Calcium channels activated by depletion of internal calcium stores in A431 cells

The inhibitory effects of somatostatin have been well documented for many physiological processes. The action of somatostatin is through G-protein-coupled receptor-mediated second-messenger signaling, which in turn affects other downstream targets including ion channels. In the retina, somatostatin is released from a specific class of amacrine cells. Here we report that there was a circadian phase-dependent effect of somatostatin-14 (SS14) on the L-type voltage-gated calcium channels (L-VGCCs) in cultured chicken cone photoreceptors, and our study reveals that this process is dependent on intracellular calcium stores. Application of 500 nM SS14 for 2 h caused a decrease in L-VGCC currents only during the subjective night but not the subjective day. We then explored the cellular mechanisms underlying the circadian phase-dependent effect of SS14. The inhibitory effect of SS14 on L-VGCCs was mediated through the pertussis-toxin-sensitive G-protein-dependent somatostatin receptor 2 (sst2). Activation of sst2 by SS14 further activated downstream signaling involving phospholipase C and intracellular calcium stores. Mobilization of intracellular Ca2+ was required for somatostatin induced inhibition of photoreceptor L-VGCCs, suggesting that somatostatin plays an important role in the modulation of photoreceptor physiology.

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Dynamics of calcium release and uptake by the internal calcium stores in rat sensory neurons

Neurophysiology ◽

10.1007/s11062-006-0062-6 ◽

2006 ◽

Vol 38 (4) ◽

pp. 305-307

Author(s):

E. V. Khomula ◽

N. V. Voitenko

Keyword(s):

Sensory Neurons ◽

Calcium Release ◽

Calcium Stores ◽

Internal Calcium

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Oxidative stress increases internal calcium stores and reduces a key mitochondrial enzyme

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease ◽

10.1016/s0925-4439(01)00091-6 ◽

2002 ◽

Vol 1586 (2) ◽

pp. 177-189 ◽

Cited By ~ 34

Author(s):

Gary E. Gibson ◽

Hui Zhang ◽

Hui Xu ◽

Larry C.H. Park ◽

Thomas M. Jeitner

Keyword(s):

Oxidative Stress ◽

Calcium Stores ◽

Mitochondrial Enzyme ◽

Internal Calcium

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Activation of calcium-independent phospholipase A2 by depletion of internal calcium stores

Biochemical Society Transactions ◽

10.1042/bst0260345 ◽

1998 ◽

Vol 26 (3) ◽

pp. 345-349 ◽

Cited By ~ 14

Author(s):

R. W. Gross

Keyword(s):

Phospholipase A2 ◽

Calcium Stores ◽

Calcium Independent Phospholipase A2 ◽

Internal Calcium

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Econazole inhibits thapsigargin-induced platelet calcium influx by mechanisms other than cytochrome P-450 inhibition

Biochemical Journal ◽

10.1042/bj2950525 ◽

1993 ◽

Vol 295 (2) ◽

pp. 525-529 ◽

Cited By ~ 25

Author(s):

J G Vostal ◽

J C Fratantoni

Keyword(s):

Plasma Membrane ◽

Antifungal Agents ◽

Calcium Influx ◽

Calcium Stores ◽

Alternative Mechanism ◽

Resting Cells ◽

Calcium Efflux ◽

Plasma Membrane Permeability ◽

Cytochrome P 450 ◽

Internal Calcium

Cytochrome P-450 has been suggested as a mediator of the signal between depleted platelet calcium stores and an increase in plasma membrane permeability to calcium which follows depletion of the stores. This hypothesis is based on the observations that inhibitors of cytochrome P-450, such as the imidazole antifungal agents, also inhibit influx of a calcium surrogate (manganese) into calcium-depleted platelets. We tested the effects of econazole and of a cytochrome P-450 inhibitor, carbon monoxide (CO), on thapsigargin (TG)-induced platelet 45Ca2+ influx. TG specifically depletes internal calcium stores and activates store-regulated calcium influx. Econazole blocked 45Ca2+ influx when it was added before TG (IC50 11 microM). Econazole at a concentration (20 microM) that inhibited 83% of TG-induced calcium influx was not inhibitory to TG-induced calcium efflux from 45Ca(2+)-loaded platelets, and did not affect calcium fluxes in resting platelets. This econazole concentration was also inhibitory to calcium influx even when it was added after the stores had been calcium-depleted by EGTA and TG for 15 min and the signal to increase calcium influx had already been generated. Inhibition of cytochrome P-450 with CO bubbled through platelet suspensions did not change calcium influx in resting cells and potentiated TG-induced calcium influx (160% of control calcium accumulation at 20 min). This effect appeared to be concentration-dependent, such that a 5 min exposure to CO produced a greater influx potentiation than a 3 min exposure. These observations indicate that (1) cytochrome P-450 does not mediate store-regulated calcium influx, and (2) econazole probably inhibits store-regulated calcium influx by an alternative mechanism, such as interaction with plasma membrane calcium channels.

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Development of functional calcium channels in cultured avian photoreceptors

Visual Neuroscience ◽

10.1017/s0952523800005058 ◽

1992 ◽

Vol 8 (4) ◽

pp. 315-327 ◽

Cited By ~ 31

Author(s):

Evanna Gleason ◽

Peter Mobbs ◽

Richard Nuccitelli ◽

Martin Wilson

Keyword(s):

Calcium Channels ◽

Time Course ◽

Lectin Binding ◽

Cytosolic Calcium ◽

Calcium Currents ◽

Oil Droplet ◽

Whole Cell Patch Clamp ◽

Cone Cells ◽

Internal Calcium ◽

Patch Clamp Method

AbstractVertebrate photoreceptors are unusual neurons in that they are capable of continuous calcium-mediated release of neurotransmitter (Trifonov, 1968; Hagins et al., 1970). In this study, we have examined the development and characteristics of calcium currents in chick cone cells placed in culture on embryonic day 8. Cone cells were identified by their lectin-binding properties, rhodopsin-like immunoreactivity, and the presence of an oil droplet. Using the whole-cell patch-clamp method, we have seen calcium currents in these cells after three days in culture, slightly before the appearance of synapses (Gleason & Wilson, 1989). Because cone calcium currents are blocked by cadmium and nifedipine but are enhanced by Bay K 8644, they most closely resemble L-type current (Nowycky et al., 1985). An unexpected feature of these currents is that their gating ranges varied widely between cells so that some cells showed the foot of their activation range at —70 mV and others as positive as —25 mV. Calcium imaging of fura-2 loaded cells was used to confirm the time course of calcium current development and describe the distribution of cytosolic calcium. As expected, depolarization of young cells failed to increase cytosolic calcium but in older cells an increase of threefold to fourfold was usually observed. Both at rest and during depolarization, most cone cells showed regional differences in internal calcium concentration. In the most mature cones, depolarization strongly elevated cytosolic calcium at the terminal end of the cell while producing a lesser change around the oil droplet and the ellipsoid region, suggesting that calcium channels are localized to the terminal.

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