title: TRPV1 channels: not so inactive on the ER.
abstract: In this issue of Neuron, Wong et al. (2014) report a remarkable evolutionarily conserved role for the Drosophila TRPV1 homolog Inactive controlling synaptic growth at larval neuromuscular junctions by facilitating Ca(2+) release from the endoplasmic reticulum.
authors.affiliation: Department of Neuroscience, University of Arizona, Tucson, AZ 85721, USA; Graduate Interdisciplinary Program in Neuroscience, University of Arizona, Tucson, AZ 85721, USA.
authors.forename: Elliot
authors.initials: E
authors.lastname: Imler
authors.affiliation: Department of Neuroscience, University of Arizona, Tucson, AZ 85721, USA; Department of Molecular and Cellular Biology, University of Arizona, Tucson, AZ 85721, USA. Electronic address: kez4@email.arizona.edu.
authors.forename: Konrad E
authors.initials: KE
authors.lastname: Zinsmaier
mesh_terms: D000818:Animals; D002118:Calcium / Q000378:metabolism*; D029721:Drosophila Proteins / Q000378:metabolism*; D007473:Ion Channels / Q000378:metabolism*; D009046:Motor Neurons / Q000378:metabolism*; D009469:Neuromuscular Junction / Q000378:metabolism*; D017729:Presynaptic Terminals / Q000378:metabolism*; D009435:Synaptic Transmission / Q000502:physiology*; D050916:TRPV Cation Channels / Q000378:metabolism*
chemical_list: D029721:Drosophila Proteins; C494780:IAV protein, Drosophila; D007473:Ion Channels; D050916:TRPV Cation Channels; D002118:Calcium