Effects of Kainic Acid on Different Populations of Cerebellar Interneurones and Astrocytes Cultured in vitro

The potent toxic action of kainic acid has been initially attributed to its excitatory effects on neuronal cells, but numerous following studies showed that the mechanism of kainate toxicity is more complex (Coyle, 1983). Several hypotheses have been formulated in order to explain the mechanism of action of kainate, since the discovery of specific receptors for this excitotoxin in the central nervous system (London and Coyle, 1979; Monaghan and Cotman, 1982). Some authors have evidenced that the presence of the glutamatergic afferent fibers is necessary for kainate to be effective in some brain areas (Biziere and Coyle, 1978, 1979; Panula, 1980), suggesting a cooperative interaction between glutamate and injected kainate to cause neuronal degeneration. On the other hand, other reports suggest that kainic acid neurotoxic effects can be manifested also in the absence of the glutamatergic input (Mc Lennan, 1980). More recently, kainate has been shown to affect neurotransmitter release and uptake in different tissue preparations of several brain areas. For example, the excitotoxin caused glutamate and aspartate release from brain synaptosomes (Pastuszko et al., 1984), cerebellar, hippocampal and striatal slices (Ferkany et al., 1982) and also stimulated GABA release from isolated, perfused chick retina (Tapia and Arias, 1982). These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.