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In these cells, several studies previously showed that extracellular sodium (Na\n                    <jats:sup>+<\/jats:sup>\n                    ) removal resulted in a negative shift of the resting membrane potential (RMP) and a subsequent inhibition of the spontaneous firing of action potentials, suggesting the contribution of a Na\n                    <jats:sup>+<\/jats:sup>\n                    background conductance. Here, we show that the Na\n                    <jats:sup>+<\/jats:sup>\n                    leak channel NALCN conducts a Ca\n                    <jats:sup>2+<\/jats:sup>\n                    \u2010 Gd\n                    <jats:sup>3+<\/jats:sup>\n                    \u2010sensitive and TTX\u2010resistant Na\n                    <jats:sup>+<\/jats:sup>\n                    background conductance in the GH\n                    <jats:sub>3<\/jats:sub>\n                    cell line, a cell model of pituitary endocrine cells. NALCN knockdown hyperpolarized the RMP, altered GH\n                    <jats:sub>3<\/jats:sub>\n                    cell electrical properties and inhibited prolactin secretion. Conversely, the overexpression of NALCN depolarized the RMP, also reshaping the electrical properties of GH\n                    <jats:sub>3<\/jats:sub>\n                    cells. Overall, our results indicate that NALCN is functional in GH\n                    <jats:sub>3<\/jats:sub>\n                    cells and involved in endocrine cell excitability as well as in hormone secretion. Indeed, the GH\n                    <jats:sub>3<\/jats:sub>\n                    cell line suitably models native pituitary cells that display a similar Na\n                    <jats:sup>+<\/jats:sup>\n                    background conductance and appears as a proper cellular model to study the role of NALCN in cellular excitability.\n                  <\/jats:p>","DOI":"10.1096\/fj.202000841rr","type":"journal-article","created":{"date-parts":[[2021,4,1]],"date-time":"2021-04-01T13:08:27Z","timestamp":1617282507000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["The sodium leak channel NALCN regulates cell excitability of pituitary endocrine cells"],"prefix":"10.1096","volume":"35","author":[{"given":"Hathaichanok","family":"Impheng","sequence":"first","affiliation":[{"name":"IGF Universit\u00e9 de Montpellier CNRS INSERM Montpellier France"},{"name":"LabEx \u2018Ion Channel Science and Therapeutics\u2019 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