Hippocampal transection attenuates kainic acid-induced amygdalar seizures in rats.
Since the dorsal and ventral hippocampus in the rat may act differently from one another in limbic seizures, we studied effects of orthogonal transection between the dorsal and ventral hippocampus upon kainic acid-induced amygdalar seizures. A total of 26 rats were divided into three groups. Ten rats underwent transection using a modified wire knife (transection group); 16 others were untransection group (n=10) and controls (n=6). All the rats then 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 introduced into the LA. Rats except controls later received 1.0 microg of kainic acid (KA) via the cannula. Controls received phosphate buffer solution alone. In 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, characterized by mastication, salivation, facial twitching, forelimb clonus, and sometimes rearing and falling, lasted 1 to 2 days. Microscopic examination revealed severe neuronal cell damage in the LA, LvH, and LdH. In the transection group, multiple spike discharges initiated from the LA and were propagated to LvH, but LdH as well as LCx involvement was slight. Status epilepticus involved only the LA and LvH 1 to 2 h following KA injection. Seizures subsided within 24 h, showing no ictal manifestations except for aggressiveness. Overall, seizures were weak and transient compared with those in controls. Histologically, hippocampal neuronal damage was slight, but damage to amygdalar neurons was similar to that in untransection group. No electroclinical and histological changes were seen in controls. These results indicated that connections between the dorsal and ventral hippocampus are important for full development of KA-induced amygdalar seizures.
Imamura
S
S
Department of Neurosurgery, University of Kagoshima, Faculty of Medicine, Sakuragaoka 8-35-1, Kagoshima, Japan. imamuras@m2.kufm.kagoshima-u.ac.jp
Tanaka
S
S
Akaike
K
K
Tojo
H
H
Takigawa
M
M
Kuratsu
J
J
D000679:Amygdala / Q000166:cytology / Q000503:physiopathology*; D000818:Animals; D001522:Behavior, Animal; D004569:Electroencephalography; D018690:Excitatory Amino Acid Agonists; D006624:Hippocampus / Q000166:cytology / Q000503:physiopathology* / Q000601:surgery; D007608:Kainic Acid; D007696:Kindling, Neurologic / Q000502:physiology; D008297:Male; D009434:Neural Pathways; D051381:Rats; D017208:Rats, Wistar; D013226:Status Epilepticus / Q000139:chemically induced / Q000503:physiopathology* / Q000601:surgery
D018690:Excitatory Amino Acid Agonists; D007608:Kainic Acid