Abstract：
:During cerebral ischemia, dysregulated glutamate release activates N-methyl-d-aspartate (NMDA) receptors which promotes excitotoxicity and intracellular acidosis. Ischemia also induces cellular adenosine (ADO) release, which activates ADO receptors and reduces neuronal injury. The aim of this research was to determine if decreasing intracellular pH (pH(i)) enhances ADO release from neurons. Rat forebrain neurons were incubated with NMDA, acetate, propionate, 5-(N)-ethyl-N-isopropyl amiloride (EIPA) or low pH buffer. pH(i) was determined with the fluorescent dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein acetoxymethyl ester (BCECF-AM) and cellular release of ADO was assayed. NMDA decreased pH(i) and increased ADO release from neurons. Acetate and propionate decreased pH(i) and evoked ADO release from neurons. EIPA, an inhibitor of sodium hydrogen exchanger 1 (NHE1), enhanced the acidosis in neurons but did not enhance ADO release. Decreasing extracellular pH (pH(e)) to 6.8 or 6.45 significantly decreased pH(i) in neurons, but was not consistently associated with increased ADO release. The main finding of this study was that acidosis per se did not enhance ADO release from neurons.
journal_name
Brain Resjournal_title
Brain researchauthors
Zamzow CR,Bose R,Parkinson FEdoi
10.1016/j.brainres.2006.01.115subject
Has Abstractpub_date
2006-04-12 00:00:00pages
23-31issue
1eissn
0006-8993issn
1872-6240pii
S0006-8993(06)00194-6journal_volume
1082pub_type
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