Abstracts

Previous studies indicated that the perirhinal cortex (PRC) is important for secondary generalization of amygdalar seizures (Yamada 1993, Imamura 1998). However, the exact pathway from PRC to sensorimotor cortex (SMC) remains elusive. An anatomic tracing study suggested that a pathway from PRC to SMC exists in the white matter adjacent to caudate nuclei (McIntyre, 1996). We named this site the [apos]anterior pericaudate white matter (APWM)[apos]. In this study, we investigated the physiologic role of the APWM in secondary generalization of kanic acid (KA)-induced amygdalar seizures in rats. 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 leisioned stereotactically in 6 rats (lesioned group) and the remaining 6 rats served as controls. All rats received KA injection (1.0 microg) into the LA to provocate KA-induced amygdalar seizures, and electroclinical observation was made for 6 h. The electroencephalographic data was statistically analyzed using Student t-test. Stereotyped KA-induced amygdalar seizures appeared in all rats after 15 to 20 min. In the controls, secondary generalization was observed behaviorally and apparent propagation to the LCx was observed on the electroencephalogram after 1 h. Such changes was further aggravated after 2 h and 6 h. In contrast, statistical analysis revealed that seizure propagation to the LCx was lower electroencepholographically and seizure manifestation was less apparant in the lesioned group after 1 h, 2 h and 6 h. In LA and LH, there were no statistical electroencephalographic changes between controls and lesioned group. It is likely that the APWM is an important pathway associated with secondary generalization of KA-induced amygdalar seizures in rats.