Abstract
Under physiological conditions, astrocytes not only passively support and nourish adjacent neurons, but also actively modulate neuronal transmission by releasing "glial transmitters," such as glutamate, ATP, and D-serine. Unlike the case for neurons, the mechanisms by which glia release transmitters are essentially unknown. Here, by using electrochemical amperometry and frequency-modulated single-vesicle imaging, we discovered that hippocampal astrocytes exhibit two modes of exocytosis of glutamate in response to various stimuli. After physiological stimulation, a glial vesicle releases a quantal content that is only 10% of that induced by nonphysiological, mechanical stimulation. The small release event arises from a brief (approximately 2 ms) opening of the fusion pore. We conclude that, after physiological stimulation, astrocytes release glutamate via a vesicular "kiss-and-run" mechanism.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Animals, Newborn
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Astrocytes / drug effects*
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Astrocytes / metabolism*
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Calcium / metabolism
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Chromaffin Cells / drug effects
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Chromaffin Cells / physiology
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Diagnostic Imaging / methods
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Dopamine / pharmacology
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Electrochemistry / methods
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Glial Fibrillary Acidic Protein / metabolism
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Glutamic Acid / metabolism*
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Glutamic Acid / pharmacology*
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Hippocampus / cytology*
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Immunohistochemistry / methods
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Microscopy, Electron / methods
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Patch-Clamp Techniques / methods
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Physical Stimulation / methods
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Pyridinium Compounds / metabolism
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Pyridinium Compounds / pharmacology
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Quaternary Ammonium Compounds / metabolism
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Quaternary Ammonium Compounds / pharmacology
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Rats
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Rats, Sprague-Dawley
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Tetanus Toxin / pharmacology
Substances
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FM1 43
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Glial Fibrillary Acidic Protein
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Pyridinium Compounds
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Quaternary Ammonium Compounds
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Tetanus Toxin
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Glutamic Acid
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Calcium
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Dopamine