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The Journal of Neuroscience, January 25, 2006, 26(4):1128-1132; doi:10.1523/JNEUROSCI.2753-05.2006

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Brief Communications
Long-Term Depression of NMDA Receptor-Mediated Synaptic Transmission Is Dependent on Activation of Metabotropic Glutamate Receptors and Is Altered to Long-Term Potentiation by Low Intracellular Calcium Buffering

Sarah C. Harney,¹ Michael Rowan,² and Roger Anwyl¹

¹Departments of Physiology and ²Pharmacology and Therapeutics, Trinity College, Dublin 2, Ireland

Correspondence should be addressed to Dr. Roger Anwyl, Department of Physiology, Trinity College, Dublin 2, Ireland. Email: ranwyl{at}tcd.ie

Synaptic plasticity of NMDA receptor (NMDAR)-mediated transmission was investigated in the rat dentate gyrus in vitro. Isolated NMDAR EPSCs were recorded from granule cells of the dentate gyrus in response to stimulation of the medial perforant path. Long-term potentiation (LTP) or long-term depression (LTD) of NMDAR EPSCs was observed in response to brief high-frequency stimulation (HFS), with the direction and extent of plasticity dependent on the concentration and type (EGTA vs BAPTA) of the intracellular Ca²⁺ buffer. LTD was induced in higher concentrations of EGTA and BAPTA than LTP, and BAPTA was 100-fold more potent than EGTA. Although LTD was induced in a high concentration of EGTA (10 mM), a high concentration of BAPTA (10 mM) blocked both LTP and LTD. LTP of AMPA receptor (AMPAR)-EPSCs exhibited a lower dependency on Ca²⁺ buffering than LTP of NMDAR EPSCs, because LTP of AMPAR EPSCs was induced by HFS in high EGTA (10 mM). We also identified a role for metabotropic glutamate receptor 5 (mGluR5) in NMDAR plasticity. HFS LTD was blocked by the group I/II mGluR antagonist LY341495 ((2S)-2-amino-2-[(1S, 2S)-2-carboxycycloprop-1-yl]-3(xanth-9-yl)propanoic acid) and by the mGluR5-selective antagonist 2-methyl-6-(phenylethynyl)pyridine hydrochloride (MPEP). Similarly, low-frequency stimulation-induced LTD of NMDAR EPSCs was also blocked by MPEP. These findings suggest that the direction of plasticity of NMDARs is determined by the intracellular free Ca²⁺ concentration and is dependent on activation of mGluR5.

Key words: NMDA; LTD; metabotropic glutamate receptor; dentate gyrus; patch clamp; calcium

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Received Jul. 4, 2005; revised Dec. 9, 2005; accepted Dec. 9, 2005.

Correspondence should be addressed to Dr. Roger Anwyl, Department of Physiology, Trinity College, Dublin 2, Ireland. Email: ranwyl{at}tcd.ie

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