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

AUTOR(ES)

Ballanyi, K

RESUMO

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.

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