Maturation of kainic acid seizure-brain damage syndrome in the rat. III. Postnatal development of kainic acid binding sites in the limbic system.
The progressive appearance of [3H]kainic acid binding sites with age has been studied in membrane suspensions prepared from various regions of the rat limbic system, and by autoradiography. Binding sites with fast dissociation rate appeared earlier than binding sites with slow dissociation rate. Scatchard analysis demonstrated apparent receptor heterogeneity for both subclasses. High affinity components were detected in the hippocampus as early as 10 days after birth, but in the amygdala + piriform lobe were found only towards the end of the third week, when animals also respond to parenteral kainic acid, for the first time, with limbic seizures accompanied by metabolic activation of the amygdala. Slice autoradiography revealed distinct labelling of the hippocampal CA3 region by postnatal day 10. A comparison with the ontogenesis of the kainic acid-induced seizure-brain damage syndrome suggests a role of high affinity receptors as mediators of metabolic nerve cell activation by kainic acid. However, this receptor interaction per se does not result in neuronal damage to the vulnerable region of the Ammon's horn, which will only occur at an age when also the amygdala is activated by the neurotoxin.
D000367:Age Factors; D000818:Animals; D001345:Autoradiography; D001665:Binding Sites; D001925:Brain Damage, Chronic / Q000139:chemically induced* / Q000378:metabolism; D004827:Epilepsy / Q000139:chemically induced* / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D007608:Kainic Acid / Q000378:metabolism*; D008032:Limbic System / Q000378:metabolism*; D011759:Pyrrolidines / Q000378:metabolism*; D051381:Rats
D011759:Pyrrolidines; D007608:Kainic Acid