Abstract
Kainic acid, a conformationally restricted glutamate derivative, may be helpful to characterize neurons using glutamate as neurotransmitter. Biochemical, histological, and physiological evidence in the central nervous system indicate a close relation between the neuronal effects of glutamate and kainic acid. However, the precise mechanism by which kainic acid acts is not known. This chapter examines the L-glutamate-sensitive binding and the neurotoxic effects of kainic acid in the pigeon optic tectum to further elucidate the relation between glutamate and kainic acid. The results in the optic tectum are very similar to those obtained in the rat neostriatum. It has been suggested that the cortico-striatal fibers use glutamate as neurotransmitter. After degeneration of these fibers, the glutamate pool and the high affinity uptake are reduced. As in the tecturn, the neurotoxicity of kainic acid depends on an intact afferent pathway and after degeneration of the cortico-striatal endings, the neurotoxicity of kainic acid can be restored with L-glutamate.
Published Version
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