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dc.contributor.author
Sun, Yuyang
dc.contributor.author
Zhang, Haopeng
dc.contributor.author
Selvaraj, Senthil
dc.contributor.author
Sukumaran, Pramod
dc.contributor.author
Lei, Saobo
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Singh, Brij B.
dc.date.available
2018-06-08T15:05:57Z
dc.date.issued
2017-03
dc.identifier.citation
Sun, Yuyang; Zhang, Haopeng; Selvaraj, Senthil; Sukumaran, Pramod; Lei, Saobo; et al.; Inhibition of L-Type Ca 2+ Channels by TRPC1-STIM1 Complex Is Essential for the Protection of Dopaminergic Neurons; Society for Neuroscience; Journal of Neuroscience; 37; 12; 3-2017; 3364-3377
dc.identifier.issn
0270-6474
dc.identifier.uri
http://hdl.handle.net/11336/47861
dc.description.abstract
Loss of dopaminergic (DA) neurons leads to Parkinson’s disease; however, the mechanism(s) for the vulnerability of DA neurons is(are) not fully understood. We demonstrate that TRPC1 regulates the L-type Ca2 channel that contributes to the rhythmic activity of adult DA neurons in the substantia nigra region. Store depletion that activates TRPC1, via STIM1, inhibits the frequency and amplitude of the rhythmic activity in DA neurons of wild-type, but not in TRPC1/, mice. Similarly, TRPC1/ substantia nigra neurons showed increased L-type Ca2 currents, decreased stimulation-dependent STIM1-Cav1.3 interaction, and decreased DA neurons. L-type Ca2 currents and the open channel probability of Cav1.3 channels were also reduced upon TRPC1 activation, whereas increased Cav1.3 currents were observed upon STIM1 or TRPC1 silencing. Increased interaction between Cav1.3-TRPC1-STIM1 was observed upon store depletion and the loss of either TRPC1 or STIM1 led to DA cell death, which was prevented by inhibiting L-type Ca2 channels. Neurotoxins that mimic Parkinson’s disease increased Cav1.3 function, decreased TRPC1 expression, inhibited Tg-mediated STIM1-Cav1.3 interaction, and induced caspase activation. Importantly, restoration of TRPC1 expression not only inhibited Cav1.3 function but increased cell survival. Together, we provide evidence that TRPC1 suppresses Cav1.3 activity by providing an STIM1-based scaffold, which is essential for DA neuron survival.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Society for Neuroscience
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Calcium
dc.subject
Cav1.3
dc.subject
Parkinson’S Disease
dc.subject
Soce
dc.subject
Trpc1-Stim1
dc.subject.classification
Inmunología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Inhibition of L-Type Ca 2+ Channels by TRPC1-STIM1 Complex Is Essential for the Protection of Dopaminergic Neurons
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-06-07T14:08:44Z
dc.journal.volume
37
dc.journal.number
12
dc.journal.pagination
3364-3377
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Baltimore
dc.description.fil
Fil: Sun, Yuyang. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Zhang, Haopeng. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Selvaraj, Senthil. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Sukumaran, Pramod. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Lei, Saobo. University of North Dakota; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institutes of Environmental Health Sciences; Estados Unidos
dc.description.fil
Fil: Singh, Brij B.. University of North Dakota; Estados Unidos
dc.journal.title
Journal of Neuroscience
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1523/JNEUROSCI.3010-16.2017
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/http://www.jneurosci.org/content/37/12/3364
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