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

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Recently we demonstrated that the increased firing rate of chemosensitive neurons in the NTS exposed to acute hypercapnia (15% CO2) was not altered by inhibition of synapses or gap junctions. It is not known, however, if pHi 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 pHi 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 (pHi) was followed in individual neurons at 37°C with a fluorescence microscopy imaging system. Medullary slices containing the NTS were exposed to 15% CO2 to cause a hypercapnic acidosis. The decreases in pHiof 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 (Ca2+, Mg2+) (n = 18) or the gap junction blocker carbenoxolone (100 µM) (n = 13) significantly (P > .05) altered the decrease in pHi 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].


Presented at the 2007 Federation of American Societies for Experimental Biology (FASEB) Science Research Conference.

Presentation Number 761.7.

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