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

Abstract

Some features of the mechanism of kainic acid neurotoxicity were tested after the injection of this substance in the optic tectum of goldfish. 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 neuronal rescue was obtained after the abolition of the excitatory input from the torus longitudinals to the tectum.