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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1998-8-5
pubmed:abstractText
Glial cells extrude acid equivalents to maintain pHi. Although four mechanisms have been described so far, pHi-control under physiological conditions is still not sufficiently explained. We therefore investigated whether a H+-translocating ATPase is involved in glial pHi homeostasis using an established glial cell line (C6 glioma). In the absence of bicarbonate, the inhibition of H+-ATPases by NEM led to a pHi decrease. The application of a more specific inhibitor (NBD-Cl) showed that the H+-ATPase involved is of the vacuolar type. Inhibition went along with delayed cell swelling. Together with the fact that glial acidification was far more pronounced in Na+-free media, this may serve as evidence for a secondary activation of Na+/H+-exchange once an activation setpoint is reached, which in turn causes secondary swelling from Na+-uptake. Stimulation of Na+/H+-exchange by PMA can increase the setpoint. pHi-recovery after an acid load was blocked by the inhibition of v-type H+-ATPase, if pHi did not reach 6.6 during the acid load. The inhibition of Na+/H+-exchange by amiloride inhibited recovery only if acidification was below the threshold. Finally, in bicarbonate-free media a v-type H+-ATPase contributes to pH-regulation in glial cells, especially during pH-homeostasis at physiological conditions, while Na+/H+-exchange gains significance during severe acid loads.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0006-3002
pubmed:author
pubmed:copyrightInfo
Copyright 1998 Elsevier Science B.V. All rights reserved.
pubmed:issnType
Print
pubmed:day
24
pubmed:volume
1372
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
28-36
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
A proton-translocating H+-ATPase is involved in C6 glial pH regulation.
pubmed:affiliation
Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University Mainz, 55101 Mainz, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't