Sodium background currents in endocrine/neuroendocrine cells: Towards unraveling channel identity and contribution in hormone secretion

•A Na+ background conductance sets the resting membrane potential.•A Na+ background conductance controls endocrine/neuroendocrine cell excitability.•A Na+ background conductance drives changes in hormone secretion.•The Na+-leak channel NALCN can contribute to the Na+ background current.•The TRP chan...

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Veröffentlicht in:Frontiers in neuroendocrinology 2021-10, Vol.63, p.100947-100947, Article 100947
Hauptverfasser: Guérineau, Nathalie C., Monteil, Arnaud, Lory, Philippe
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Sprache:eng
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Zusammenfassung:•A Na+ background conductance sets the resting membrane potential.•A Na+ background conductance controls endocrine/neuroendocrine cell excitability.•A Na+ background conductance drives changes in hormone secretion.•The Na+-leak channel NALCN can contribute to the Na+ background current.•The TRP channel family can contribute to the Na+ background current. In endocrine/neuroendocrine tissues, excitability of secretory cells is patterned by the repertoire of ion channels and there is clear evidence that extracellular sodium (Na+) ions contribute to hormone secretion. While voltage-gated channels involved in action potential generation are well-described, the background 'leak' channels operating near the resting membrane potential are much less known, and in particular the channels supporting a background entry of Na+ ions. These background Na+ currents (called here 'INab') have the ability to modulate the resting membrane potential and subsequently affect action potential firing. Here we compile and analyze the data collected from three endocrine/neuroendocrine tissues: the anterior pituitary gland, the adrenal medulla and the endocrine pancreas. We also model how INab can be functionally involved in cellular excitability. Finally, towards deciphering the physiological role of INab in endocrine/neuroendocrine cells, its implication in hormone release is also discussed.
ISSN:0091-3022
1095-6808
DOI:10.1016/j.yfrne.2021.100947