QUICK SEARCH:   [advanced] Author: Keyword(s):
Home     Help     Feedback     Subscriptions     Archive     Search     Table of Contents

Help viewing high resolution images Return to article

Fig. 3. Relationship between intracellular Ca²⁺ concentration (Ca_i) and anoxic K_ATP channel activation in dorsal vagal neurons from juvenile rats. (A) Chemical anoxia due to 1 mmol l^–1 CN^– produces a persistent hyperpolarisation and block of tonic spiking while Ca_i increases by <50 nmol l^–1. Tolbutamide (200 µmol l^–1) reverses the anoxic hyperpolarisation. The concomitant reappearance of spiking induces a further stable increase of Ca_i that is, nevertheless, not much larger than Ca_i levels during physiological activity of these cells. (B) The persistence of the anoxic Ca_i rise in Ca²⁺-free superfusate suggests that this Ca²⁺ signal is due to release from intracellular stores. (C) The Ca_i rise associated with chemical anoxia is not substantially attenuated following depletion of endoplasmic reticulum Ca²⁺ stores with the Ca²⁺ pump blocker cyclopiazonic acid (CPA; 30 µmol l^–1), while the anoxia response is mimicked and occluded by the mitochondrial blocker FCCP (1 µmol l^–1). (D) Simultaneous recording of Ca_i, mitochondrial potential () and membrane current (I_m) in a voltage-clamped dorsal vagal neuron filled via the patch-electrode with both 100 µmol l^–1 fura-2 and 5 mg ml^–1 rhodamine-123. A rapid increase of Ca_i during an outward current due to depolarisation from –50 to 0 mV (20 s) is followed by a modest increase in rhodamine-123 fluorescence, indicating a depolarisation of . In response to CN^– (1 mmol l^–1), a considerably larger mitochondrial depolarisation whose onset kinetics correlate with that of the K_ATP outward current is observed, while the rise of Ca_i is notably slower. A, reproduced from Ballanyi and Kulik (1998); B–D, data from K. Ballanyi and A. Kulik.

Return to article