Usefulness of parenteral kainic acid as a model of temporal lobe epilepsy.
Systemic injections of kainic acid (KA) in adult rats rapidly induce sustained motor seizures preferentially involving the limbic structures and culminating in status epilepticus. The hippocampal formation and amygdala seem to occupy a central position for the onset of paroxysmal discharge and for the manifestation of limbic signs respectively. With long survival periods, the animals spontaneously display limbic motor seizures and a second administration of KA produces more severe effects. The brain damage, found in several limbic structures subsequent to KA-induced seizures, is reminiscent of that seen in human epileptics, and electrographical and metabolic studies (using the 2-deoxyglucose method) reveal that it follows increased neuronal and metabolic activation. The crucial role of the mossy fiber system in the particular vulnerability to KA of the CA3 neurons of Ammon's horn is also suggested by a study of the maturation of the KA-induced seizure and brain damage syndrome.
D000679:Amygdala / Q000378:metabolism; D000818:Animals; D001925:Brain Damage, Chronic / Q000139:chemically induced; D004195:Disease Models, Animal; D004833:Epilepsy, Temporal Lobe / Q000139:chemically induced / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D007608:Kainic Acid; D011759:Pyrrolidines; D051381:Rats; D013577:Syndrome
D011759:Pyrrolidines; D005947:Glucose; D007608:Kainic Acid