Abstract
NEUROTRANSMISSION at most excitatory synapses in the brain operates through two types of glutamate receptor termed α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMP A) andN-methyl-D-aspartate (NMDA) receptors; these mediate the fast and slow components of excitatory postsynaptic potentials respectively1–3. Activation of NMDA receptors can also lead to a long-lasting modification in synaptic efficiency at glutamatergic synapses; this is exemplified in the CA1 region of the hippocampus, where NMDA receptors mediate the induction of long-term potentiation (LTP)4. It is believed that in this region LTP is maintained by a specific increase in the AMPA receptor-mediated component of synaptic transmission5,6. We now report, however, that a pharmacologically isolated NMDA receptor-mediated synaptic response can undergo robust, synapse-specific LTP. This finding has implications for neuropathologies such as epilepsy and neurodegeneration, in which excessive NMDA receptor activation has been implicated7. It adds fundamentally to theories of synaptic plasticity because NMDA receptor activation may, in addition to causing increased synaptic efficiency, directly alter the plasticity of synapses.
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References
Watkins, J. C. & Evans, R. H. A. Rev. Pharmaco. Toxicol. 21, 165–204 (1981).
Dale, N. & Roberts, A. J. Physiol., Lond. 363, 35–59 (1985).
Collingridge, G. L., Herron, C. E. & Lester, R. A. J. Physiol., Lond. 399, 283–300 (1988).
Collingridge, G. L., Kehl, S. J. & McLennan, H. J. Physiol., Lond. 334, 33–46 (1983).
Muller, D., Joly, M. & Lynch, G. Science 242, 1694–1697 (1988).
Kauer, J. A., Malenka, R. C. & Nicoll, R. A. Neuron 1, 911–917 (1988).
Meldrum, B. Clin. Sci. 68, 113–122 (1985).
Davies, C. H., Davies, S. N. & Collingridge, G. L. J. Physiol., Lond. 424, 513–531 (1990).
D'Angelo, E., Rossi, P. & Garthwaite, J. Nature 346, 467–470 (1990).
Hestrin, S., Nicoll, R. A., Perkel, D. J. & Sah, P. J. Physiol., Lond. 422, 203–225 (1990).
Randall, A. D., Schofield, J. G. & Collingridge, G. L. Neurosci. Lett. 114, 191–196 (1990).
Malinow, R. & Tsien, R. W. Nature 346, 177–180 (1990).
Dingledine, R., Hynes, M. A. & King, G. L. J. Physiol., Lond. 380, 175–189 (1986).
Coan, E. J., Irving, A. J. & Collingridge, G. L. Neurosci. Lett. 105, 205–210 (1989).
Nowak, L., Bregestovski, P., Ascher, P., Herbet, A. & Prochiantz, A. Nature 307, 462–465 (1984).
Mayer, M. L., Westbrook, G. L. & Guthrie, P. B. Nature 309, 261–263 (1984).
Bindman, L. J. & Murphy, K. P. S. J. J. Physiol., Lond. 406, 176P (1988).
Artola, A. & Singer, W. Eur. J. Neurosci. 2, 254–269 (1990).
Dolphin, A. C., Errington, M. L. & Bliss, T. V. P. Nature 297, 496–498 (1982).
Bliss, T. V. P. & Lynch, M. A. in Long-Term Potentiation: From Biophysics to Behavior (eds Landfield, P. W. & Deadwyler, S. A.) 3–72 (Liss, New York, 1988).
Davies, S. N., Lester, R. A., Reymann, K. G. & Collingridge, G. L. Nature 338, 500–503 (1989).
Bekkers, J. M. & Stevens, C. F., Nature 346, 724–729 (1990).
Leonard, J. P. & Kelso, S. R. Soc. Neurosci. Abstr. 15, 535 (1989).
MacDermott, A. B., Mayer, M. L., Westbrook, G. L., Smith, S. J. & Barker, J. L. Nature 321, 519–522 (1986).
Jahr, C. E. & Stevens, C. F. Nature 325, 522–525 (1987).
Ascher, P., & Nowak, L. J. Physiol., Lond. 399, 247–266 (1988).
Slater, N. T., Stelzer, A. & Galvan, M. Neurosci. Lett. 60, 25–31 (1985).
Stasheff, S. F., Anderson, W. W., Clark, S. & Wilson, W. A. Science 245, 648–651 (1989).
Scharfman, H. E. & Schwartzkroin, P. A. Science 246, 257–260 (1989).
Blanton, M. G., LoTurco, J. J. & Kreigstein, A. R. J. Neurosci. Meth. 30, 203–210 (1989).
Horn, R. & Marty, A. J. gen. Physiol. 92, 145–159 (1988).
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Bashir, Z., Alford, S., Davies, S. et al. Long-term potentiation of NMDA receptor-mediated synaptic transmission in the hippocampus. Nature 349, 156–158 (1991). https://doi.org/10.1038/349156a0
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DOI: https://doi.org/10.1038/349156a0
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