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Presynaptic store-operated Ca2+ entry drives excitatory spontaneous neurotransmission and augments endoplasmic reticulum stress
Authors:Natali L. Chanaday  Elena Nosyreva  Ok-Ho Shin  Hua Zhang  Iltan Aklan  Deniz Atasoy  Ilya Bezprozvanny  Ege T. Kavalali
Affiliation:1. Department of Pharmacology, School of Medicine, Vanderbilt University, Nashville, TN 37240-7933, USA;2. Department of Neuroscience, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA;3. Department of Physiology, The University of Texas Southwestern Medical Center, Dallas, TX 75390-9040, USA;4. Department of Neuroscience and Pharmacology, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA;5. Iowa Neuroscience Institute, University of Iowa, Iowa City, IA 52242, USA;6. FOE Diabetes Research Center, University of Iowa, Iowa City, IA 52242, USA;7. Laboratory of Molecular Neurodegeneration, Peter the Great St Petersburg State Polytechnic University, St. Petersburg, Russia;8. Vanderbilt Brain Institute, Vanderbilt University, Nashville, TN 37240-7933, USA
Abstract:
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  • Keywords:synaptic vesicle  calcium  store operated calcium entry  spontaneous neurotrasnmission  synaptotagmin-7  STIM2  Orai  endoplasmic reticulum stress
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