L-type Ca2+ channel–mediated Ca2+ influx adjusts neuronal mitochondrial function to physiological and pathophysiological conditions

Matej Hotka; Michal Cagalinec; Karlheinz Hilber; Livia Hool; Stefan Boehm; Helmut Kubista

doi:10.1126/scisignal.aaw6923

Research ArticleCalcium signaling

L-type Ca²⁺ channel–mediated Ca²⁺ influx adjusts neuronal mitochondrial function to physiological and pathophysiological conditions

View ORCID ProfileMatej Hotka¹,*,
View ORCID ProfileMichal Cagalinec¹,²,³,
View ORCID ProfileKarlheinz Hilber¹,
View ORCID ProfileLivia Hool⁴,⁵,
View ORCID ProfileStefan Boehm¹, and
View ORCID ProfileHelmut Kubista ¹,*

¹Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Währingerstrasse 13a, 1090, Vienna, Austria.
²Department of Cellular Cardiology, Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05 Bratislava, Slovakia.
³Laboratory of Mitochondrial Dynamics, Department of Pharmacology, Institute of Biomedicine and Translational Medicine, Faculty of Medicine, University of Tartu, Ravila 19, 50 411 Tartu, Estonia.
⁴School of Human Sciences (Physiology), The University of Western Australia, Crawley, WA 6009, Australia.
⁵Victor Chang Cardiac Research Institute, Sydney, NSW 2010, Australia.

↵*Corresponding author. Email: matej.hotka{at}meduniwien.ac.at (M.H.); helmut.kubista{at}meduniwien.ac.at (H.K.)

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Science Signaling 11 Feb 2020:
Vol. 13, Issue 618, eaaw6923
DOI: 10.1126/scisignal.aaw6923

Matej Hotka

1Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Währingerstrasse 13a, 1090, Vienna, Austria.

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ORCID record for Matej Hotka
For correspondence: matej.hotka@meduniwien.ac.at helmut.kubista@meduniwien.ac.at

Michal Cagalinec

1Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Währingerstrasse 13a, 1090, Vienna, Austria.

2Department of Cellular Cardiology, Institute of Experimental Endocrinology, Biomedical Research Center, Slovak Academy of Sciences, Dúbravská cesta 9, 845 05 Bratislava, Slovakia.

3Laboratory of Mitochondrial Dynamics, Department of Pharmacology, Institute of Biomedicine and Translational Medicine, Faculty of Medicine, University of Tartu, Ravila 19, 50 411 Tartu, Estonia.

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ORCID record for Michal Cagalinec

Karlheinz Hilber

1Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Währingerstrasse 13a, 1090, Vienna, Austria.

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Livia Hool

4School of Human Sciences (Physiology), The University of Western Australia, Crawley, WA 6009, Australia.

5Victor Chang Cardiac Research Institute, Sydney, NSW 2010, Australia.

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Stefan Boehm

1Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Währingerstrasse 13a, 1090, Vienna, Austria.

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Helmut Kubista

1Center of Physiology and Pharmacology, Department of Neurophysiology and Neuropharmacology, Medical University of Vienna, Währingerstrasse 13a, 1090, Vienna, Austria.

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For correspondence: matej.hotka@meduniwien.ac.at helmut.kubista@meduniwien.ac.at

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vol. 13 no. 618

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https://doi.org/10.1126/scisignal.aaw6923

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Received January 16, 2019
Resubmitted September 12, 2019
Accepted January 23, 2020
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Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works http://www.sciencemag.org/about/science-licenses-journal-article-reuseThis is an article distributed under the terms of the Science Journals Default License.

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L-type Ca²⁺ channel–mediated Ca²⁺ influx adjusts neuronal mitochondrial function to physiological and pathophysiological conditions

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