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3 Department of Biology, St. Lawrence University, Canton, New York 13617; 1 Department of Biology, Allegheny College, Meadville, Pennsylvania 16335; and 2 Departments of Physiology and Medicine, Dartmouth Medical School, Lebanon, New Hampshire 03756
We examined intracellular pH (pHi) regulation in the retrotrapezoid nucleus (RTN), a CO2-sensitive site, and the hypoglossal nucleus, a nonchemosensitive site, during development (postnatal days 2-18) in rats. Respiratory acidosis [10% CO2, extracellular pH (pHo) 7.18] caused acidification without pHi recovery in the RTN at all ages. In the hypoglossal nucleus, pHi recovered in young animals, but as animal age increased, the slope of pHi recovery diminished. In animals older than postnatal day 11, the pHi responses to hypercapnia were identical in the hypoglossal nucleus and the RTN, but hypoglossal nucleus and RTN neurons could regulate pHi during intracellular acidification at constant pHo at all ages. Recovery of pHi from acidification in the RTN depended on extracellular Na+ and was inhibited by amiloride but was unaffected by DIDS, suggesting a role for Na+/H+ exchange. Hence, pHi regulation during acidosis is more effective in the hypoglossal nucleus in younger animals, possibly as a requirement of development, but in older juvenile animals (older than postnatal day 11), pHi regulation is relatively poor in chemosensitive (RTN) and nonchemosensitive nuclei (hypoglossal nucleus).
chemoreceptor; brain slice
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