ACIDOSIS OF RAT DORSAL VAGAL NEURONS IN-SITU DURING SPONTANEOUS AND EVOKED ACTIVITY

1. Rat brainstem slices were taken for simultaneous measurements of in tracellular pH (pH(i)) and membrane currents or potentials in dorsal v agal neurons, dialysed with the pH-sensitive dye BCECF. 2. Intrinsic i ntracellular buffering power was 18 mM per pH unit, as determined by e xposure to trimethylamine in CO2/HCO3--free, Hepes-buffered saline. 3. Tonic spike activity led to a stable fall in pH(i) of 0.05-0.2 pH uni ts from a baseline of 7.19 in current-clamp mode, whereas depolarizati on from -60 to 0 mV for 1 min in voltage-clamp mode produced an intrac ellular acidification of 0.3 pH units. The depolarization-evoked fall in pH(i) was suppressed by 1 mM Ni2+ or 0.2 mM Cd2+, but not by 0.5 mu M TTX or CO2/HCO3--free saline. 4. Kainate (100 mu M) led to an an in ward current of -620 pA and a threefold increase in membrane conductan ce, accompanied by a fall in pH(i) of 0.33 pH units. 5. GABA (1 mM) ev oked a bicuculline-blockable,le conductance increase and fall in pH(i) of up to 0.5 pH units. The GABA-induced pH(i) decrease, but not the c onductance increase, was suppressed in Hepes solution. 6. Neither toni c spike activity, nor resting current or conductance were markedly cha nged upon Hepes-induced intracellular alkalinizations of up to 0.35 pH units, or by an anoxia-induced fall in pH(i) of a maximum of 0.36 pH units. 7. The data show that neuronal activity produces profound chang es in pH(i). It appears that spontaneous spike discharge of dorsal vag al neurons is rather tolerant of major perturbations in pH(i).