Abstract

Abstract Anterior Pericaudate White Matter Is Important for the Secondary Generalization of Kanic Acid-induced Amygdalar Seizures in Rats. 1 Shin-ichi Imamura, 3 Shigeya Tanaka, 2 Koichi Akaike, 2,4 Hideshi Tojo, 2 Norihiko Sakoda, 2 Tatsuro Yamaguchi, 2 Motofumi Kasugai, 2 Akira Sano, and 1 Jun-ichi Kuratsu ( 1 Department of Neurosurgery, Graduate School of Medical and Dental Sciences 2 Department of Neuropsychiatry, Kagoshima University, Graduate School of Medical and Dental Sciences 3 Tanaka Neurosurgical Clinic 4 Himawari Hospital, Kagoshima, Japan ). Rationale: Previous studies indicated that the perirhinal cortex (PRC) is critical for the secondary generalization of amygdalar seizures (Yamada 1993, Imamura 1998). However, the exact pathway from the PRC to the sensorimotor cortex (SMC) remains obscure. McIntyre et al. suggested that a pathway from the PRC to the SMC exists in the white matter adjacent to the caudate nuclei, and we named this site the "anterior pericaudate white matter (APWM)." In this study, we investigated the role of the APWM in the secondary generalization of kanic acid (KA)-induced amygdalar seizures in rats. Methods: Twelve male Wistar rats were used in the experiment. All received stereotactic implantation of electrodes in the left amygdala (LA), left dorsal hippocampus (LH), and left sensorimotor cortex (LCx). A cannula was also inserted into the LA for the preparation of KA injection. The APWM was lesioned stereotactically in six rats (lesioned group) and the remaining six rats served as controls. All rats received KA injection (1.0 μg) into the LA to provocate KA-induced amygdalar seizures, and electroclinical observation was made for 6 hours. Results: Stereotyped KA-induced amygdalar seizures appeared in all rats after 15 to 20 minutes. In the controls, secondary generalization was observed behaviorally and the apparent propagation to the LCx was observed with the electroencephalogram after 60 minutes. Seizure manifestations were less severe. In contrast, seizure propagation to the LCx was weaker in the lesioned group. Conclusions: The APWM may be an important area associated with the secondary generalization of KA-induced amygdalar seizures in rats.

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