Effect of kainic acid on ultrastructure and γ-aminobutyrate-related circuits in the optic tectum of the goldfish

Abstract

Following unilateral microelectrophoretic delivery of kainic acid in the optic tectum of the goldfish, an ultrastructural and biochemical study was carried out. Kainic acid exerted a powerful neurotoxic effect against several types of tectal neurons, noticeably the periventricular neurons and the pyramidal and fusiform neurons of the stratum fibrosum et griseum superficiale. The neurotoxic effect of kainic acid was found to be highly selective. In fact, only some of the different neuronal populations underwent degenerative changes, while other neurons of the same type, and often in very close vicinity, were completely unaffected. Kainic acid neurotoxicity allows us therefore to discriminate between apparently homogeneous neuronal populations, probably on the basis of different neurochemical characteristics possessed by neurons of the same morphological type. The lack of neurotoxic effect against afferent fibres and axon terminals was assessed. Long-term observations of the affected optic tectum after kainic acid treatment demonstrated a remarkable level of structural rearrangement. A sharp decrease in the level of glutamate decarboxylase activity was noticed during the first six days after kainic acid treatment. This was followed by a partial recovery of enzyme activity, which, however, did not progress from 15 days to 2 months after operation. On the other hand no decrease of glutamate decarboxylase activity occurred in the left optic tectum six days and one month after surgical ablation of the right eye. These results suggest the presence of intrinsic γ-aminobutyrate-containing systems in the goldfish optic tectum. The existence of intrinsic neurons that take up γ-aminobutyrate was confirmed by light-microscopic autoradiography of the optic tectum of normal goldfish after local injection of [ 3H]γ-aminobutyrate.