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This Article Full Text Full Text (PDF) All Versions of this Article: 297/5/R1409    most recent 91038.2008v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Kersh, A. E. Articles by Putnam, R. W. PubMed PubMed Citation Articles by Kersh, A. E. Articles by Putnam, R. W.

Articles

pH regulating transporters in neurons from various chemosensitive brainstem regions in neonatal rats

¹Department of Neuroscience, Cell Biology and Physiology, Wright State University Boonshoft School of Medicine, Dayton, Ohio; and ²Department of Molecular Pharmacology and Physiology, College of Medicine, University of South Florida, Tampa, Florida

Submitted December 22, 2008 ; accepted in final form August 19, 2009

We studied the membrane transporters that mediate intracellular pH (pH_i) recovery from acidification in brainstem neurons from chemosensitive regions of neonatal rats. Individual neurons within brainstem slices from the retrotrapezoid nucleus (RTN), the nucleus tractus solitarii (NTS), and the locus coeruleus (LC) were studied using a pH-sensitive fluorescent dye and fluorescence imaging microscopy. The rate of pH_i recovery from an NH₄Cl-induced acidification was measured, and the effects of inhibitors of various pH-regulating transporters determined. Hypercapnia (15% CO₂) resulted in a maintained acidification in neurons from all three regions. Recovery in RTN neurons was nearly entirely eliminated by amiloride, an inhibitor of Na⁺/H⁺ exchange (NHE). Recovery in RTN neurons was blocked 50% by inhibitors of isoform 1 of NHE (NHE-1) but very little by an inhibitor of NHE-3 or by DIDS (an inhibitor of HCO₃-dependent transport). In NTS neurons, amiloride blocked over 80% of the recovery, which was also blocked 65% by inhibitors of NHE-1 and 26% blocked by an inhibitor of NHE-3. Recovery in LC neurons, in contrast, was unaffected by amiloride or blockers of NHE isoforms but was dependent on Na⁺ and increased by external HCO₃^–. On the basis of these findings, pH_i recovery from acidification appears to be largely mediated by NHE-1 in RTN neurons, by NHE-1 and NHE-3 in NTS neurons, and by a Na- and HCO₃-dependent transporter in LC neurons. Thus, pH_i recovery is mediated by different pH-regulating transporters in neurons from different chemosensitive regions, but recovery is suppressed by hypercapnia in all of the neurons.

hypercapnia; locus coeruleus; Na⁺/H⁺ exchange; HCO₃ transport; NTS; retrotrapezoid nucleus