Premium
Intracellular Ca 2+ during metabolic activation of K ATP channels in spontaneously active dorsal vagal neurons in medullary slices
Author(s) -
Ballanyi Klaus,
Kulik Anna
Publication year - 1998
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1046/j.1460-9568.1998.00269.x
Subject(s) - dorsum , chemistry , intracellular , neuroscience , medullary cavity , biophysics , anatomy , biology , biochemistry
Intracellular Ca 2+ ([Ca 2+ ] i ) and membrane properties were measured in fura‐2 dialysed dorsal vagal neurons (DVN) spontaneously active at a frequency of 0.5–5 Hz. [Ca 2+ ] i increased by about 30 n m upon rising spike frequency by more than 200% due to 20–50 pA current pulses or 10 μ m serotonin. It fell by 30 n m upon block of spiking by current‐injection, tetrodotoxin or Ni 2+ and also during hyperpolarization due to γ‐aminobutyric acid or opening of adenosine triphosphate (ATP) ‐sensitive K + (K ATP ) channels with diazoxide. K ATP channel‐mediated hyperpolarizations during anoxia or cyanide produced an initial [Ca 2+ ] i decrease which reversed into a secondary Ca 2+ rise by less than 100 n m . Similar moderate rises of [Ca 2+ ] i were observed during block of aerobic metabolism under voltage‐clamp as well as in intact cells, loaded with fura‐2 AM. The magnitude of the metabolism‐related [Ca 2+ ] i transients did not correlate with the amplitude of the K ATP channel‐mediated outward current. [Ca 2+ ] i did not change during diazoxide‐induced or spontaneous activation of K ATP outward current observed in 10% of cells after establishing whole‐cell recording. Increasing [Ca 2+ ] i with cyclopiazonic acid did not activate K ATP channels. [Ca 2+ ] i was not affected upon block of outward current with sulphonylureas, but these K ATP channel blockers were effective to reverse inhibition of spike discharge and, thus, the initial [Ca 2+ ] i fall upon spontaneous or diazoxide‐, anoxia‐ and cyanide‐induced K ATP channel activation. A sulphonylurea‐sensitive hyperpolarization and [Ca 2+ ] i fall was also revealed in the early phase of iodoacetate‐induced metabolic arrest, whereas after about 20 min, occurrence of a progressive depolarization led to an irreversible rise of [Ca 2+ ] i to more than 1 μ m . The results indicate that K ATP channel activity in DVN is not affected by physiological changes of intracellular Ca 2+ and the lack of a major perturbance of Ca 2+ homeostasis contributes to their high tolerance to anoxia.