title: The role of mitochondrial function in glutamate-dependent metabolism in neuronal cells.
abstract: Glutamate 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 glutamateinduced 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.
authors.affiliation: Departamento de Farmacologia, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo/SP, Brazil. ssmaili@unifesp.br
authors.forename: S S
authors.initials: SS
authors.lastname: Smaili
authors.forename: R P
authors.initials: RP
authors.lastname: Ureshino
authors.forename: L
authors.initials: L
authors.lastname: Rodrigues
authors.forename: K K
authors.initials: KK
authors.lastname: Rocha
authors.forename: J T
authors.initials: JT
authors.lastname: Carvalho
authors.forename: K T
authors.initials: KT
authors.lastname: Oseki
authors.forename: C
authors.initials: C
authors.lastname: Bincoletto
authors.forename: G S
authors.initials: GS
authors.lastname: Lopes
authors.forename: H
authors.initials: H
authors.lastname: Hirata
mesh_terms: D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism; D000818:Animals; D001343:Autophagy / Q000187:drug effects; D020013:Calcium Signaling / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D018683:Excitatory Amino Acid Agents / Q000378:metabolism / Q000494:pharmacology; D018698:Glutamic Acid / Q000378:metabolism*; D006801:Humans; D006816:Huntington Disease / Q000188:drug therapy / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009457:Neuroglia / Q000187:drug effects / Q000378:metabolism*; D009473:Neuronal Plasticity / Q000187:drug effects; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D020258:Neurotoxicity Syndromes / Q000188:drug therapy / Q000378:metabolism / Q000517:prevention & control; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism; D009435:Synaptic Transmission / Q000187:drug effects
chemical_list: D018683:Excitatory Amino Acid Agents; D018698:Glutamic Acid