Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 14-Day Trial for You or Your Team.

Learn More →

Activation of polyphosphoinositide metabolism as a signal‐transducing system coupled to excitatory amino acid receptors in astroglial cells

Activation of polyphosphoinositide metabolism as a signal‐transducing system coupled to... Excitatory amino acids (EAA) are known to induce an increase in the breakdown of polyphosphoinositides (PI) in brain slices and in dispersed cultures of neurons. We have now used astroglia cultured from newborn rat cerebra to demonstrate that glutamate provokes, in (3H)inositol‐labeled cells, an accumulation of inositol phosphates in a time‐ and concentration‐dependent manner. The ED50 value for glutamate was 40 μM. Quisqualate, ibotenate, and kainate were also active, with their relative potencies in the order of quisqualate > ibotenate >> kainate. No effect was detected with N‐methyl‐D‐aspartate and quinolinic acid in the absence of Mg2+. The nonselective glutamate receptor antagonist γ‐D‐glutamylglycine fully inhibited glutamate agonist‐induced PI breakdown. A brief pretreatment of the astroglial cells with phorbol esters negated these effects of EAA receptor agonists, suggesting a feedback role for protein kinase C in phospholipase C action. Glutamate also elevated cytosolic free Ca2+ in Fura‐2‐loaded astroglial cells, as assessed by digital fluorescence imaging microscopy. Since a close metabolic partnership is known to exist between neurons and glia, these findings may have important functional consequences for neural cells in vivo. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Glia Wiley

Activation of polyphosphoinositide metabolism as a signal‐transducing system coupled to excitatory amino acid receptors in astroglial cells

Loading next page...
 
/lp/wiley/activation-of-polyphosphoinositide-metabolism-as-a-signal-transducing-C8i3XQ0Uu0

References (66)

Publisher
Wiley
Copyright
Copyright © 1989 Alan R. Liss, Inc.
ISSN
0894-1491
eISSN
1098-1136
DOI
10.1002/glia.440020305
pmid
2568342
Publisher site
See Article on Publisher Site

Abstract

Excitatory amino acids (EAA) are known to induce an increase in the breakdown of polyphosphoinositides (PI) in brain slices and in dispersed cultures of neurons. We have now used astroglia cultured from newborn rat cerebra to demonstrate that glutamate provokes, in (3H)inositol‐labeled cells, an accumulation of inositol phosphates in a time‐ and concentration‐dependent manner. The ED50 value for glutamate was 40 μM. Quisqualate, ibotenate, and kainate were also active, with their relative potencies in the order of quisqualate > ibotenate >> kainate. No effect was detected with N‐methyl‐D‐aspartate and quinolinic acid in the absence of Mg2+. The nonselective glutamate receptor antagonist γ‐D‐glutamylglycine fully inhibited glutamate agonist‐induced PI breakdown. A brief pretreatment of the astroglial cells with phorbol esters negated these effects of EAA receptor agonists, suggesting a feedback role for protein kinase C in phospholipase C action. Glutamate also elevated cytosolic free Ca2+ in Fura‐2‐loaded astroglial cells, as assessed by digital fluorescence imaging microscopy. Since a close metabolic partnership is known to exist between neurons and glia, these findings may have important functional consequences for neural cells in vivo.

Journal

GliaWiley

Published: Jan 1, 1989

There are no references for this article.