We examined intracellular pH (pH(i)) regulation in the retrotrapezoid nucle
us (RTN), a CO2-sensitive site, and the hypoglossal nucleus, a nonchemosens
itive site, during development (postnatal days 2-18) in rats. Respiratory a
cidosis [10% CO2, extracellular pH (pH(o)) 7.18] caused acidification witho
ut pH(i) recovery in the RTN at all ages. In the hypoglossal nucleus, pH(i)
recovered in young animals, but as animal age increased, the slope of pH(i
) recovery diminished. In animals older than postnatal day 11, the pH(i) re
sponses to hypercapnia were identical in the hypoglossal nucleus and the RT
N, but hypoglossal nucleus and RTN neurons could regulate pH(i) during intr
acellular acidification at constant pHo at all ages. Recovery of pH(i) from
acidification in the RTN depended on extracellular Na+ and was inhibited b
y amiloride but was unaffected by DIDS, suggesting a role for Na+/H+ exchan
ge. Hence, pH(i) regulation during acidosis is more effective in the hypogl
ossal nucleus in younger animals, possibly as a requirement of development,
but in older juvenile animals (older than postnatal day 11), pH(i) regulat
ion is relatively poor in chemosensitive (RTN) and nonchemosensitive nuclei
(hypoglossal nucleus).