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The Journal of Neuroscience, October 4, 2006, 26(40):10270-10280; doi:10.1523/JNEUROSCI.3091-06.2006

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Cellular/Molecular
NMDA-Dependent, But Not Group I Metabotropic Glutamate Receptor-Dependent, Long-Term Depression at Schaffer Collateral–CA1 Synapses Is Associated with Long-Term Reduction of Release from the Rapidly Recycling Presynaptic Vesicle Pool

Xiao-lei Zhang,¹ Zhen-yu Zhou,¹ Jochen Winterer,^3,4 Wolfgang Müller,⁵ and Patric K. Stanton^1,2

Departments of ¹Cell Biology and Anatomy and ²Neurology, New York Medical College, Valhalla, New York 10595, ³Neuroscience Research Institute and ⁴Department of Psychiatry, Charité, Humboldt University, D-10117 Berlin, Germany, and ⁵Departments of Neurosurgery, Neurology, and Neuroscience, University of New Mexico School of Medicine, Albuquerque, New Mexico 87131

Correspondence should be addressed to Dr. Patric K. Stanton, Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595. Email: patric_stanton{at}nymc.edu

Postsynaptic alterations have been suggested to account for NMDA receptor (NMDAR)-dependent long-term depression (LTD) and long-term potentiation of synaptic strength, although there is substantial evidence supporting changes in presynaptic release. Direct chemical activation of either NMDA or group I metabotropic glutamate receptor (mGluR1) elicits LTD of similar magnitudes, but it is unknown whether they share common expression mechanisms. Using dual-photon laser-scanning microscopy of FM1-43 [N-(3-triethylammoniumpropyl)-4-(4-(dibutylamino)styryl)pyridinium dibromide] to directly visualize presynaptic vesicular release from the rapidly recycling vesicle pool (RRP) at Schaffer collateral terminals in field CA1 of rat hippocampal slices, we found that a persistent reduction in vesicular release from the RRP is induced by NMDA-LTD but not by mGluR1-LTD. Variance-mean analyses of Schaffer collateral release probability (P_r) at varying extracellular calcium concentrations confirmed that NMDA-LTD was associated with reduced P_r, whereas mGluR1-LTD was not. Pharmacological isolation of NMDAR-dependent and mGluR-dependent forms of stimulus-evoked LTD revealed that both are composed of a combination of presynaptic and postsynaptic alterations. However, when group I mGluR-dependent LTD was isolated by combining an NMDAR blocker with a group II mGluR antagonist, this form of LTD was purely postsynaptic. The nitric oxide synthase inhibitor N-nitro-L-arginine blocked the induction of NMDA-LTD but did not alter mGluR-LTD, consistent with a selective role for nitric oxide as a retrograde messenger mediating NMDA-LTD. These data demonstrate that single synapses can express multiple forms of LTD with different sites of expression, that NMDA-LTD is a combination of presynaptic and postsynaptic alterations, but that group I mGluR-LTD appears to be expressed entirely postsynaptically.

Key words: CA1; hippocampus; long-term depression; metabotropic glutamate receptors; NMDA; presynaptic; rapidly recycling vesicle pool; Schaffer collateral; transmitter release

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Received April 5, 2006; revised Aug. 21, 2006; accepted Aug. 22, 2006.

Correspondence should be addressed to Dr. Patric K. Stanton, Department of Cell Biology and Anatomy, New York Medical College, Valhalla, NY 10595. Email: patric_stanton{at}nymc.edu

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