Inositol 1,4,5-trisphosphate (IP3) evokes release of Ca2+ from the endoplasmic reticulum (ER), but the resulting Ca2+ signals are shaped by interactions with additional intracellular organelles. Bafilomycin A1, which prevents lysosomal Ca2+ uptake by inhibiting H+ pumping into lysosomes, increased the amplitude of the initial Ca2+ signals evoked by carbachol in human embryonic kidney (HEK) cell...

We present here evidence for the enhancement of an inositol 1,4,5-trisphosphate (IP3) mediated calcium signaling pathway in myotubes from dystrophin-deficient cell lines (SolC1(-)) as compared to a cell line from the same origin but transfected with mini-dystrophin (SolD(+)). With confocal microscopy, we demonstrated that calcium rise, induced by the perifusion of a solution containing a high p...

Ca2+ liberation through inositol 1,4,5-trisphosphate receptor (IP3R) channels generates complex patterns of spatiotemporal cellular Ca2+ signals owing to the biphasic modulation of channel gating by Ca2+ itself. These processes have been extensively studied in Xenopus oocytes, where imaging studies have revealed local Ca2+ signals ("puffs") arising from clusters of IP3R, and patch-clamp studies...

Domeier TL, Zima AV, Maxwell JT, Huke S, Mignery GA, Blatter LA. IP3 receptor-dependent Ca release modulates excitation-contraction coupling in rabbit ventricular myocytes. Am J Physiol Heart Circ Physiol 294: H596–H604, 2008. First published November 30, 2007; doi:10.1152/ajpheart.01155.2007.— Inositol 1,4,5-trisphosphate (IP3) receptor (IP3R)-dependent Ca signaling exerts positive inotropic, ...

Ion channel regulation is key to the control of excitability and behaviour. In the bag cell neurons of Aplysia californica, a voltageand Ca-dependent nonselective cation channel drives a ~30-minute afterdischarge, culminating in the release of egglaying hormone. Using excised, inside-out single channel patch-clamp, this study tested the hypothesis that inositol 1,4,5-trisphosphate (IP3), which ...

gamma-Aminobutyric acid (GABA)A receptor-mediated inhibitory synaptic transmission in visual cortex undergoes long-term potentiation (LTP), which is input-specific and associative. The present study, conducted under a blockade of ionotropic glutamate receptors, demonstrates an induction mechanism of LTP considerably different from those of associative LTP at excitatory synapses. Inhibitory resp...

We have previously visualized three Ca2+ transients, generated by release from intracellular stores, which are associated with cytokinesis during the early cell division cycles of zebrafish embryos: the furrow positioning, propagation and deepening transients. Here we demonstrate the requirement of the latter for furrow deepening, and identify the Ca2+ release channels responsible for generatin...

1. Guanosine 5'-[gamma-thio]triphosphate (GTP[S]), if added before GTP, blocks both Ca2+ efflux promoted by GTP and the effect of GTP on enhancement of inositol 1,4,5-triphosphate (IP3)-promoted Ca2+ release from preloaded microsomal vesicles. If, however, GTP[S] is added after GTP, it does not reverse the Ca2+ efflux promoted by GTP, nor does it inhibit IP3-promoted Ca2+ release. 2. The effect...

Cyclic ADP-ribose (cADPR) is a potentially important intracellular Ca2+ releasing messenger [1-5]. In pancreatic acinar cells where intracellular infusion of both inositol trisphosphate (IP3) and cADPR evoke repetitive Ca2+ spiking [6], the cADPR antagonist 8-NH2-cADPR [7], which blocks cADPR-evoked but not IP3-evoked Ca2+ spiking, can abolish Ca2+ spiking induced by physiological levels of the...

Resting platelets maintain a stable level of low cytoplasmic calcium ([Ca(2+)]cyt) and high dense tubular system calcium ([Ca(2+)]dts). During thrombosis, activators cause a transient rise in inositol trisphosphate (IP3) to trigger calcium mobilization from stores and elevation of [Ca(2+)]cyt. Another major source of [Ca(2+)]cyt elevation is store-operated calcium entry (SOCE) through plasmalem...