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      Physiological and pathophysiological roles of excitatory amino acids during central nervous system development

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      Brain Research Reviews
      Elsevier BV

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          Most cited references188

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          Glutamate neurotoxicity and diseases of the nervous system.

          D Choi (1988)
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            Glycine potentiates the NMDA response in cultured mouse brain neurons.

            Transmitters mediating 'fast' synaptic processes in the vertebrate central nervous system are commonly placed in two separate categories that are believed to exhibit no interaction at the receptor level. The 'inhibitory transmitters' (such as glycine and GABA) are considered to act only on receptors mediating a chloride conductance increase, whereas 'excitatory transmitters' (such as L-glutamate) are considered to activate receptors mediating a cationic conductance increase. The best known excitatory receptor is that specifically activated by N-methyl-D-aspartate (NMDA) which has recently been characterized at the single channel level. The response activated by NMDA agonists is unique in that it exhibits a voltage-dependent Mg block. We report here that this response exhibits another remarkable property: it is dramatically potentiated by glycine. This potentiation is not mediated by the inhibitory strychnine-sensitive glycine receptor, and is detected at a glycine concentration as low as 10 nM. The potentiation can be observed in outside-out patches as an increase in the frequency of opening of the channels activated by NMDA agonists. Thus, in addition to its role as an inhibitory transmitter, glycine may facilitate excitatory transmission in the brain through an allosteric activation of the NMDA receptor.
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              Voltage-dependent block by Mg2+ of NMDA responses in spinal cord neurones

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                Author and article information

                Journal
                Brain Research Reviews
                Brain Research Reviews
                Elsevier BV
                01650173
                January 1990
                January 1990
                : 15
                : 1
                : 41-70
                Article
                10.1016/0165-0173(90)90011-C
                4bb09f16-714c-4ed0-91bd-2b27b202a80e
                © 1990

                http://www.elsevier.com/tdm/userlicense/1.0/

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