Vesicular Glutamate Transporter-Dependent Glutamate Release from Astrocytes

Journal of Neuroscience - Tập 24 Số 11 - Trang 2633-2642 - 2004
Vedrana Montana1, Yingchun Ni, Vice Sunjara, Xue Jun Hua, Vladimir Parpura
1Department of Cell Biology and Neuroscience and Center for Nanoscale Science and Engineering, University of California, Riverside, California 92521, USA.

Tóm tắt

Astrocytes exhibit excitability based on variations of their intracellular Ca2+concentrations, which leads to glutamate release, that in turn can signal to adjacent neurons. This glutamate-mediated astrocyte–neuron signaling occurs at physiological intracellular Ca2+levels in astrocytes and includes modulation of synaptic transmission. The mechanism underlying Ca2+-dependent glutamate release from astrocytes is most likely exocytosis, because astrocytes express the protein components of the solubleN-ethyl maleimide-sensitive fusion protein attachment protein receptors complex, including synaptobrevin 2, syntaxin, and synaptosome-associated protein of 23 kDa. Although these proteins mediate Ca2+-dependent glutamate release from astrocytes, it is not well understood whether astrocytes express functional vesicular glutamate transporters (VGLUTs) that are critical for vesicle refilling. Here, we find in cultured and freshly isolated astrocytes the presence of brain-specific Na+-dependent inorganic phosphate cotransporter and differentiation-associated Na+-dependent inorganic phosphate cotransporter that have recently been identified as VGLUTs 1 and 2. Indirect immunocytochemistry showed a punctate pattern of VGLUT immunoreactivity throughout the entire cell body and processes, whereas pharmacological inhibition of VGLUTs abolished mechanically and agonist-evoked Ca2+-dependent glutamate release from astrocytes. Taken together, these data indicate that VGLUTs play a functional role in exocytotic glutamate release from astrocytes.

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Journal of Neuroscience

Tập 24 Số 11

2633-2642

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