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The Journal of Neuroscience, April 4, 2007, 27(14):3753-3758; doi:10.1523/JNEUROSCI.0069-07.2007

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Brief Communications
Plasma Membrane Ca²⁺ ATPase 2 Contributes to Short-Term Synapse Plasticity at the Parallel Fiber to Purkinje Neuron Synapse

Ruth M. Empson,^1,3 Molly L. Garside,¹ and Thomas Knöpfel²

¹School of Biological Sciences, Royal Holloway University of London, Egham, Surrey TW20 0EX, United Kingdom, ²Laboratory for Neuronal Circuit Dynamics, RIKEN Brain Science Institute, Wako-shi, Saitama 351-0198, Japan, and ³Department of Physiology, University of Otago School of Medical Sciences, 9054 Dunedin, New Zealand

Correspondence should be addressed to Ruth M. Empson, Department of Physiology, Otago School of Medicine, P. O. Box 913, 9054 Dunedin, New Zealand. Email: ruth.empson{at}stonebow.otago.ac.nz

Plasma membrane Ca²⁺ ATPase 2 (PMCA2) is a fast, highly effective mechanism to control resting cytosolic Ca²⁺ and Ca²⁺ excursions in neurons and other excitable cells. The strong expression of PMCA2 in the cerebellum and the cerebellar behavioral deficits presented by PMCA2–/– knock-out mice all point to its importance for cerebellar circuit dynamics. Here, we provide direct functional evidence for the influence of presynaptic PMCA2-mediated Ca²⁺ extrusion for short-term plasticity at cerebellar parallel fiber to Purkinje neuron synapses. Dramatic structural alterations to the Purkinje neurons in the absence of PMCA2 also suggest a strong influence of this fast PMCA2 isoform for development and maintenance of cerebellar function.

Key words: plasma membrane Ca²⁺ ATPase; synapse; cerebellum; parallel fibers; plasticity; presynaptic

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Received Jan. 8, 2007; revised Feb. 16, 2007; accepted Feb. 25, 2007.

Correspondence should be addressed to Ruth M. Empson, Department of Physiology, Otago School of Medicine, P. O. Box 913, 9054 Dunedin, New Zealand. Email: ruth.empson{at}stonebow.otago.ac.nz

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