{"intvolume":" 1657","date_created":"2018-12-11T11:46:59Z","author":[{"first_name":"Florin","full_name":"Gherghina, Florin L","last_name":"Gherghina"},{"last_name":"Tica","full_name":"Tica, Andrei A","first_name":"Andrei"},{"full_name":"Elena Deliu","id":"37A40D7E-F248-11E8-B48F-1D18A9856A87","last_name":"Deliu","orcid":"0000-0002-7370-5293","first_name":"Elena"},{"last_name":"Abood","full_name":"Abood, Mary E","first_name":"Mary"},{"first_name":"G.","full_name":"Brailoiu, G. Christina","last_name":"Brailoiu"},{"first_name":"Eugen","last_name":"Brǎiloiu","full_name":"Brǎiloiu, Eugen"}],"day":"15","title":"Effects of VPAC1 activation in nucleus ambiguus neurons","quality_controlled":0,"citation":{"chicago":"Gherghina, Florin, Andrei Tica, Elena Deliu, Mary Abood, G. Brailoiu, and Eugen Brǎiloiu. “Effects of VPAC1 Activation in Nucleus Ambiguus Neurons.” Brain Research. Elsevier, 2017. https://doi.org/10.1016/j.brainres.2016.12.026.","short":"F. Gherghina, A. Tica, E. Deliu, M. Abood, G. Brailoiu, E. Brǎiloiu, Brain Research 1657 (2017) 297–303.","ista":"Gherghina F, Tica A, Deliu E, Abood M, Brailoiu G, Brǎiloiu E. 2017. Effects of VPAC1 activation in nucleus ambiguus neurons. Brain Research. 1657, 297–303.","ama":"Gherghina F, Tica A, Deliu E, Abood M, Brailoiu G, Brǎiloiu E. Effects of VPAC1 activation in nucleus ambiguus neurons. Brain Research. 2017;1657:297-303. doi:10.1016/j.brainres.2016.12.026","ieee":"F. Gherghina, A. Tica, E. Deliu, M. Abood, G. Brailoiu, and E. Brǎiloiu, “Effects of VPAC1 activation in nucleus ambiguus neurons,” Brain Research, vol. 1657. Elsevier, pp. 297–303, 2017.","apa":"Gherghina, F., Tica, A., Deliu, E., Abood, M., Brailoiu, G., & Brǎiloiu, E. (2017). Effects of VPAC1 activation in nucleus ambiguus neurons. Brain Research. Elsevier. https://doi.org/10.1016/j.brainres.2016.12.026","mla":"Gherghina, Florin, et al. “Effects of VPAC1 Activation in Nucleus Ambiguus Neurons.” Brain Research, vol. 1657, Elsevier, 2017, pp. 297–303, doi:10.1016/j.brainres.2016.12.026."},"publist_id":"7290","date_published":"2017-02-15T00:00:00Z","publication":"Brain Research","volume":1657,"year":"2017","status":"public","_id":"529","publisher":"Elsevier","date_updated":"2021-01-12T08:01:26Z","acknowledgement":"This study was supported by startup funds from the Jefferson College of Pharmacy, and by the National Institutes of Health DA023204 (to M.E.A) and P30 DA 013429 to Center for Substance Abuse Research, Temple University.","publication_status":"published","extern":1,"doi":"10.1016/j.brainres.2016.12.026","month":"02","page":"297 - 303","abstract":[{"text":"The pituitary adenylyl cyclase-activating polypeptide (PACAP) and its G protein-coupled receptors, PAC1, VPAC1 and VPAC2 form a system involved in a variety of biological processes. Although some sympathetic stimulatory effects of this system have been reported, its central cardiovascular regulatory properties are poorly characterized. VPAC1 receptors are expressed in the nucleus ambiguus (nAmb), a key center controlling cardiac parasympathetic tone. In this study, we report that selective VPAC1 activation in rhodamine-labeled cardiac vagal preganglionic neurons of the rat nAmb produces inositol 1,4,5-trisphosphate receptor-mediated Ca2+ mobilization, membrane depolarization and activation of P/Q-type Ca2+ channels. In vivo, this pathway converges onto transient reduction in heart rate of conscious rats. Therefore we demonstrate a VPAC1-dependent mechanism in the central parasympathetic regulation of the heart rate, adding to the complexity of PACAP-mediated cardiovascular modulation.","lang":"eng"}],"type":"journal_article"}