{"author":[{"first_name":"Nicholas","last_name":"Vyleta","full_name":"Vyleta, Nicholas","id":"36C4978E-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Smith, Stephen","last_name":"Smith","first_name":"Stephen"}],"status":"public","intvolume":"        31","month":"03","citation":{"ama":"Vyleta N, Smith S. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. <i>European Journal of Neuroscience</i>. 2011;31(12):4593-4606. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">10.1523/JNEUROSCI.6398-10.2011</a>","mla":"Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” <i>European Journal of Neuroscience</i>, vol. 31, no. 12, Wiley-Blackwell, 2011, pp. 4593–606, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">10.1523/JNEUROSCI.6398-10.2011</a>.","short":"N. Vyleta, S. Smith, European Journal of Neuroscience 31 (2011) 4593–4606.","ieee":"N. Vyleta and S. Smith, “Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor,” <i>European Journal of Neuroscience</i>, vol. 31, no. 12. Wiley-Blackwell, pp. 4593–4606, 2011.","apa":"Vyleta, N., &#38; Smith, S. (2011). Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. <i>European Journal of Neuroscience</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">https://doi.org/10.1523/JNEUROSCI.6398-10.2011</a>","chicago":"Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” <i>European Journal of Neuroscience</i>. Wiley-Blackwell, 2011. <a href=\"https://doi.org/10.1523/JNEUROSCI.6398-10.2011\">https://doi.org/10.1523/JNEUROSCI.6398-10.2011</a>.","ista":"Vyleta N, Smith S. 2011. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. 31(12), 4593–4606."},"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","page":"4593 - 4606","issue":"12","publication":"European Journal of Neuroscience","_id":"469","publication_status":"published","publist_id":"7353","title":"Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor","date_updated":"2021-01-12T08:00:49Z","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097128/"}],"day":"23","publisher":"Wiley-Blackwell","type":"journal_article","oa":1,"department":[{"_id":"PeJo"}],"date_published":"2011-03-23T00:00:00Z","date_created":"2018-12-11T11:46:39Z","year":"2011","language":[{"iso":"eng"}],"scopus_import":1,"abstract":[{"lang":"eng","text":"Spontaneous release of glutamate is important for maintaining synaptic strength and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report that external Ca2+ triggers spontaneous glutamate release more weakly than evoked release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement of spontaneous release by extracellular calcium is insensitive to chelation of intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased spontaneous glutamate release. The frequency of spontaneous synaptic transmission was decreased in CaSR mutant neurons. The concentration-effect relationship for extracellular calcium regulation of spontaneous release was well described by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these results indicate that extracellular Ca2+ does not trigger spontaneous glutamate release by simply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate release. "}],"volume":31,"quality_controlled":"1","doi":"10.1523/JNEUROSCI.6398-10.2011","oa_version":"Submitted Version"}