Response of membrane potential and intracellular pH to hypercapnia in neurons and astrocytes from rat retrotrapezoid nucleus

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Abstract
We compared the response to hypercapnia (10%) in neurons and astrocytes among a distinct area of the retrotrapezoid nucleus (RTN), the mediocaudal RTN (mcRTN), and more intermediate and rostral RTN areas (irRTN) in medullary brain slices from neonatal rats. Hypercapnic acidosis (HA) caused pHo to decline from 7.45 to 7.15 and a maintained intracellular acidification of 0.15 ± 0.02 pH unit in 90% of neurons from both areas ( n = 16). HA excited 44% of mcRTN (7/16) and 38% of irRTN neurons (6/16), increasing firing rate by 167 ± 75% (chemosensitivity index, CI, 256 ± 72%) and 310 ± 93% (CI 292 ± 50%), respectively. These responses did not vary throughout neonatal development. We compared the responses of mcRTN neurons to HA (decreased pHi and pHo) and isohydric hypercapnia (IH; decreased pHi with constant pHo). Neurons excited by HA (firing rate increased 156 ± 46%; n = 5) were similarly excited by IH (firing rate increased 167 ± 38%; n = 5). In astrocytes from both RTN areas, HA caused a maintained intracellular acidification of 0.17 ± 0.02 pH unit ( n = 6) and a depolarization of 5 ± 1 mV ( n = 12). In summary, many neurons (42%) from the RTN are highly responsive (CI 248%) to HA; this may reflect both synaptically driven and intrinsic mechanisms of CO2 sensitivity. Changes of pHi are more significant than changes of pHo in chemosensory signaling in RTN neurons. Finally, the lack of pHi regulation in response to HA suggests that astrocytes do not enhance extracellular acidification during hypercapnia in the RTN.