KAINIC ACID NEUROTOXICITY IN THE GOLDFISH OPTIC TECTUM - NO PROTECTION BY THE NMDA RECEPTOR ANTAGONIST MK801 AND PARTIAL PROTECTION BY ABOLITION OF A TECTAL EXCITATORY INPUT

Some features of the mechanism of kainic acid neurotoxicity were teste d after the injection of this substance in the optic tectum of goldfis h. A systemic treatment with the N-methyl-D-aspartate (NMDA) receptor antagonist MK801 did not influence the degree of toxicity, assessed by a decrement of enzymatic neuronal markers; instead, a significant neu ronal rescue was obtained after the abolition of the excitatory input from the torus longitudinalis to the tectum.