The Role of Mitochondrial Function in Glutamate-Dependent Metabolism in Neuronal Cells

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dc.contributor.authorSmaili, Soraya Soubhi [UNIFESP]
dc.contributor.authorUreshino, Rodrigo Portes [UNIFESP]
dc.contributor.authorRodrigues, L. [UNIFESP]
dc.contributor.authorRocha, Katiucha Karolina [UNIFESP]
dc.contributor.authorCarvalho, J. T. [UNIFESP]
dc.contributor.authorOseki, Karen Tubono [UNIFESP]
dc.contributor.authorBincoletto, Claudia [UNIFESP]
dc.contributor.authorLopes, Guiomar Silva [UNIFESP]
dc.contributor.authorHirata, Hanako [UNIFESP]
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2018-06-15T17:05:15Z
dc.date.available2018-06-15T17:05:15Z
dc.date.issued2011-12-01
dc.description.abstractGlutamate is an important neurotransmitter in neurons and glial cells and it is one of the keys to the neuron-glial interaction in the brain. Glutamate transmission is strongly dependent on calcium homeostasis and on mitochondrial function. In the present work we presented several aspects related to the role of mitochondria in glutamate signaling and in brain diseases. We focused on glutamate-induced calcium signaling and its relation to the organelle dysfunction with cell death processes. In addition, we have discussed how alterations in this pathway may lead or aggravate a variety of neurodegenerative diseases. We compiled information on how mitochondria can influence cell fate during glutamate stimulation and calcium signaling. These organelles play a pivotal role in neuron and glial exchange, in synaptic plasticity and several pathological conditions related to Aging, Alzheimer's, Parkinson's and Huntington's diseases. We have also presented autophagy as a mechanism activated during mitochondrial dysfunction which may function as a protective mechanism during injury. Furthermore, some new perspectives and approaches to treat these neurodegenerative diseases are offered and evaluated.en
dc.description.affiliationUniv Fed Sao Paulo EPM UNIFESP, Dept Farmacol, Escola Paulista Med, Sao Paulo, Brazil
dc.description.affiliationUnifespUniv Fed Sao Paulo EPM UNIFESP, Dept Farmacol, Escola Paulista Med, Sao Paulo, Brazil
dc.description.sourceWeb of Science
dc.format.extent3865-3877
dc.identifierhttp://dx.doi.org/10.2174/138161211798357782
dc.identifier.citationCurrent Pharmaceutical Design. Sharjah: Bentham Science Publ Ltd, v. 17, n. 35, p. 3865-3877, 2011.
dc.identifier.doi10.2174/138161211798357782
dc.identifier.issn1381-6128
dc.identifier.urihttp://repositorio.unifesp.br/handle/11600/43466
dc.identifier.wosWOS:000299637300006
dc.language.isoeng
dc.publisherBentham Science Publ Ltd
dc.relation.ispartofCurrent Pharmaceutical Design
dc.rightsinfo:eu-repo/semantics/restrictedAccess
dc.subjectGlutamateen
dc.subjectCalcium Signalingen
dc.subjectMitochondrial Dysfunctionen
dc.subjectAutophagyen
dc.subjectApoptosisen
dc.subjectCell Deathen
dc.titleThe Role of Mitochondrial Function in Glutamate-Dependent Metabolism in Neuronal Cellsen
dc.typeinfo:eu-repo/semantics/article
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