Hippocampal transection attenuates kainic acid-induced amygdalar seizures in rats

Since the dorsal and ventral hippocampus in the rat may act differently fro m one another in limbic seizures, we studied effects of orthogonal transect ion between the dorsal and ventral hippocampus upon kainic acid-induced amy gdalar seizures. A total of 26 rats were divided into three groups. Ten rat s underwent transection using a modified wire knife (transection group); 16 others were untransection group (n=10) and controls (n=6). All the rats th en underwent stereotactic implantation of electrodes in the left amygdala ( LA), left dorsal hippocampus (LdH), left ventral hippocampus (LVH), and the left sensorimotor cortex (LCx). A stainless steel cannula also was introdu ced into the LA. Rats except controls later received 1.0 mug of kainic acid (KA) via the cannula. Controls received phosphate buffer solution alone. I n the untransection group, multiple spike discharges in the LA immediately propagated concurrently to the LVH and LdH. Propagation involved the LCx to become status epilepticus 1 to 2 h after KA injection. Seizures, character ized by mastication, salivation, facial twitching, forelimb clonus, and som etimes rearing and falling, lasted 1 to 2 days. Microscopic examination rev ealed severe neuronal cell damage in the LA, LVH, and LdH. In the transecti on group, multiple spike discharges initiated from the LA and were propagat ed to LVH, but LdH as well as LCx involvement was slight. Status epilepticu s involved only the LA and LvH 1 to 2 h following KA injection. Seizures su bsided within 24 h, showing no ictal manifestations except for aggressivene ss. Overall, seizures were weak and transient compared with those in contro ls. Histologically, hippocampal neuronal damage was slight, but damage to a mygdalar neurons was similar to that in untransection group. No electroclin ical and histological changes were seen in controls. These results indicate d that connections between the dorsal and ventral hippocampus are important for full development of KA-induced amygdalar seizures. (C) 2001 Elsevier S cience B.V. All rights reserved.