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Science 20 May 1994:
Vol. 264. no. 5162, pp. 1148 - 1152
DOI: 10.1126/science.7909958
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Articles

Science, Vol 264, Issue 5162, 1148-1152
Copyright © 1994 by American Association for the Advancement of Science

articles

Postsynaptic induction and presynaptic expression of hippocampal long-term depression

VY Bolshakov and SA Siegelbaum

Department of Pharmacology, Howard Hughes Medical Institute, Columbia University, New York, NY 10032.

Long-term depression (LTD) is an activity-dependent decrease in synaptic efficacy that together with its counterpart, long-term potentiation, is thought to be an important cellular mechanism for learning and memory in the mammalian brain. The induction of LTD in hippocampal CA1 pyramidal neurons in neonatal rats is shown to depend on postsynaptic calcium ion entry through L-type voltage-gated calcium channels paired with the activation of metabotropic glutamate receptors. Although induced postsynaptically, LTD is due to a long-term decrease in transmitter release from presynaptic terminals. This suggests that LTD is likely to require the production of a retrograde messenger.


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GABA Activity Mediating Cytosolic Ca2+ Rises in Developing Neurons Is Modulated by cAMP-Dependent Signal Transduction.
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Group 1 and 2 Metabotropic Glutamate Receptors Play Differential Roles in Hippocampal Long-Term Depression and Long-Term Potentiation in Freely Moving Rats.
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J. Neurosci. 17, 3303-3311
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Decreased probability of neurotransmitter release underlies striatal long-term depression and postnatal development of corticostriatal synapses.
S. Choi and D. M. Lovinger (1997)
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Contribution of Voltage-Gated Ca2+ Channels to Homosynaptic Long-Term Depression in the CA1 Region In Vitro.
B. R. Christie, L. K. Schexnayder, and D. Johnston (1997)
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P. C. Kind, G. M. Kelly, H. J. L. Fryer, C. Blakemore, and S. Hockfield (1997)
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Nitric oxide-related species inhibit evoked neurotransmission but enhance spontaneous miniature synaptic currents in central neuronal cultures.
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Induction of Hippocampal Long-Term Depression Requires Release of Ca2+ from Separate Presynaptic and Postsynaptic Intracellular Stores.
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