Contribution of plasma membrane Ca^(2+) ATPase to cerebellar synapse function

作     者：Helena Huang Raghavendra Y Nagaraja Molly L Garside Walther Akemann Thomas Knpfel Ruth M Empson 

作者机构：Department of PhysiologyBrain Health and Repair Research CentreUniversity of Otago School of Biological SciencesRoyal Holloway University of London Laboratory for Neuronal Circuit DynamicsRIKEN Brain Science Institute 

出 版 物：《World Journal of Biological Chemistry》 (世界生物化学杂志（英文版）（电子版）)

年 卷 期：2010年第1卷第5期

页      面：95-102页

学科分类：0710[理学-生物学] 07[理学] 071006[理学-神经生物学] 

基　　金：Supported by An Health Research Council-Japanese Society for the Promotion of Science fellowship and the Neurological Foundation of New Zealand(Empson RM and Nagaraja RY) a British Biological and Biotechnology Research Council award(Empson RM and Garside ML) a Department of Physiology MSc studentship(Huang H) RIKEN intramural funding(Knpfel T) 

主　　题：Plasma membrane Ca2+ ATPase Cerebellum Calcium Purkinje neuron 

摘      要：The cerebellum expresses one of the highest levels of the plasma membrane Ca2+ATPase,isoform 2 in the mammalian *** highly efficient plasma membrane calcium transporter protein is enriched within the main output neurons of the cerebellar cortex;i.e. the Purkinje neurons(PNs) .Here we review recent evidence,including electrophysiological and calcium imaging approaches using the plasma membrane calcium ATPase 2(PMCA2) knockout mouse,to show that PMCA2 is critical for the physiological control of calcium at cerebellar synapses and cerebellar dependent *** studies have also revealed that deletionof PMCA2 throughout cerebellar development in the PMCA2 knockout mouse leads to permanent signalling and morphological alterations in the PN dendrites. Whilst these findings highlight the importance of PMCA2 during cerebellar synapse function and development,they also reveal some limitations in the use of the PMCA2 knockout mouse and the need for additional experimental approaches including cell-specific and reversible manipulation of PMCAs.