AMPA Receptors in Disease

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Arecently proposed model of glutamate excitotoxicity highlights the importance of molecular diversity of AMPA subunit expression. It hypothesizes that cells are vulnerable to injury from excessive Ca++ influx after any of a number primary insults affecting the expression of edited GluR2 subunits (such as ischemia, hypoxia, hypoglycemia, or epilepsy). AMPA receptor expression is also altered under conditions of stress in the hippocampus. Perhaps a peak in the expression of AMPA receptors at 20 to 22 weeks of gestation in the human may increase vulnerability to excitox-icity at that time, because AMPA receptors have been shown to increase during the prenatal period in rats, when there is also observed a greater vulnerability to excitotoxic injury.

In Rassmussen's encephalitis, a severe childhood form of epilepsy often requiring cerebral hemispherectomy because of its poor response to available anticonvulsive regimens, recent evidence supports an autoimmune mechanism involving the GluR3 subunit as an autoantigen.

Thus, current evidence supports roles for AMPA receptor involvement in excitotoxic injury through various pathophysiologic mechanisms such as epilepsy, stroke, ischemia, hypoxia, trauma, extreme stress, hypoglycemia, or hypercortisolemia, as well as in neurodegenerative diseases (e.g., Huntington's disease, Alzheimer's disease, Parkinson's disease). Pathophysiological roles for AMPAre-ceptors have been suggested, and are under continuing study, in other neuropsychiatric disorders such as mood disorders, Schizophrenia, and anxiety disorders.

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