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

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

机构地区：[1]Department of Physiology,Brain Health and Repair Research Centre,University of Otago [2]School of Biological Sciences,Royal Holloway University of London [3]Laboratory for Neuronal Circuit Dynamics,RIKEN Brain Science Institute

出　　处：《World Journal of Biological Chemistry》2010年第5期95-102,共8页世界生物化学杂志（英文版）（电子版）

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(Knpfel T)

摘　　要：The cerebellum expresses one of the highest levels of the plasma membrane Ca2+ATPase,isoform 2 in the mammalian brain.This 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 behaviour.These 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.The cerebellum expresses one of the highest levels of the plasma membrane Ca2+ATPase,isoform 2 in the mammalian brain.This 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 behaviour.These 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.

关 键 词：Plasma membrane Ca2+ ATPASE CEREBELLUM Calcium PURKINJE neuron 

分 类 号：R338[医药卫生—人体生理学]