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Mary C McKenna

Publication Detail

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Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam.

C M Tang; Q Y Shi; A Katchman; G Lynch (Profiled Author: Cha-Min Tang)

Department of Neurology, University of Pennsylvania, Philadelphia.
Science (New York, N.Y.) 1991;254(5029):288-90.

Abstract

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.

1 Originating Grant

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