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The Journal of Neuroscience, April 23, 2008, 28(17):4350-4355; doi:10.1523/JNEUROSCI.0284-08.2008

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Brief Communications
Transient Upregulation of Postsynaptic IP₃-Gated Ca Release Underlies Short-Term Potentiation of Metabotropic Glutamate Receptor 1 Signaling in Cerebellar Purkinje Cells

Sang Jeong Kim,¹ Yunju Jin,¹ Jun Kim,¹ Jung Hoon Shin,² Paul F. Worley,^2,3 and David J. Linden²

¹Department of Physiology, Seoul National University College of Medicine, Seoul 110-799, Korea, and Departments of ²Neuroscience and ³Neurology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Correspondence should be addressed to David J. Linden, Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205. Email: dlinden{at}jhmi.edu

Synaptic plasticity lasting 100 s has been suggested to function as a temporary buffer for neural information. One example of this was reported by Batchelor and Garthwaite (1997), who found that a slow metabotropic glutamate receptor 1 (mGluR1)-evoked EPSP produced by burst stimulation of cerebellar parallel fiber–Purkinje cell synapses could be potentiated by a conditioning stimulus consisting of prior activation of climbing fiber synapses (or injection of depolarizing current) with a delay of up to 90 s. What is the molecular basis of the signal that spans this temporal gap? Here, we show that mGluR1-evoked slow EPSCs evoked by parallel fiber burst test stimuli show a similar form of short-term potentiation (mGluR1-STP) and that this phenomenon is also observed when parallel fiber bursts are replaced by pressure pulses of an exogenous mGluR1 agonist. Ca imaging experiments revealed that cytosolic Ca levels returned to baseline within several seconds after conditioning depolarization, indicating that this cannot underlie mGluR1-STP. To test the hypothesis that transient upregulation of inositol-1,4,5-trisphosphate (IP₃)-gated Ca release underlies this phenomenon, we used local photolytic uncaging of IP₃ to deplete IP₃-gated Ca stores. IP₃ uncaging in the interval between conditioning depolarization and the test pulse produced a complete blockade of mGluR1-STP, as did blockade of IP₃ receptors with heparin. When Ca transients evoked by IP₃ uncaging were used as a test stimulus, conditioning depolarization produced a large STP of Ca response amplitudes. These data suggest that transient upregulation of postsynaptic IP₃-gated Ca signaling constitutes a novel form of short-term synaptic plasticity.

Key words: Purkinje cell; mGluR1; potentiation; IP₃; Ca stores; cerebellum

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Received Nov. 15, 2006; revised March 13, 2008; accepted March 17, 2008.

Correspondence should be addressed to David J. Linden, Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205. Email: dlinden{at}jhmi.edu

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