Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.
Receptor-mediated glutamate release from volume sensitive channels in astrocytes
Takahiro Takano *,
Jian Kang ,,
Jyoti K. Jaiswal,
Sanford M. Simon,
Jane H.-C. Lin ¶,
Yufei Yu ¶,
Yuxing Li ¶,
Jay Yang ||,
Gerald Dienel **,
H. Ronald Zielke, and
Maiken Nedergaard *,
*Center for Aging and Developmental Biology, University of Rochester Medical Center, 601 Elmwood Avenue, Rochester, NY 14642; Departments of Cell Biology and ¶Pathology, New York Medical College, 30 Sunshine Cottage Road, Valhalla, NY 10595; Laboratory of Cellular Biophysics, The Rockefeller University, 1230 York Avenue, New York, NY 10021; ||Department of Anesthesiology, Columbia University Physicians and Surgeons, New York, NY 10032; **Department of Neurology, University of Arkansas for Medical Sciences, Little Rock, AR 77205; and Department of Pediatrics, University of Maryland, 655 West Baltimore Street, Baltimore, MD 21201
Edited by Charles F. Stevens, The Salk Institute for Biological Studies, La Jolla, CA, and approved September 22, 2005
Received for publication July 26, 2005.
Several lines of work have shown that astrocytes release glutamatein response to receptor activation, which results in a modulationof local synaptic activity. Astrocytic glutamate release isCa2+-dependent and occurs in conjunction with exocytosis ofglutamate containing vesicles. However, astrocytes contain amillimolar concentration of cytosolic glutamate and expresschannels permeable to small anions, such as glutamate. Here,we tested the idea that astrocytes respond to receptor stimulationby dynamic changes in cell volume, resulting in volume-sensitivechannel activation, and efflux of cytosolic glutamate. Confocalimaging and whole-cell recordings demonstrated that astrocytesexhibited a transient Ca2+-dependent cell volume increase, whichactivated glutamate permeable channels. HPLC analysis revealedthat glutamate was released in conjunction with other aminoacid osmolytes. Our observations indicate that volume-sensitivechannel may constitute a previously uncharacterized target formodulation of astrocyte-neuronal interactions.
Lack of Evidence for Vesicular Glutamate Transporter Expression in Mouse Astrocytes.
D. Li, K. Herault, K. Silm, A. Evrard, S. Wojcik, M. Oheim, E. Herzog, and N. Ropert (2013)
|Abstract »|Full Text »|PDF »
Neuronal D-Serine and Glycine Release Via the Asc-1 Transporter Regulates NMDA Receptor-Dependent Synaptic Activity.
D. Rosenberg, S. Artoul, A. C. Segal, G. Kolodney, I. Radzishevsky, E. Dikopoltsev, V. N. Foltyn, R. Inoue, H. Mori, J.-M. Billard, et al. (2013)
|Abstract »|Full Text »|PDF »
Optogenetic activation of LiGluR-expressing astrocytes evokes anion channel-mediated glutamate release.