce a functional map of the seizure generalization pathway from these limbic foci, we also stained for Fos protein in sections of the PRC-, AM- and dHIPP-kindled brains using an immunohistochemistry technique. In the generalized seizures of PRC kindling the duration of afterdischarges (ADs) and the latency to forelimb clonus were significantly shorter than those of AM kindling or dHIPP kindling. Typically, the PRC-kindled rats demonstrated moving arrest or exploratory behavior for about 10 days, and then a characteristic 'rapid backward moving' behavior for 1 day, followed by the sudden appearance of generalized motor seizures. Fos protein induction after a single stimulation of the PRC is more widely observed than after a single stimulation of the AM, in that the PRC stimulation produced Fos protein expression in the temporal and parietal neocortices. Following AM and PRC kindling, the Fos-positive areas were asymmetrically propagated from the ipsilateral to the contralateral hemisphere. The contralateral PRC was primarily activated at the generalization of epileptic activity in the contralateral hemisphere. In contrast, the Fos protein distribution of the dHIPP-kindled rats was restricted to the bilateral hippocampi during the early stages, followed by the symmetrical propagation from the limbic system to the neocortex during the generalized seizures. These results indicate that the PRC plays a characteristic role in the seizure generalization of kindling.
KW - Amygdala
KW - Dorsal hippocampus
KW - Epilepsy
KW - Fos protein
KW - Kindling
KW - Perirhinal cortex
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U2 - 10.1016/S0006-8993(98)00895-6
DO - 10.1016/S0006-8993(98)00895-6
M3 - Article
C2 - 9804919
AN - SCOPUS:0032539055
VL - 811
SP - 122
EP - 132
JO - Molecular Brain Research
JF - Molecular Brain Research
SN - 0006-8993
IS - 1-2
ER -