Intracellular Ca2+ Release and Synaptic Plasticity: A Tale of Many Stores. (June 2019)

• Record Type: Journal Article
• Authors: Padamsey, Zahid; Foster, William J.; Emptage, Nigel J.
• Is Part Of: Neuroscientist. Volume 25:Number 3(2019)
• Page Start: 208
• Page End: 226
• Publication Date: 2019-06
• Subjects: synaptic plasticity -- endoplasmic reticulum -- mitochondria -- lysosomes -- Ca2+ stores -- hippocampus -- LTP -- LTD -- acidic stores -- Ca2+ signaling; Neurosciences -- Periodicals; Neurology -- Periodicals; Neurobiology -- Periodicals; 616.8005
• DOI: 10.1177/1073858418785334
• Languages: English
• ISSNs: 1073-8584

Abstract

Ca 2+ is an essential trigger for most forms of synaptic plasticity. Ca 2+ signaling occurs not only by Ca 2+ entry via plasma membrane channels but also via Ca 2+ signals generated by intracellular organelles. These organelles, by dynamically regulating the spatial and temporal extent of Ca 2+ elevations within neurons, play a pivotal role in determining the downstream consequences of neural signaling on synaptic function. Here, we review the role of three major intracellular stores: the endoplasmic reticulum, mitochondria, and acidic Ca 2+ stores, such as lysosomes, in neuronal Ca 2+ signaling and plasticity. We provide a comprehensive account of how Ca 2+ release from these stores regulates short- and long-term plasticity at the pre- and postsynaptic terminals of central synapses.