Kainic acid seizure syndrome and binding sites in developing rats.
In rats up to 16 days after birth, parenteral kainic acid (KA) produced tonico-clonic convulsions, metabolic activation limited to the hippocampus, and no brain damage. Starting with the 19th day after birth, KA produced limbic seizures associated with metabolic activation and subsequent damage in the hippocampus, the amygdala, and other limbic structures. Membranes prepared from hippocampi 10 days after birth bound [3H]KA with a high affinity component, which was localized in the mossy fiber region by slice autoradiography. In contrast, on amygdaloid membranes this component appeared only 17-19 days after birth. Our results further stress the crucial role of the amygdala in the KA seizure syndrome.
D000679:Amygdala / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D001665:Binding Sites; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D007608:Kainic Acid / Q000378:metabolism*; D008297:Male; D011759:Pyrrolidines / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000139:chemically induced* / Q000473:pathology; D013577:Syndrome
D011759:Pyrrolidines; D007608:Kainic Acid