Excitatory amino acid neurotransmission, excitotoxicity and excitotoxins.
Exciting recent developments have begun to define the molecular basis for excitatory amino acid (EAA) receptor diversity and function. Clarification of the roles of these receptors will require identification of the entire repertoire of EAA subunit genes, the subunit composition of each receptor subtype and the mapping of subunits within the central nervous system (CNS). This may allow the development of selective receptor targeting by therapeutic agents. Further evidence is emerging about the molecular processes underlying excitotoxic injury and the importance of free radical formation acting in concert with calcium-dependent processes is being increasingly recognized. There are many clues indicating that primary or secondary excitotoxic mechanisms may play a part in the pathogenesis of some chronic human neurodegenerative disorders. Further work is needed to clarify the mechanisms of selective vulnerability of particular neuronal types given the widespread distribution of EAA receptors within the CNS.
Shaw
P J
PJ
Department of Neurology, University of Newcastle upon Tyne, UK.
D000544:Alzheimer Disease / Q000503:physiopathology; D000596:Amino Acids / Q000502:physiology*; D001925:Brain Damage, Chronic / Q000503:physiopathology*; D006801:Humans; D006816:Huntington Disease / Q000503:physiopathology; D016472:Motor Neuron Disease / Q000503:physiopathology; D009410:Nerve Degeneration / Q000502:physiology*; D009474:Neurons / Q000502:physiology; D010300:Parkinson Disease / Q000503:physiopathology; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface / Q000502:physiology*; D009435:Synaptic Transmission / Q000502:physiology*
D000596:Amino Acids; D017459:Receptors, Amino Acid; D011956:Receptors, Cell Surface