Membrane potentials and microenvironment of rat dorsal vagal cells in vitro during energy depletion.

1. Brainstem slices were taken from mature rats. In the dorsal vagal nucleus (DVNX), membrane potentials (Em) of neurons (DVNs) and glia, as well as extracellular oxygen, K+ and pH (Po2, aKo, pHo), were analysed during metabolic disturbances. 2. Postsynaptic potentials of DVNs, elicited by repetitive electrical stimulation of the solitary tract (TS), led to a secondary glial depolarization of up to 25 mV, a fall in Po2 of up to 150 mmHg, a rise in extracellular aKo of up to 9 mM, and a fall in pHo of about 0.2 pH units. 3. Hypoxic superfusates produced tissue anoxia, leading to an aKo increase of less than 2 mM and a pHo fall of 0.24 +/‐ 0.04 pH units (mean +/‐ S.D.). Glucose‐free solution evoked, after a delay of more than 8 min, a slow rise in aKo of 1.9 +/‐ 0.8 mM, accompanied by a mean increase in pHo of 0.24 +/‐ 0.13 pH units. After pre‐incubation in glucose‐free solution, anoxia elevated aKo by up to 15 mM, whereas the anoxia‐induced pHo decrease was completely blocked. 4. In 45 of 118 DVNs, anoxia elicited a persistent hyperpolarization of 15.6 +/‐ 5.0 mV. In the remaining DVNs, anoxic exposure either did not produce a change in Em (37%) or led to a depolarization of less than 10 mV (25%). A stable depolarization of 9 +/‐ 3.8 mV was detected in glial cells during anoxia. Similar responses were revealed in oxygenated glucose‐free solution after a delay of 12‐60 min. 5. The metabolism‐related hyperpolarizations were blocked by 100‐500 microM tolbutamide or 20‐100 microM glibenclamide, leading to recovery of spontaneous (0.5‐6 Hz) spike discharge. In these cells, 400‐500 microM diazoxide evoked hyperpolarizations and blockade of spontaneous activity. 6. In DVNs and glial cells, a progressive depolarization of up to 40 mV in amplitude developed during anoxic exposure after pre‐incubation in glucose‐free solution. 7. The results show that oxygen or glucose depletion does not impair the viability of DVNX cells. The contribution of neuronal ATP‐sensitive K+ (KATP) channels to this tolerance is discussed.