Excitatory synaptic currents generated by glutamate receptor activation medi ate rapid transmission between neurons in the central nervous system. The review on Nicotinic Acetylcholine Receptors (see B Edmonds et ai, this vol ume) deals with muscle-type nicotinic receptors and with some general prin ciples and experimental methods that are germane to the study of synaptic currents. Here we discuss glutamate receptors. The aims are to (a) summarize recent work concerning the structure of these classes of receptors, (b) address current understanding of the mechanisms underlying activation of glutamate receptors, and (c) discuss present views of the role of channel gating in determining the time course of synaptic currents. At glutamatergic synapses, the situation is more complicated than at the endplate because of at least two factors. First. glutamate usually acts on two distinct classes of receptors (4, 36, 59, 101 , 1 1 2); a non-N-methyl-D-aspartate (non-NMDA) receptor characterized by insensitivity to the synthetic agonist N-methyl-D-aspartate (NMDA), which produces a synaptic response with a rapid rate of onset and decay, similar in time course to that produced by ACh
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