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Perirhinal cortical lesion suppresses the secondary generalization in kainic acid‐induced limbic seizure
Author(s) -
FUKUMOTO SHINICHIRO,
TANAKA SHIGEYA,
TOJO HIDESHI,
AKAIKE KOICHI,
TAKIGAWA MORIKUNI
Publication year - 2002
Publication title -
psychiatry and clinical neurosciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.609
H-Index - 74
eISSN - 1440-1819
pISSN - 1323-1316
DOI - 10.1046/j.1440-1819.2002.01055.x
Subject(s) - kainic acid , ibotenic acid , perirhinal cortex , neuroscience , lesion , limbic system , clonus , motor cortex , epilepsy , psychology , hippocampus , medicine , temporal lobe , central nervous system , pathology , glutamate receptor , receptor , stimulation
To elucidate the role of the perirhinal cortex (PRC) in experimental epilepsy, the effects of the lesion of the PRC on kainic acid (KA)‐induced limbic seizure were investigated. The PRC lesion was made by means of ibotenic acid (IBO) microinjection. The electroencephalogram in the PRC‐lesioned rats demonstrated suppression of the propagation of epileptic discharges from the limbic structures to the sensorimotor cortex. Behaviorally, motor manifestations such as mastication, facial twitching and forelimb clonus were attenuated. These results indicate that the PRC seems to be a potent relay station of the secondary generalization from the limbic structures to the sensorimotor cortex.