Ibotenic acid mediates neurotoxicity and phosphoinositide hydrolysis by independent receptor mechanisms.

Article date: 1992/2/1

PubMed ID: 1325800

Journal name: Molecular and chemical neuropathology (ISSN: 1044-7393)


Ibotenic acid (Ibo) has been shown to have agonist activity at both the N-methyl-D-aspartate (NMDA) and trans-ACPD or metabolotropic quisqualate (Qm) receptor sites in several systems. Both of these receptor sites have been implicated in excitotoxicity. Like NMDA neurotoxicity, Ibo neurotoxicity can be enhanced by glycine and blocked by MK-801. Ibo induced stimulation of phosphoinositide (PI) hydrolysis, on the other hand, is unaffected by either of these treatments. We therefore conclude that Ibo is capable of acting at both NMDA and trans-ACPD receptors in the CNS, although only activation of NMDA receptors is involved in Ibo neurotoxicity. This conclusion leads us to postulate that stimulation of phosphoinositide hydrolysis is neither necessary nor sufficient for neurotoxicity.

Author List: Zinkand W C, Moore W C, Thompson C, Salama A I, Patel J

Publication Types: Journal Article

Substances mentioned in the article: Phosphatidylinositols; Receptors, Glycine; Receptors, Metabotropic Glutamate; Receptors, N-Methyl-D-Aspartate; Receptors, Neurotransmitter; metabotropic quisqualate receptor; Ibotenic Acid; N-Methylaspartate; Dizocilpine Maleate; Quisqualic Acid; Type C Phospholipases; Glycine;

Mesh terms: Animals; Cell Death/drug effects; Cells, Cultured; Cerebral Cortex/cytology; Dizocilpine Maleate/pharmacology; Drug Interactions; Enzyme Activation; Glycine/pharmacology; Hydrolysis; Ibotenic Acid/pharmacology; N-Methylaspartate/antagonists & inhibitors; Neurons/drug effects; Phosphatidylinositols/metabolism; Quisqualic Acid/pharmacology; Rats; Receptors, Glycine; Receptors, Metabotropic Glutamate; Receptors, N-Methyl-D-Aspartate/drug effects; Receptors, Neurotransmitter/drug effects; Second Messenger Systems/drug effects; Type C Phospholipases/metabolism;

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