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dc.contributor.author
Lutas , Andrew
dc.contributor.author
Birnbaumer, Lutz
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dc.contributor.author
Yellen, Gary
dc.date.available
2020-03-05T14:43:02Z
dc.date.issued
2014-12-03
dc.identifier.citation
Lutas , Andrew; Birnbaumer, Lutz; Yellen, Gary; Metabolism regulates the spontaneous firing of substantia nigra pars reticulata neurons via KATP and nonselective cation channels; Society for Neuroscience; Journal of Neuroscience; 34; 49; 03-12-2014; 16336-16347
dc.identifier.issn
0270-6474
dc.identifier.uri
http://hdl.handle.net/11336/98825
dc.description.abstract
Neurons use glucose to fuel glycolysis and provide substrates for mitochondrial respiration, but neurons can also use alternative fuels that bypass glycolysis and feed directly into mitochondria. To determine whether neuronal pacemaking depends on active glucose metabolism, we switched the metabolic fuel from glucose to alternative fuels, lactate or β-hydroxybutyrate, while monitoring the spontaneous firing of GABAergic neurons in mouse substantia nigra pars reticulata (SNr) brain slices. We found that alternative fuels, in the absence of glucose, sustained SNr spontaneous firing at basal rates, but glycolysis may still be supported by glycogen in the absence of glucose. To prevent any glycogen-fueled glycolysis, we directly inhibited glycolysis using either 2-deoxyglucose or iodoacetic acid. Inhibiting glycolysis in the presence of alternative fuels lowered SNr firing to a slower sustained firing rate. Surprisingly, we found that the decrease in SNr firing was not mediated by ATP-sensitive potassium (KATP) channel activity, but if we lowered the perfusion flow rate or omitted the alternative fuel, KATP channels were activated and could silence SNr firing. The KATP-independent slowing of SNr firing that occurred with glycolytic inhibition in the presence of alternative fuels was consistent with a decrease in a nonselective cationic conductance. Although mitochondrial metabolism alone can prevent severe energy deprivation and KATP channel activation in SNr neurons, active glucose metabolism appears important for keeping open a class of ion channels that is crucial for the high spontaneous firing rate of SNr neurons.
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
EXCITABILITY
dc.subject
GLYCOLYSIS
dc.subject
KATP
dc.subject
TRP CHANNEL
dc.subject.classification
Bioquímica y Biología Molecular
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dc.subject.classification
Ciencias Biológicas
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dc.subject.classification
CIENCIAS NATURALES Y EXACTAS
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dc.title
Metabolism regulates the spontaneous firing of substantia nigra pars reticulata neurons via KATP and nonselective cation channels
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2019-10-28T18:26:55Z
dc.identifier.eissn
1529-2401
dc.journal.volume
34
dc.journal.number
49
dc.journal.pagination
16336-16347
dc.journal.pais
Estados Unidos
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dc.journal.ciudad
Washington
dc.description.fil
Fil: Lutas , Andrew. Harvard Medical School; Estados Unidos
dc.description.fil
Fil: Birnbaumer, Lutz. National Institutes of Health; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.description.fil
Fil: Yellen, Gary. Harvard Medical School; Estados Unidos
dc.journal.title
Journal of Neuroscience
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dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.jneurosci.org/content/34/49/16336
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1523/JNEUROSCI.1357-14.2014
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