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 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 longitudinalis to the tectum.
Migani
P
P
Faculty Center for Biological Sciences, University of Ancona, Italy.
D000818:Animals; D015415:Biomarkers; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D006054:Goldfish / Q000502:physiology*; D007267:Injections; D007608:Kainic Acid / Q000008:administration & dosage / Q000633:toxicity*; D009498:Neurotoxins / Q000008:administration & dosage / Q000633:toxicity*; D010275:Parasympathetic Nervous System / Q000166:cytology / Q000187:drug effects; D011950:Receptors, Cholinergic / Q000187:drug effects; D016194:Receptors, N-Methyl-D-Aspartate / Q000037:antagonists & inhibitors*; D013477:Superior Colliculi / Q000201:enzymology / Q000473:pathology / Q000502:physiology*; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D015415:Biomarkers; D009498:Neurotoxins; D011950:Receptors, Cholinergic; D016194:Receptors, N-Methyl-D-Aspartate; D005680:gamma-Aminobutyric Acid; D016291:Dizocilpine Maleate; D007608:Kainic Acid