Glutamatergic involvement in psychomotor stimulant action.
The sympathomimetic psychomotor stimulants, including cocaine, amphetamines, and the phenylethylamine amphetamine-like derivatives, exert actions in mammalian systems that implicate involvement of the excitatory neurotransmitter, glutamate and its receptors. Despite evidence that psychomotor stimulants do not directly stimulate glutamate receptors, blockade of acute lethal, convulsive, circulatory, thermoregulatory, locomotor and stereotypical responses, as well as interference with slowly developing behavioral sensitization and brain monoaminergic neurotoxicities, can be achieved by receptor antagonists at both N-methyl-D-aspartate and AMPA/kainate glutamate receptor subtypes. Alterations in glutamatergic neurobiology, including elevations in extracellular glutamate levels, changes in glutamate receptor properties and glutamatergic neuronal degeneration, have also been attributed to psychomotor stimulant administration. Blockade of glutamate receptors offers therapeutic options in management of psychomotor stimulant toxicity.
Rockhold
R W
RW
Department of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson 39216-4505, USA.
D000818:Animals; D001921:Brain / Q000187:drug effects; D000697:Central Nervous System Stimulants / Q000494:pharmacology*; D003042:Cocaine / Q000494:pharmacology; D018698:Glutamic Acid / Q000502:physiology*; D006801:Humans; D009043:Motor Activity / Q000187:drug effects; D010627:Phenethylamines / Q000494:pharmacology; D011597:Psychomotor Performance / Q000187:drug effects*; D013566:Sympathomimetics / Q000494:pharmacology*
D000697:Central Nervous System Stimulants; D010627:Phenethylamines; D013566:Sympathomimetics; C029261:phenethylamine; D018698:Glutamic Acid; D003042:Cocaine