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

Author(s): S. S. Smaili, R. P. Ureshino, L. Rodrigues, K. K. Rocha, J. T. Carvalho, K. T. Oseki, C. Bincoletto, G. S. Lopes, H. Hirata

Journal Name: Current Pharmaceutical Design

Volume 17 , Issue 35 , 2011

Become EABM
Become Reviewer


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, Alzheimers, Parkinsons and Huntingtons 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.

Keywords: Glutamate, Calcium Signaling, Mitochondrial Dysfunction, Autophagy, Apoptosis, Cell Death, neurons, glial cells, glutamine synthase, aging

Rights & PermissionsPrintExport Cite as

Article Details

Year: 2011
Page: [3865 - 3877]
Pages: 13
DOI: 10.2174/138161211798357782
Price: $65

Article Metrics

PDF: 29