Document Detail


Glutamate blocks astroglial stellation: effect of glutamate uptake and volume changes.
MedLine Citation:
PMID:  7915251     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neurotransmitters which increase intracellular cAMP levels can cause cultured astroglia to change from a flat, polygonal shape to a stellate morphology. Little is known about how glial stellation can be regulated by other transmitters. In the present study, we demonstrated that L-glutamate blocked isoproterenol (ISO) or dibutyryl-cAMP induced stellation in astroglia. The glutamate inhibition was concentration dependent, with its maximal effect on > 90% of cells at 500 microM. Glutamate also reversed glial stellation within a short period (< 30 min). Glutamate uptake analogues, D-glutamate and D-aspartate, rather than receptor agonists, kainate and quisqualate, mimicked the glutamate effect. Likewise, the glutamate uptake blocker, D-thero-beta-hydroxyaspartate, blocked the glutamate effect. The glutamate inhibition was not a result of inhibition of cAMP formation, since norepinephrine, which inhibited 80% of ISO-stimulated cAMP, also caused glial stellation. Increases in extracellular K+ to 50 mM also reduced glial stellation, whereas 25 mM K+ had little effect. Since 25 mM K+ caused much greater depolarization than 400 microM glutamate, it was unlikely that the effects of both glutamate and high [K+] on glial stellation were due to membrane depolarization. Hypotonic treatment (120 mOsm) enhanced, whereas hypertonic treatment (520 mOsm) prevented, the glutamate reversal of glial stellation. Thus, glial swelling appeared to be a primary mechanism for the inhibitory effect of glutamate and high [K+] on glial stellation. This mechanism could also explain the observation that glutamate inhibited stellation induced by PMA, a PKC activator. Our data suggest that glutamate released from neurons during neuronal activity or pathology can be taken up by astrocytes and alter their morphology. Changes in glial morphology may in turn affect the volume and composition of the extracellular space and, as a result, neuronal activity.
Authors:
Y Shao; M O Enkvist; K D McCarthy
Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Glia     Volume:  11     ISSN:  0894-1491     ISO Abbreviation:  Glia     Publication Date:  1994 May 
Date Detail:
Created Date:  1994-09-29     Completed Date:  1994-09-29     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8806785     Medline TA:  Glia     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1-10     Citation Subset:  IM    
Affiliation:
Department of Pharmacology, University of North Carolina at Chapel Hill 27599-7365.
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Astrocytes / drug effects*,  ultrastructure*
Bucladesine / antagonists & inhibitors,  pharmacology
Cells, Cultured
Cerebral Cortex / cytology,  drug effects,  ultrastructure
Culture Media
Cytoskeleton / metabolism
Glutamates / antagonists & inhibitors,  metabolism,  pharmacology*
Glutamic Acid
Immunohistochemistry
Isoproterenol / antagonists & inhibitors,  pharmacology
Membrane Potentials / drug effects
Neurotransmitter Agents / antagonists & inhibitors,  metabolism,  pharmacology*
Norepinephrine / physiology
Osmolar Concentration
Rats
Grant Support
ID/Acronym/Agency:
NS 20212/NS/NINDS NIH HHS
Chemical
Reg. No./Substance:
0/Culture Media; 0/Glutamates; 0/Neurotransmitter Agents; 362-74-3/Bucladesine; 51-41-2/Norepinephrine; 56-86-0/Glutamic Acid; 7683-59-2/Isoproterenol

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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