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Such cellular events are known to potentiate intracellular calcium ([Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>); however, the role of NE with respect to modulating [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> in <jats:styled-content style=\"fixed-case\">PVN<\/jats:styled-content> neurones and the mechanisms by which this may occur remain unclear. We evaluated the effects of <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content> on [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> of acutely isolated <jats:styled-content style=\"fixed-case\">PVN<\/jats:styled-content> neurones using Fura\u20102 imaging. <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content> induced a slow increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> compared to artificial cerebrospinal fluid vehicle. <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content>\u2010induced Ca<jats:sup>2+<\/jats:sup> elevations were mimicked by the \u03b1<jats:sub>1<\/jats:sub>\u2010<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content> agonist phenylephrine (<jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content>) but not by \u03b1<jats:sub>2<\/jats:sub>\u2010<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content> agonist clonidine (<jats:styled-content style=\"fixed-case\">CLON<\/jats:styled-content>). <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content> but not <jats:styled-content style=\"fixed-case\">CLON<\/jats:styled-content> also increased the overall number of neurones that increase [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> (ie, responders). Elimination of extracellular Ca<jats:sup>2+<\/jats:sup> or intracellular endoplasmic reticulum Ca<jats:sup>2+<\/jats:sup> stores abolished the increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and reduced responders. Blockade of voltage\u2010dependent Ca<jats:sup>2+<\/jats:sup> channels abolished the \u03b1<jats:sub>1<\/jats:sub>\u2010<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content> induced increase in [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> and number of responders, as did inhibition of phospholipase C inhibitor, protein kinase C and inositol triphosphate receptors. Spontaneous phasic Ca<jats:sup>2+<\/jats:sup> events, however, were not altered by <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> PE<\/jats:styled-content> or <jats:styled-content style=\"fixed-case\">CLON<\/jats:styled-content>. Repeated K<jats:sup>+<\/jats:sup>\u2010induced membrane depolarisation produced repetitive [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub> elevations. <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content> and <jats:styled-content style=\"fixed-case\">PE<\/jats:styled-content> increased baseline Ca<jats:sup>2+<\/jats:sup>, whereas <jats:styled-content style=\"fixed-case\">NE<\/jats:styled-content> decreased the peak amplitude. <jats:styled-content style=\"fixed-case\">CLON<\/jats:styled-content> also decreased peak amplitude but did not affect baseline [Ca<jats:sup>2+<\/jats:sup>]<jats:sub>i<\/jats:sub>. Taken together, these data suggest receptor\u2010specific influence of \u03b1<jats:sub>1<\/jats:sub> and \u03b1<jats:sub>2<\/jats:sub> receptors on the various modes of calcium entry in <jats:styled-content style=\"fixed-case\">PVN<\/jats:styled-content> neurones. They further suggest Ca<jats:sup>2+<\/jats:sup> increase via \u03b1<jats:sub>1<\/jats:sub>\u2010<jats:styled-content style=\"fixed-case\">AR<\/jats:styled-content>s is co\u2010dependent on extracellular Ca<jats:sup>2+<\/jats:sup> influx and intracellular Ca<jats:sup>2+<\/jats:sup> release, possibly via a phospholipase C inhibitor\u2010mediated signalling cascade.<\/jats:p>","DOI":"10.1111\/jne.12791","type":"journal-article","created":{"date-parts":[[2019,9,8]],"date-time":"2019-09-08T13:41:16Z","timestamp":1567950076000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Activation of alpha\u20101 adrenergic receptors increases cytosolic calcium in neurones of the paraventricular nucleus of the hypothalamus"],"prefix":"10.1111","volume":"31","author":[{"given":"William J.","family":"Milanick","sequence":"first","affiliation":[{"name":"Department of Biomedical Sciences University of Missouri Columbia MO 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