Inhibiting Synapses and Gap Junctions in the Nucleus of Solitary Tract (NTS) Had No Effect on the Magnitude of the Decrease in pH_i Associated With Acute Hypercapnic Acidosis

Recently we demonstrated that the increased firing rate of chemosensitive neurons in the NTS exposed to acute hypercapnia (15% CO ₂ ) was not altered by inhibition of synapses or gap junctions. It is not known, however, if pH _i during hypercapnic acidosis in the NTS is affected by synapses and gap junctions. The purpose of this study was to investigate whether inhibition of synapses and gap junctions in the NTS would alter the decrease in pH _i during hypercapnic acidosis. Medullary brain slices from neonatal Sprague-Dawley rats (P1–P18) were loaded with 2', 7'-bis (carboxyethyl)-5(6)-carboxyfluorescein-acetomethyl ester (BCECF-AM) and intracellular pH (pH _i ) was followed in individual neurons at 37°C with a fluorescence microscopy imaging system. Medullary slices containing the NTS were exposed to 15% CO ₂ to cause a hypercapnic acidosis. The decreases in pH _i of NTS chemosensitive neurons in artificial spinal fluid during acute hypercapnia were on average from 7.49 ± .002 to 7.28 ± .002. Neither synaptic block medium (Ca ²⁺ , Mg ²⁺ ) (n = 18) or the gap junction blocker carbenoxolone (100 µM) (n = 13) significantly (P > .05) altered the decrease in pH _i of chemosensitive neurons in the NTS. These data suggest that neither chemical nor electrical transmission contributes to the level of intracellular acidification of neurons within the NTS. [NIH HL56683, AHA Postdoctoral Fellowship].