New mechanisms of excitatory transmitter neurotoxicity.
Accumulating evidence suggests that either excessive activation or suppression of either ionotropic or metabotropic EAA receptors can have neurotoxic consequences, and a variety of different mechanisms may be involved. The major excitatory neurotransmitters in the mammalian CNS-glutamate (Glu) and acetylcholine (ACh)--have vitally important beneficial functions, but also harbor treacherous neurotoxic potential which, as will be described in this review, can be expressed as classical excitotoxicity or in several other ways that have yet to be studied in detail.
Olney
J W
JW
Department of Psychiatry, Washington University School of Medicine, St. Louis, MO.
D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D018698:Glutamic Acid / Q000502:physiology*; D006801:Humans; D016202:N-Methylaspartate / Q000037:antagonists & inhibitors; D009422:Nervous System Diseases / Q000139:chemically induced; D009498:Neurotoxins / Q000378:metabolism*; D017459:Receptors, Amino Acid / Q000145:classification; D018094:Receptors, Metabotropic Glutamate / Q000037:antagonists & inhibitors / Q000502:physiology; D013577:Syndrome
D009498:Neurotoxins; D017459:Receptors, Amino Acid; D018094:Receptors, Metabotropic Glutamate; D018698:Glutamic Acid; D016202:N-Methylaspartate; D000109:Acetylcholine