Synaptic localization of kainic acid binding sites

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Abstract
The heterocyclic compound kainic acid (KA) is a potent excitant when applied to mammalian neurons. Lesions caused by injections of KA into the rat striatum and hippocampus cause similar patterns of damage to those seen in Huntington''s chorea in humans and status epilepticus, respectively. Although it was originally thought to be a glutamate agonist, KA does not act on the majority of the receptors for glutamate, but seems to act on a class of receptors which are distinct from those which mediate responses to other excitatory amino acids. The potent and selective neurotoxic effects of this compound may be mediated by these same receptors. Knowledge of the relative distribution of junctional and extrajunctional (non-synaptic) receptors would provide important insights into the action of KA on the CNS. KA binding sites are greatly enriched in isolated synaptic junctions from rat brain. As demonstrated by in vitro autoradiography, these binding sites are concentrated specifically in terminal fields where KA acts as a potent neurotoxin.