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Science 11 October 1991: Vol. 254. no. 5029, pp. 288 - 290 DOI: 10.1126/science.1681589
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Articles
Science, Vol 254, Issue 5029, 288-290
Copyright © 1991 by American Association for the Advancement of Science
Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam
CM Tang,
QY Shi,
A Katchman,
and
G Lynch
Department of Neurology, University of Pennsylvania, Philadelphia.
It is generally accepted that glutamate serves as the neurotransmitter at most excitatory synapses in the mammalian central nervous system (CNS). Synaptic release of glutamate may trigger a fast and a slow excitatory postsynaptic current (EPSC). The slow EPSC is mediated by N-methyl-D-aspartate (NMDA) receptor channels, whereas the fast EPSC is mediated by non-NMDA receptor channels. The nootropic agent aniracetam selectively and reversibly slows the desensitization kinetics of non-NMDA channels and lengthens their single-channel open times. Antiracetam also modulates the kinetics of the fast EPSC in a manner that mirrors its action on the kinetics of the non-NMDA channels. These results support the hypothesis that the properties of the non-NMDA glutamate channels rather than the rate of neurotransmitter clearance are the primary determinants of the kinetics of the fast EPSC in the mammalian CNS.
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