Linked Life Data

8779924

Source:http://linkedlifedata.com/resource/pubmed/id/8779924

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2 Pt 1
pubmed:dateCreated
1996-12-20
pubmed:abstractText
A 30-s exposure to N-methyl-D-aspartate (NMDA) produced a dose-dependent and long-lasting (10-20 min) reduction in intracellular pH in cultured cortical neurons, detected by the fluorescent dye 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. This intracellular acidification could be blocked by addition of the NMDA antagonist, D-(-)-2-amino-5-phosphonovalerate, or by removal of extracellular Ca2+. Removal of extracellular HCO3- markedly impaired recovery from NMDA-induced intracellular acidification. Recovery was also impaired when 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid or 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid, inhibitors of HCO3- transport, were added to the cultures immediately after NMDA exposure. In contrast, the Na+/H+ exchange blocker, 5-(N-ethyl-N-isopropyl)amiloride, did not affect pH recovery. Removal of extracellular Cl- partially prevented pH recovery after NMDA stimulation. In addition, extracellular HCO3- increased intracellular Na+ after NMDA exposure, consistent with HCO3- activation of a Na(+)-dependent exchanger. These results demonstrate that stimulation of cortical neuronal NMDA receptors is followed by long-lasting intracellular acidification and that the presence of extracellular HCO3- is important in the subsequent recovery of normal intracellular pH, likely acting at least in part via the Na(+)-dependent Cl-/HCO3- exchanger.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
270
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
C593-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Recovery from NMDA-induced intracellular acidification is delayed and dependent on extracellular bicarbonate.
pubmed:affiliation
Center for the Study of Nervous System Injury, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.