Astrocyte Heterogeneity: Endogenous Amino Acid Levels and Release Evoked by Non‐ N ‐Methyl‐D‐Aspartate Receptor Agonists and by Potassium‐Induced Swelling in Type‐1 and Type‐2 Astrocytes

Astrocyte Heterogeneity: Endogenous Amino Acid Levels and Release Evoked by Non‐ N... Abstract: The aim of the present study was to determine whether endogenous amino acids are released from type‐1 and type‐2 astrocytes following non‐N‐methyl‐D‐aspartate (NMDA) receptor activation and whether such release is related to cell swelling. Amino acid levels and release were measured by HPLC in secondary cultures from neonatal rat cortex, highly enriched in type‐1 or type‐2 astrocytes. The following observations were made. (a) The endogenous level of several amino acids (glutamate, alanine, glutamine, asparagine, taurine, serine, and threonine) was substantially higher in type‐1 than in type‐2 astrocytes. (b) The spontaneous release of glutamine and taurine was higher in type‐1 than in type‐2 astrocytes; that of other amino acids was similar. (c) Exposure of type‐2 astrocyte cultures to 50 μM kainate or quisqualate doubled the release of glutamate and caused a lower, but significant increase in that of aspartate, glycine, taurine, alanine, serine (only in the case of kainate), and glutamine (only in the case of quisqualate). These effects were reversed by the antagonist CNQX. (d) Exposure of type‐1 astrocyte cultures to 50–200 μM kainate or 50 μM quisqualate did not affect endogenous amino acid release, even after treating the cultures with dibutyryl cyclic AMP. (e) Exposure of type‐1 or type‐2 astrocyte cultures to 50 mM KCl (replacing an equimolar concentration of NaCl) enhanced the release of taurine > glutamate > aspartate. The effect was somewhat more pronounced in type‐2 than in type‐1 astrocytes. Veratridine (50 μM) did not cause any increase in amino acid release. (f) The release of amino acids induced by high (K+) appeared to be related to cell swelling, in both type‐1 and type‐2 astrocytes. Swelling and K+‐induced release were somewhat higher in type‐2 than in type‐1 astrocytes. In contrast, neither kainate nor quisqualate caused any appreciable increase in cell volume. It is concluded that non‐NMDA receptor agonists stimulate the release of several endogenous amino acids (some of which are neuroactive) from type‐2 but not from type‐1 astrocytes. The effect does not seem to be related to cell swelling, which causes a different release profile in both type‐1 and type‐2 astrocytes. The absence of kainate‐ and quisqualate‐evoked release in type‐1 astrocytes suggests that the density of non‐NMDA receptors in this cell type is very low. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Astrocyte Heterogeneity: Endogenous Amino Acid Levels and Release Evoked by Non‐ N ‐Methyl‐D‐Aspartate Receptor Agonists and by Potassium‐Induced Swelling in Type‐1 and Type‐2 Astrocytes

Journal of Neurochemistry, Volume 58 (5) – May 1, 1992

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Publisher
Wiley
Copyright
Copyright © 1992 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
D.O.I.
10.1111/j.1471-4159.1992.tb10073.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: The aim of the present study was to determine whether endogenous amino acids are released from type‐1 and type‐2 astrocytes following non‐N‐methyl‐D‐aspartate (NMDA) receptor activation and whether such release is related to cell swelling. Amino acid levels and release were measured by HPLC in secondary cultures from neonatal rat cortex, highly enriched in type‐1 or type‐2 astrocytes. The following observations were made. (a) The endogenous level of several amino acids (glutamate, alanine, glutamine, asparagine, taurine, serine, and threonine) was substantially higher in type‐1 than in type‐2 astrocytes. (b) The spontaneous release of glutamine and taurine was higher in type‐1 than in type‐2 astrocytes; that of other amino acids was similar. (c) Exposure of type‐2 astrocyte cultures to 50 μM kainate or quisqualate doubled the release of glutamate and caused a lower, but significant increase in that of aspartate, glycine, taurine, alanine, serine (only in the case of kainate), and glutamine (only in the case of quisqualate). These effects were reversed by the antagonist CNQX. (d) Exposure of type‐1 astrocyte cultures to 50–200 μM kainate or 50 μM quisqualate did not affect endogenous amino acid release, even after treating the cultures with dibutyryl cyclic AMP. (e) Exposure of type‐1 or type‐2 astrocyte cultures to 50 mM KCl (replacing an equimolar concentration of NaCl) enhanced the release of taurine > glutamate > aspartate. The effect was somewhat more pronounced in type‐2 than in type‐1 astrocytes. Veratridine (50 μM) did not cause any increase in amino acid release. (f) The release of amino acids induced by high (K+) appeared to be related to cell swelling, in both type‐1 and type‐2 astrocytes. Swelling and K+‐induced release were somewhat higher in type‐2 than in type‐1 astrocytes. In contrast, neither kainate nor quisqualate caused any appreciable increase in cell volume. It is concluded that non‐NMDA receptor agonists stimulate the release of several endogenous amino acids (some of which are neuroactive) from type‐2 but not from type‐1 astrocytes. The effect does not seem to be related to cell swelling, which causes a different release profile in both type‐1 and type‐2 astrocytes. The absence of kainate‐ and quisqualate‐evoked release in type‐1 astrocytes suggests that the density of non‐NMDA receptors in this cell type is very low.

Journal

Journal of NeurochemistryWiley

Published: May 1, 1992

References

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