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The Journal of Neuroscience, September 24, 2008, 28(39):9682-9691; doi:10.1523/JNEUROSCI.3484-08.2008

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Cellular/Molecular
Mitochondria Modulate Ca²⁺-Dependent Glutamate Release from Rat Cortical Astrocytes

Reno C. Reyes and Vladimir Parpura

Department of Neurobiology, Center for Glial Biology in Medicine, Atomic Force Microscopy and Nanotechnology Laboratories, Civitan International Research Center, Evelyn F. McKnight Brain Institute, University of Alabama, Birmingham, Alabama 35294

Correspondence should be addressed to Vladimir Parpura, Department of Neurobiology, 1719 Sixth Avenue South, CIRC 429, University of Alabama, Birmingham, AL 35294. Email: vlad{at}uab.edu

Vesicular glutamate release from astrocytes depends on mobilization of free Ca²⁺ from the endoplasmic reticulum (ER), and extracellular space to elevate cytosolic Ca²⁺ (Ca²⁺_cyt). Although mitochondria in neurons, and other secretory cells, have been shown to sequester free Ca²⁺ and have been implicated in the modulation of Ca²⁺-dependent transmitter release, the role of mitochondria in Ca²⁺-dependent glutamate release from astrocytes is not known. A pharmacological approach was taken to manipulate Ca²⁺ accumulation in mitochondria and thereby affect Ca²⁺_cyt of solitary astrocytes in response to mechanical stimuli. Ca²⁺_cyt responses and levels of glutamate release were measured optically in parallel experiments using a fluorescent Ca²⁺ indicator and an enzyme-linked assay, respectively. It was observed that inhibiting mitochondrial Ca²⁺ accumulation is correlated to increased Ca²⁺_cyt and glutamate release, whereas enhancing mitochondrial Ca²⁺ accumulation is correlated to decreased Ca²⁺_cyt and glutamate release. These observations suggest that, in addition to the activity of ER and plasma membrane ion channels, mitochondria modulate Ca²⁺_cyt dynamics in astrocytes and play a role in Ca²⁺-dependent glutamate release from astrocytes.

Key words: mitochondria; astrocyte; calcium; glutamate; release; exocytosis

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Received July 24, 2008; accepted Aug. 18, 2008.

Correspondence should be addressed to Vladimir Parpura, Department of Neurobiology, 1719 Sixth Avenue South, CIRC 429, University of Alabama, Birmingham, AL 35294. Email: vlad{at}uab.edu

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