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Department of Physiology and Biophysics, Wright State University, Dayton, Ohio 45435
Intracellular pH
(pHi) regulation was studied in
neurons from two chemosensitive [nucleus of the solitary tract
(NTS) and ventrolateral medulla (VLM)] and two nonchemosensitive
[hypoglossal (Hyp) and inferior olive (IO)] areas of the
medulla oblongata. Intrinsic buffering power
(
int) was the same in neurons
from all regions (46 mM/pH U).
Na+/H+
exchange mediated recovery from acidification in all neurons [Ritucci, N. A., J. B. Dean, and R. W. Putnam.
Am. J. Physiol. 273 (Regulatory Integrative Comp. Physiol.
42): R433-R441, 1997]. Cl
/HCO3
exchange mediated recovery from alkalinization in VLM, Hyp, and IO
neurons but was absent from most NTS neurons. The
Na+/H+
exchanger from NTS and VLM neurons was fully inhibited when
extracellular pH (pHo) <7.0,
whereas the exchanger from Hyp and IO neurons was fully inhibited only
when pHo <6.7. The
Cl/HCO3
exchanger from VLM, but not Hyp and IO neurons, was inhibited by
pHo of 7.9. These pH regulatory
properties resulted in steeper
pHi-pHo
relationships in neurons from chemosensitive regions compared with
those from nonchemosensitive regions. These differences are consistent
with a role for changes of pHi as
the proximate signal in central chemoreception and changes of
pHo in modulating
pHi changes.
brain stem; central chemoreceptor; carbon dioxide; fluorescence imaging; respiration; Na+/H+ exchange
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