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Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease

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Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease. / Benkert, Julia; Hess, Simon; Roy, Shoumik; Beccano-Kelly, Dayne; Wiederspohn, Nicole; Duda, Johanna; Simons, Carsten; Patil, Komal; Gaifullina, Aisylu; Mannal, Nadja; Dragicevic, Elena; Spaich, Desirée; Müller, Sonja; Nemeth, Julia; Hollmann, Helene; Deuter, Nora; Mousba, Yassine; Kubisch, Christian; Poetschke, Christina; Striessnig, Joerg; Pongs, Olaf; Schneider, Toni; Wade-Martins, Richard; Patel, Sandip; Parlato, Rosanna; Frank, Tobias; Kloppenburg, Peter; Liss, Birgit.

in: NAT COMMUN, Jahrgang 10, Nr. 1, 08.11.2019, S. 5094.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Benkert, J, Hess, S, Roy, S, Beccano-Kelly, D, Wiederspohn, N, Duda, J, Simons, C, Patil, K, Gaifullina, A, Mannal, N, Dragicevic, E, Spaich, D, Müller, S, Nemeth, J, Hollmann, H, Deuter, N, Mousba, Y, Kubisch, C, Poetschke, C, Striessnig, J, Pongs, O, Schneider, T, Wade-Martins, R, Patel, S, Parlato, R, Frank, T, Kloppenburg, P & Liss, B 2019, 'Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease', NAT COMMUN, Jg. 10, Nr. 1, S. 5094. https://doi.org/10.1038/s41467-019-12834-x

APA

Benkert, J., Hess, S., Roy, S., Beccano-Kelly, D., Wiederspohn, N., Duda, J., Simons, C., Patil, K., Gaifullina, A., Mannal, N., Dragicevic, E., Spaich, D., Müller, S., Nemeth, J., Hollmann, H., Deuter, N., Mousba, Y., Kubisch, C., Poetschke, C., ... Liss, B. (2019). Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease. NAT COMMUN, 10(1), 5094. https://doi.org/10.1038/s41467-019-12834-x

Vancouver

Benkert J, Hess S, Roy S, Beccano-Kelly D, Wiederspohn N, Duda J et al. Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease. NAT COMMUN. 2019 Nov 8;10(1):5094. https://doi.org/10.1038/s41467-019-12834-x

Bibtex

@article{43ca0088237b45399fa1baaed2bd6fe1,
title = "Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease",
abstract = "Degeneration of dopaminergic neurons in the substantia nigra causes the motor symptoms of Parkinson's disease. The mechanisms underlying this age-dependent and region-selective neurodegeneration remain unclear. Here we identify Cav2.3 channels as regulators of nigral neuronal viability. Cav2.3 transcripts were more abundant than other voltage-gated Ca2+ channels in mouse nigral neurons and upregulated during aging. Plasmalemmal Cav2.3 protein was higher than in dopaminergic neurons of the ventral tegmental area, which do not degenerate in Parkinson's disease. Cav2.3 knockout reduced activity-associated nigral somatic Ca2+ signals and Ca2+-dependent after-hyperpolarizations, and afforded full protection from degeneration in vivo in a neurotoxin Parkinson's mouse model. Cav2.3 deficiency upregulated transcripts for NCS-1, a Ca2+-binding protein implicated in neuroprotection. Conversely, NCS-1 knockout exacerbated nigral neurodegeneration and downregulated Cav2.3. Moreover, NCS-1 levels were reduced in a human iPSC-model of familial Parkinson's. Thus, Cav2.3 and NCS-1 may constitute potential therapeutic targets for combatting Ca2+-dependent neurodegeneration in Parkinson's disease.",
author = "Julia Benkert and Simon Hess and Shoumik Roy and Dayne Beccano-Kelly and Nicole Wiederspohn and Johanna Duda and Carsten Simons and Komal Patil and Aisylu Gaifullina and Nadja Mannal and Elena Dragicevic and Desir{\'e}e Spaich and Sonja M{\"u}ller and Julia Nemeth and Helene Hollmann and Nora Deuter and Yassine Mousba and Christian Kubisch and Christina Poetschke and Joerg Striessnig and Olaf Pongs and Toni Schneider and Richard Wade-Martins and Sandip Patel and Rosanna Parlato and Tobias Frank and Peter Kloppenburg and Birgit Liss",
year = "2019",
month = nov,
day = "8",
doi = "10.1038/s41467-019-12834-x",
language = "English",
volume = "10",
pages = "5094",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease

AU - Benkert, Julia

AU - Hess, Simon

AU - Roy, Shoumik

AU - Beccano-Kelly, Dayne

AU - Wiederspohn, Nicole

AU - Duda, Johanna

AU - Simons, Carsten

AU - Patil, Komal

AU - Gaifullina, Aisylu

AU - Mannal, Nadja

AU - Dragicevic, Elena

AU - Spaich, Desirée

AU - Müller, Sonja

AU - Nemeth, Julia

AU - Hollmann, Helene

AU - Deuter, Nora

AU - Mousba, Yassine

AU - Kubisch, Christian

AU - Poetschke, Christina

AU - Striessnig, Joerg

AU - Pongs, Olaf

AU - Schneider, Toni

AU - Wade-Martins, Richard

AU - Patel, Sandip

AU - Parlato, Rosanna

AU - Frank, Tobias

AU - Kloppenburg, Peter

AU - Liss, Birgit

PY - 2019/11/8

Y1 - 2019/11/8

N2 - Degeneration of dopaminergic neurons in the substantia nigra causes the motor symptoms of Parkinson's disease. The mechanisms underlying this age-dependent and region-selective neurodegeneration remain unclear. Here we identify Cav2.3 channels as regulators of nigral neuronal viability. Cav2.3 transcripts were more abundant than other voltage-gated Ca2+ channels in mouse nigral neurons and upregulated during aging. Plasmalemmal Cav2.3 protein was higher than in dopaminergic neurons of the ventral tegmental area, which do not degenerate in Parkinson's disease. Cav2.3 knockout reduced activity-associated nigral somatic Ca2+ signals and Ca2+-dependent after-hyperpolarizations, and afforded full protection from degeneration in vivo in a neurotoxin Parkinson's mouse model. Cav2.3 deficiency upregulated transcripts for NCS-1, a Ca2+-binding protein implicated in neuroprotection. Conversely, NCS-1 knockout exacerbated nigral neurodegeneration and downregulated Cav2.3. Moreover, NCS-1 levels were reduced in a human iPSC-model of familial Parkinson's. Thus, Cav2.3 and NCS-1 may constitute potential therapeutic targets for combatting Ca2+-dependent neurodegeneration in Parkinson's disease.

AB - Degeneration of dopaminergic neurons in the substantia nigra causes the motor symptoms of Parkinson's disease. The mechanisms underlying this age-dependent and region-selective neurodegeneration remain unclear. Here we identify Cav2.3 channels as regulators of nigral neuronal viability. Cav2.3 transcripts were more abundant than other voltage-gated Ca2+ channels in mouse nigral neurons and upregulated during aging. Plasmalemmal Cav2.3 protein was higher than in dopaminergic neurons of the ventral tegmental area, which do not degenerate in Parkinson's disease. Cav2.3 knockout reduced activity-associated nigral somatic Ca2+ signals and Ca2+-dependent after-hyperpolarizations, and afforded full protection from degeneration in vivo in a neurotoxin Parkinson's mouse model. Cav2.3 deficiency upregulated transcripts for NCS-1, a Ca2+-binding protein implicated in neuroprotection. Conversely, NCS-1 knockout exacerbated nigral neurodegeneration and downregulated Cav2.3. Moreover, NCS-1 levels were reduced in a human iPSC-model of familial Parkinson's. Thus, Cav2.3 and NCS-1 may constitute potential therapeutic targets for combatting Ca2+-dependent neurodegeneration in Parkinson's disease.

U2 - 10.1038/s41467-019-12834-x

DO - 10.1038/s41467-019-12834-x

M3 - SCORING: Journal article

C2 - 31704946

VL - 10

SP - 5094

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -