Ca2+ -dependent inactivation of the mitochondrial Ca2+ uniporter involves proton flux through the ATP synthase.

Stimulation of receptors on the surface of animal cells often evokes cellular responses by raising intracellular Ca(2+) concentration. The rise in cytoplasmic Ca(2+) drives a plethora of processes, including neurotransmitter release, muscle contraction, and cell growth and proliferation. Mitochondria help shape intracellular Ca(2+) signals through their ability to rapidly take up significant amounts of Ca(2+) from the cytosol via the uniporter, a Ca(2+)-selective ion channel in the inner mitochondrial membrane.

Biphasic regulation of mitochondrial Ca2+ uptake by cytosolic Ca2+ concentration.

A rise in cytosolic Ca(2+) concentration is used as a key activation signal in virtually all animal cells, where it triggers a range of responses including neurotransmitter release, muscle contraction, and cell growth and proliferation [1]. During intracellular Ca(2+) signaling, mitochondria rapidly take up significant amounts of Ca(2+) from the cytosol, and this stimulates energy production, alters the spatial and temporal profile of the intracellular Ca(2+) signal, and triggers cell death [2-10]. Mitochondrial Ca(2+) uptake occurs via a ruthenium-red-sensitive uniporter channel found in the inner membrane [11].

Ca2+-calmodulin-dependent facilitation and Ca2+ inactivation of Ca2+ release-activated Ca2+ channels.

In non-excitable cells, one major route for Ca2+ influx is through store-operated Ca2+ channels in the plasma membrane. These channels are activated by the emptying of intracellular Ca2+ stores, and in some cell types store-operated influx occurs through Ca2+ release-activated Ca2+ (CRAC) channels. Here, we report that intracellular Ca2+ modulates CRAC channel activity through both positive and negative feedback steps in RBL-1 cells.

Effect of pain and audiovisual stimulation on the depression of acute hypoxic ventilatory response by low-dose halothane in humans.

Background: The effects of different low-dose volatile agents in blunting the acute hypoxic ventilatory response (AHVR) are variable. Arousal (due to audiovisual stimulation) may prevent isoflurane-induced blunting of AHVR. The purpose of this study was to assess whether this was also the case for halothane.