Intracellular Calcium Transients and Potassium Current Oscillations Evoked by Glutamate in Cultured Rat Astrocytes

• Published in: The Journal of neuroscience Vol. 17; no. 19; pp. 7278 - 7287
• Main Authors: Chen, Jianguo, Backus, Kurt H, Deitmer, Joachim W
• Format: Journal Article
• Language: English
• Published: United States Soc Neuroscience 01-10-1997; Society for Neuroscience
• Subjects: Animals; Astrocytes - drug effects; Astrocytes - metabolism; Astrocytes - physiology; Biological Transport; Calcium - physiology; Cells, Cultured; Electric Conductivity; Glutamic Acid - pharmacology; Hydrogen-Ion Concentration; Intracellular Membranes - metabolism; Ligands; Oscillometry; Osmolar Concentration; Patch-Clamp Techniques; Potassium - physiology; Rats; Receptors, Glutamate - metabolism
• ISSN: 0270-6474; 1529-2401
• DOI: 10.1523/jneurosci.17-19-07278.1997

Glutamate responses in cultured rat astrocytes from cerebella of neonatal rats were investigated using the perforated-patch configuration to record membrane currents without rundown of intracellular messenger cascades, and microfluorometric measurements to measure the intracellular Ca2+ concentration ([Ca2+]i) and intracellular pH (pHi) with fura-2 AM and 2',7'-bis-(2-carboxyethyl)-5,6-carboxyfluorescein acetoxy methylester respectively. In the perforated-patch mode, glutamate evoked single or multiple outward current transients in 82% of the cells, which disappeared when the recording technique was converted into a conventional whole-cell mode. The outward current transients were accompanied by [Ca2+]i transients, whereas pHi fell monophasically, without any sign of oscillation. Pharmacological analysis of the glutamate-induced responses indicated that ionotropic receptor activation evoked an inward current but no outward current transients, and metabotropic receptor activation (of the mGluR1/5 type) elicited outward current transients but no inward current. The outward current transients were reduced in frequency, or even abolished, after depletion of the intracellular Ca2+-stores by the Ca2+-ATPase inhibitor cyclopiaconic acid (10 microM). They reversed near -85 mV and were reduced by tetraethylammonium (10 mM), suggesting that they were caused by K+ channel activation. It is concluded that glutamate evoked these K+ outward current transients by oscillatory Ca2+ release mediated by mGluR activation. The corresponding membrane potential waves across the astroglial syncytium could provide spatial and temporal dynamics to the glial K+ uptake capacity and other voltage-dependent processes.