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Persistent Na+ influx drives L-type channel resting Ca2+ entry in rat melanotrophs

T. Kayano, Y. Sasaki, N. Kitamura, N. Harayama, T. Moriya, G. Dayanithi, A. Verkhratsky, I. Shibuya,

. 2019 ; 79 (-) : 11-19. [pub] 20190206

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc20025865

Rat melanotrophs express several types of voltage-gated and ligand-gated calcium channels, although mechanisms involved in the maintenance of the resting intracellular Ca2+ concentration ([Ca2+]i) remain unknown. We analyzed mechanisms regulating resting [Ca2+]i in dissociated rat melanotrophs by Ca2+-imaging and patch-clamp techniques. Treatment with antagonists of L-type, but not N- or P/Q-type voltage-gated Ca2+ channels (VGCCs) as well as removal of extracellular Ca2+ resulted in a rapid and reversible decrease in [Ca2+]i, indicating constitutive Ca2+ influx through L-type VGCCs. Reduction of extracellular Na+ concentration (replacement with NMDG+) similarly decreased resting [Ca2+]i. When cells were champed at -80 mV, decrease in the extracellular Na+ resulted in a positive shift of the holding current. In cell-attached voltage-clamp and whole-cell current-clamp configurations, the reduction of extracellular Na+ caused hyperpolarisation. The holding current shifted in negative direction when extracellular K+ concentration was increased from 5 mM to 50 mM in the presence of K+ channel blockers, Ba2+ and TEA, indicating cation nature of persistent conductance. RT-PCR analyses of pars intermedia tissues detected mRNAs of TRPV1, TRPV4, TRPC6, and TRPM3-5. The TRPV channel blocker, ruthenium red, shifted the holding current in positive direction, and significantly decreased the resting [Ca2+]i. These results indicate operation of a constitutive cation conductance sensitive to ruthenium red, which regulates resting membrane potential and [Ca2+]i in rat melanotrophs.

Citace poskytuje Crossref.org

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$a Rat melanotrophs express several types of voltage-gated and ligand-gated calcium channels, although mechanisms involved in the maintenance of the resting intracellular Ca2+ concentration ([Ca2+]i) remain unknown. We analyzed mechanisms regulating resting [Ca2+]i in dissociated rat melanotrophs by Ca2+-imaging and patch-clamp techniques. Treatment with antagonists of L-type, but not N- or P/Q-type voltage-gated Ca2+ channels (VGCCs) as well as removal of extracellular Ca2+ resulted in a rapid and reversible decrease in [Ca2+]i, indicating constitutive Ca2+ influx through L-type VGCCs. Reduction of extracellular Na+ concentration (replacement with NMDG+) similarly decreased resting [Ca2+]i. When cells were champed at -80 mV, decrease in the extracellular Na+ resulted in a positive shift of the holding current. In cell-attached voltage-clamp and whole-cell current-clamp configurations, the reduction of extracellular Na+ caused hyperpolarisation. The holding current shifted in negative direction when extracellular K+ concentration was increased from 5 mM to 50 mM in the presence of K+ channel blockers, Ba2+ and TEA, indicating cation nature of persistent conductance. RT-PCR analyses of pars intermedia tissues detected mRNAs of TRPV1, TRPV4, TRPC6, and TRPM3-5. The TRPV channel blocker, ruthenium red, shifted the holding current in positive direction, and significantly decreased the resting [Ca2+]i. These results indicate operation of a constitutive cation conductance sensitive to ruthenium red, which regulates resting membrane potential and [Ca2+]i in rat melanotrophs.
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$a Sasaki, Yuto $u Laboratory of Veterinary Physiology, Joint Department of Veterinary Medicine, Faculty of Agriculture, Tottori University, Tottori, Japan.
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$a Harayama, Nobuya $u Intensive Care Medicine, University Hospital, University of Occupational and Environmental Health, Kitakyushu, Japan.
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$a Dayanithi, Govindan $u Institut des Sciences Biologiques-Neurosciences, cognition, Centre National de la Recherche Scientifique, 3 rue Michel-Ange, Paris, France; MMDN, Institut National de la Santé et de la Recherche Médicale U1198, Université Montpellier, Montpellier, France; Ecole Pratique des Hautes Etudes-Sorbonne, Paris, France; Department of Pharmacology and Toxicology, Faculty ofMedicine, Charles University at Plzen, Plzen, Czech Republic. Electronic address: gdaya@univ-montp2.fr.
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$a Verkhratsky, Alexei $u Faculty of Biology, Medicine and Health, University of Manchester, M13 9PT Manchester, UK; Achucarro Centre for Neuroscience, IKERBASQUE, Basque Foundation for Science, 48011, Bilbao, Spain.
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