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Physiology of spontaneous [Ca(2+)]i oscillations in the isolated vasopressin and oxytocin neurones of the rat supraoptic nucleus

S. Kortus, C. Srinivasan, O. Forostyak, Y. Ueta, E. Sykova, A. Chvatal, M. Zapotocky, A. Verkhratsky, G. Dayanithi,

. 2016 ; 59 (6) : 280-8. [pub] 20160406

Jazyk angličtina Země Nizozemsko

Typ dokumentu časopisecké články

Perzistentní odkaz   https://www.medvik.cz/link/bmc17031792

The magnocellular vasopressin (AVP) and oxytocin (OT) neurones exhibit specific electrophysiological behaviour, synthesise AVP and OT peptides and secrete them into the neurohypophysial system in response to various physiological stimulations. The activity of these neurones is regulated by the very same peptides released either somato-dendritically or when applied to supraoptic nucleus (SON) preparations in vitro. The AVP and OT, secreted somato-dendritically (i.e. in the SON proper) act through specific autoreceptors, induce distinct Ca(2+) signals and regulate cellular events. Here, we demonstrate that about 70% of freshly isolated individual SON neurones from the adult non-transgenic or transgenic rats bearing AVP (AVP-eGFP) or OT (OT-mRFP1) markers, produce distinct spontaneous [Ca(2+)]i oscillations. In the neurones identified (through specific fluorescence), about 80% of AVP neurones and about 60% of OT neurones exhibited these oscillations. Exposure to AVP triggered [Ca(2+)]i oscillations in silent AVP neurones, or modified the oscillatory pattern in spontaneously active cells. Hyper- and hypo-osmotic stimuli (325 or 275 mOsmol/l) respectively intensified or inhibited spontaneous [Ca(2+)]i dynamics. In rats dehydrated for 3 or 5days almost 90% of neurones displayed spontaneous [Ca(2+)]i oscillations. More than 80% of OT-mRFP1 neurones from 3 to 6-day-lactating rats were oscillatory vs. about 44% (OT-mRFP1 neurones) in virgins. Together, these results unveil for the first time that both AVP and OT neurones maintain, via Ca(2+) signals, their remarkable intrinsic in vivo physiological properties in an isolated condition.

Citace poskytuje Crossref.org

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$a Physiology of spontaneous [Ca(2+)]i oscillations in the isolated vasopressin and oxytocin neurones of the rat supraoptic nucleus / $c S. Kortus, C. Srinivasan, O. Forostyak, Y. Ueta, E. Sykova, A. Chvatal, M. Zapotocky, A. Verkhratsky, G. Dayanithi,
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$a The magnocellular vasopressin (AVP) and oxytocin (OT) neurones exhibit specific electrophysiological behaviour, synthesise AVP and OT peptides and secrete them into the neurohypophysial system in response to various physiological stimulations. The activity of these neurones is regulated by the very same peptides released either somato-dendritically or when applied to supraoptic nucleus (SON) preparations in vitro. The AVP and OT, secreted somato-dendritically (i.e. in the SON proper) act through specific autoreceptors, induce distinct Ca(2+) signals and regulate cellular events. Here, we demonstrate that about 70% of freshly isolated individual SON neurones from the adult non-transgenic or transgenic rats bearing AVP (AVP-eGFP) or OT (OT-mRFP1) markers, produce distinct spontaneous [Ca(2+)]i oscillations. In the neurones identified (through specific fluorescence), about 80% of AVP neurones and about 60% of OT neurones exhibited these oscillations. Exposure to AVP triggered [Ca(2+)]i oscillations in silent AVP neurones, or modified the oscillatory pattern in spontaneously active cells. Hyper- and hypo-osmotic stimuli (325 or 275 mOsmol/l) respectively intensified or inhibited spontaneous [Ca(2+)]i dynamics. In rats dehydrated for 3 or 5days almost 90% of neurones displayed spontaneous [Ca(2+)]i oscillations. More than 80% of OT-mRFP1 neurones from 3 to 6-day-lactating rats were oscillatory vs. about 44% (OT-mRFP1 neurones) in virgins. Together, these results unveil for the first time that both AVP and OT neurones maintain, via Ca(2+) signals, their remarkable intrinsic in vivo physiological properties in an isolated condition.
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$a Srinivasan, Chinnapaiyan $u Department of Molecular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic.
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$a Forostyak, Oksana $u Department of Molecular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Department of Neuroscience, Charles University, Second Medical Faculty, V Uvalu 84, 15006 Prague, Czech Republic.
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$a Ueta, Yoichi $u Department of Physiology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.
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$a Sykova, Eva $u Department of Neuroscience, Charles University, Second Medical Faculty, V Uvalu 84, 15006 Prague, Czech Republic; Department of Neuroscience, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic.
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$a Chvatal, Alexandr $u Department of Neuroscience, Charles University, Second Medical Faculty, V Uvalu 84, 15006 Prague, Czech Republic; Department of Cellular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic.
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$a Zapotocky, Martin $u Institute of Physiology, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Institute of Biophysics and Informatics, First Faculty of Medicine, Charles University in Prague, Salmovska 1, 12000 Prague, Czech Republic.
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$a Verkhratsky, Alexei $u University of Manchester, School of Biological Sciences, D.4417 Michael Smith Building, Oxford Road, M13 9PT Manchester, United Kingdom; Achucarro Center for Neuroscience, IKERBASQUE, Basque Foundation for Science, 48011 Bilbao, Spain; Department of Neurosciences, University of the Basque Country UPV/EHU and CIBERNED, Leioa, Spain; University of Nizhny Novgorod, Nizhny Novgorod 603022, Russia. Electronic address: Alexej.Verkhratsky@manchester.ac.uk.
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$a Dayanithi, Govindan $u Department of Molecular Neurophysiology, Institute of Experimental Medicine, Czech Academy of Sciences, Videnska 1083, 14220 Prague, Czech Republic; Institut National de la Santé et de la Recherche Médicale, Unité de recherche U1198, Université Montpellier 2, 34095 Montpellier, France; Ecole Pratique des Hautes Etudes, Sorbonne, 75014 Paris, France. Electronic address: gdaya@univ-montp2.fr.
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