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It is now widely accepted that glutamate is the major excitatory
neurotrans- mitter in the mammalian central nervous system. The
main criteria for accept- ing a molecule as a chemical transmitter
appear to be fulfilled at several synapses: Glutamate mimics the
action of the natural transmitter in the post- synaptic neuron
(CURTIS et al. 1959), glutamate is present in presynaptic ele-
ments (OTTERSEN and STORM-MATHISEN 1984), and glutamate is released
from central neurons in an activity-dependent manner (BRADFORD
1970). The postsynaptic receptors that mediate the effects of
glutamate are markedly diverse. Based on their activation by
agonists that act more selec- tively than the natural transmitter
itself, a-amino-3-hydroxy-5-methyl- isoxazolepropionate (AMPA)
receptors, kainate receptors, and N-methyl-D- aspartate (NMDA)
receptors can be distinguished. Molecular cloning has revealed
additional structural diversity. To date, almost 20 glutamate
receptor subunit genes have been identified, and an even larger
number of splice vari- ants and edited versions are present in the
mammalian brain. Analysis of synaptic transmission revealed that
"the" excitatory synapse does not exist. Glutamatergic synapses in
different circuitries differ substan- tially in their signaling
properties, although they use the same transmitter. We have learned
that cellular, subcellular, and molecular factors determine synap-
tic function, and that glutamate receptor subunit diversity is of
direct relevance in shaping the unique signaling properties of a
glutamatergic synapse.
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