Nicotinic cholinergic signaling in hippocampal astrocytes involves calcium-induced calcium release from intracellular stores
- Department of Physiology and Biophysics, University of Colorado Health Sciences Center, Denver, CO 80262
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Edited by Charles F. Stevens, The Salk Institute for Biological Studies, La Jolla, CA, and approved January 25, 2001 (received for review November 12, 2000)
Abstract
In this report we provide evidence that neuronal nicotinic acetylcholine receptors (nAChRs) are present on hippocampal astrocytes and their activation produces rapid currents and calcium transients. Our data indicate that these responses obtained from astrocytes are primarily mediated by an AChR subtype that is functionally blocked by α-bungarotoxin (αBgt) and contains the α7 subunit (αBgt-AChRs). Furthermore, their action is unusual in that they effectively increase intracellular free calcium concentrations by activating calcium-induced calcium release from intracellular stores, triggered by influx through the receptor channels. These results reveal a mechanism by which αBgt-AChRs on astrocytes can efficiently modulate calcium signaling in the central nervous system in a manner distinct from that observed with these receptors on neurons.
Footnotes
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↵ * To whom reprint requests should be addressed at: Department of Physiology and Biophysics, C-240, University of Colorado Health Sciences Center, 4200 East 9th Avenue, Denver, CO 80262. E-mail: sukumar.v{at}uchsc.edu.
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This paper was submitted directly (Track II) to the PNAS office.
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See commentary on page 3631.
- Abbreviations:
- αBgt,
- α-bungarotoxin;
- ACh,
- acetylcholine;
- AChR,
- ACh receptor;
- nAChR,
- neuronal AChR;
- CICR,
- calcium-induced calcium release;
- MLA,
- methyllycaconitine;
- TG,
- thapsigargin;
- Xe-C,
- Xestospongin C;
- VGCC,
- voltage-gated calcium channel;
- InsP3,
- inositol trisphosphate
- Copyright © 2001, The National Academy of Sciences
