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The Journal of Neuroscience, June 28, 2006, 26(26):6935-6944; doi:10.1523/JNEUROSCI.0784-06.2006

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Cellular/Molecular
Long-Term Depression at the Mossy Fiber–Deep Cerebellar Nucleus Synapse

Wei Zhang and David J. Linden

Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Correspondence should be addressed to David J. Linden, 725 North Wolfe Street, 916 Hunterian Building, Baltimore, MD 21205. Email: dlinden{at}jhmi.edu

Several lines of evidence have indicated that the deep cerebellar nuclei (DCN) are a site of memory storage for certain forms of motor learning, most notably associative eyelid conditioning. In particular, these experiments, together with network models, have implicated the excitatory glutamatergic synapse between mossy fibers and DCN neurons in this memory trace. However, to date, evidence for persistent use-dependent change in the strength of this synapse has been almost entirely absent. Here, we report that high-frequency burst stimulation of mossy fibers, either alone or paired with postsynaptic depolarization, gives rise to long-term depression (LTD) of the mossy fiber–DCN synapse. This form of LTD is not associated with changes in the paired-pulse ratio and is blocked by loading with a postsynaptic Ca²⁺ chelator but not by bath application of an NMDA receptor antagonist. Mossy fiber–DCN LTD requires activation of a group I metabotropic glutamate receptor (mGluR) and protein translation. Unlike mGluR/translation-dependent LTD in other brain regions, this form of LTD requires mGluR1 and is mGluR5 independent.

Key words: mGluR1; mGluR5; slow EPSC; synaptic plasticity; protein synthesis; burst detection

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Received Feb. 21, 2006; revised May 5, 2006; accepted May 22, 2006.

Correspondence should be addressed to David J. Linden, 725 North Wolfe Street, 916 Hunterian Building, Baltimore, MD 21205. Email: dlinden{at}jhmi.edu

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