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Cortical death caused by striatal administration of AMPA and interleukin-1 is mediated by activation of cortical NMDA receptors.
Allan S, Rothwell NJ
J Cereb Blood Flow Metab. 2000;20( 10):1409-13.
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Abstract
Striatal coadministration of interleukin-1beta (IL-1beta) with alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (S-AMPA) in rats results in widespread cortical cell death not caused by either treatment alone. This cortical damage was unaffected by cortical infusion of the AMPA-receptor antagonist NBQX. Cortical infusion of an NMDA-receptor antagonist D-AP5 significantly inhibited (57%; P < 0.05) cortical death, but had no effect on the local striatal death. Thus, cortical neuronal death induced by striatal S-AMPA and human recombinant interleukin-1beta (hrIL-1beta) is mediated by activation of NMDA receptors in the cortex. The authors propose that IL-1beta actions on AMPA-receptor mediated cell death may involve the activation of polysynaptic pathways from the striatum to the cortex.
Keyword(s)
Animals; Drug Synergism; Human; Male; Rats; Rats, Sprague-Dawley; Support, Non-U.S. Gov't; antagonists & inhibitors: Receptors, AMPA; antagonists & inhibitors: Receptors, N-Methyl-D-Aspartate; drug effects: Cell Death; drug effects: Cerebral Cortex; drug effects: Corpus Striatum; pharmacology: 2-Amino-5-phosphonovalerate; pharmacology: Excitatory Amino Acid Agonists; pharmacology: Excitatory Amino Acid Antagonists; pharmacology: Interleukin-1; pharmacology: Quinoxalines; pharmacology: Recombinant Proteins; pharmacology: alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid