Kainic acid: neurotoxic effects after intraocular injection.
Intraocular injection of 120 nmol. of kainic acid, a powerful glutamate receptor agonist, induces a marked degeneration of cells in the inner nuclear layer of the retina. Within 2 hours after injection there is a significant decrement in the specific activities of tyrosine hydroxylase, choline acetyltransferase, and glutamic acid decarboxylase; by 48 hours after injection there is nearly a complete loss in the presynaptic neurochemical markers for the cholinergic and GABAergic neurons. The dopaminergic neurons, as assessed by activity of tyrosine hydroxylase and concentration of endogenous dopamine, are reduced only 50% by the kainic acid treatment. Although basal adenylate cyclase activity is unaffected by kainic acid, there is a 90 percent reduction in the activating effects of dopamine on adenylate cyclase in the kainic acid-treated retina.
D000109:Acetylcholine / Q000096:biosynthesis; D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives / Q000494:pharmacology; D002645:Chickens; D002799:Cholinergic Fibers / Q000187:drug effects; D004298:Dopamine / Q000096:biosynthesis; D007267:Injections; D009474:Neurons / Q000187:drug effects; D011759:Pyrrolidines / Q000008:administration & dosage / Q000009:adverse effects*; D012160:Retina / Q000187:drug effects* / Q000201:enzymology / Q000473:pathology; D012162:Retinal Degeneration / Q000139:chemically induced; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000096:biosynthesis
D011759:Pyrrolidines; D001224:Aspartic Acid; D005680:gamma-Aminobutyric Acid; D000109:Acetylcholine; D004298:Dopamine