Document Detail


Regulation of Ca2+ homeostasis by glucose metabolism in rat brain.
MedLine Citation:
PMID:  9406177     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In a previous communication we reported that glucose deprivation from KHRB medium resulted in a marked stimulation of Ca2+ uptake by brain tissue, suggesting a relationship between glucose and Ca2+ homeostasis in brain tissue. Experiments were carried out to investigate the significance of glucose in Ca2+ transport in brain cells. The replacement of glucose with either D-methylglucoside or 2-deoxyglucose, non-metabolizable analogues of glucose, resulted in stimulation of Ca2+ uptake just as by glucose deprivation. These data show that glucose metabolism rather than glucose transfer was necessary to stimulate Ca2+ uptake in brain tissue. Inhibition of glucose metabolism with either NaF, NaCN, or iodoacetate resulted in stimulation of Ca2+ uptake similar to that produced by glucose deprivation. These results lend further support for the concept that glucose metabolism is essential for Ca2+ homeostasis in brain. Anoxia promotes glucose metabolism through glycolytic pathway to keep up with the demand for ATP by cellular processes (the Pasteur effect). Incubation of brain slices under nitrogen gas did not alter Ca2+ uptake by brain tissue, as did glucose deprivation and the inhibitors of glucose metabolism. We conclude that glucose metabolism resulting in the synthesis of ATP is essential for Ca2+ homeostasis in brain. Verapamil and nifedipine which block voltage-gated Ca2+ channels, did not alter Ca2+ uptake stimulated by glucose deprivation, indicating that glucose deprivation-enhanced Ca2+ uptake was not mediated by Ca2+ channels. Tetrodotoxin which specifically blocks Na2+ channels, abolished Ca2+ uptake enhanced by glucose deprivation, but had no effect on Ca2+ uptake in presence of glucose (controls). These results suggest that stimulation of Ca2+ uptake by glucose deprivation may be related to Na2+ transfer via NaCa exchange in brain.
Authors:
M Nijjar; R L Belgrave
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Molecular and cellular biochemistry     Volume:  176     ISSN:  0300-8177     ISO Abbreviation:  Mol. Cell. Biochem.     Publication Date:  1997 Nov 
Date Detail:
Created Date:  1998-01-23     Completed Date:  1998-01-23     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0364456     Medline TA:  Mol Cell Biochem     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  317-26     Citation Subset:  IM    
Affiliation:
Department of Anatomy and Physiology, Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Brain / drug effects,  metabolism*
Calcium / metabolism*
Cytosol / drug effects,  metabolism
Glucose / metabolism*
Homeostasis*
Male
Membranes / drug effects,  metabolism
Rats
Rats, Sprague-Dawley
Sodium Cyanide / pharmacology
Sodium Fluoride / pharmacology
Chemical
Reg. No./Substance:
143-33-9/Sodium Cyanide; 50-99-7/Glucose; 7440-70-2/Calcium; 7681-49-4/Sodium Fluoride

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


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