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C(a2+)-dependent glutamate release involves two classes of endoplasmic reticulum Ca(2+) stores in astrocytes
Xue Hua1, Erik B Malarkey, Vice Sunjara
1Department of Cell Biology and Neuroscience, and Center for Nanoscale Science and Engineering, University of California, Riverside, California 92521, USA.
Journal of Neuroscience Research
|March 30, 2004
Summary
Astrocytes release glutamate in a calcium-dependent manner. Both inositol 1,4,5-trisphosphate (IP3)-sensitive and caffeine/ryanodine-sensitive internal calcium stores regulate this essential process.
Area of Science:
- Neuroscience
- Cell Biology
- Biochemistry
Background:
- Astrocytes modulate synaptic transmission via glutamate release, a process dependent on intracellular calcium (Ca2+).
- The specific internal Ca2+ stores contributing to this glutamate release are not fully understood.
Purpose of the Study:
- To investigate the distinct roles of different intracellular Ca2+ stores in regulating mechanically induced glutamate release from cortical astrocytes.
- To elucidate the pharmacological mechanisms controlling Ca2+-dependent glutamate release.
Main Methods:
- Cultured solitary cortical astrocytes were used.
- Intracellular Ca2+ levels were monitored using fluo-3 and quantitative fluorescence microscopy.
- Glutamate release was quantified using an L-glutamate dehydrogenase-linked detection system.
- Pharmacological agents, including Cd2+, diphenylboric acid 2-aminoethyl ester, caffeine, and ryanodine, were employed.
Main Results:
- Mechanical stimulation of astrocytes induced Ca2+ increases and glutamate release.
- Extracellular Cd2+ significantly reduced glutamate release, confirming Ca2+ dependence.
- Internal Ca2+ stores were confirmed as the primary Ca2+ source.
- Inositol 1,4,5-trisphosphate (IP3) receptor antagonism and caffeine/ryanodine treatment both significantly reduced glutamate release.
Conclusions:
- Astrocytes utilize dual intracellular Ca2+ stores, sensitive to both IP3 and caffeine/ryanodine, to regulate glutamate release.
- These findings highlight the complex intracellular mechanisms governing astrocyte-mediated synaptic modulation.