Abstract

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 (betaint) 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-/HCO-3 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-/HCO-3 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.

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