Inositol Trisphosphate and Calcium Signaling

Berridge, M. J.; Taylor, Colin W.

doi:10.1101/sqb.1988.053.01.107

Cited by 187 publications

(248 citation statements)

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“…The underlying molecular machinery appears to engage Ca 2+ -dependent Ca 2+ release controlled by inositol 1,4,5-trisphosphate (IP 3 ) and possibly ryanodine receptor-channels displaying a highly non-linear (sometimes bell-shaped) dependence between channel activity and Ca 2+ concentration 50 . Recently, local Ca 2+ transients (but not global waves) have been documented in astroglia lacking IP 3 receptors 51,52 .…”

Section: Resultsmentioning

confidence: 99%

Disentangling astroglial physiology with a realistic cell model in silico

et al. 2018

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Electrically non-excitable astroglia take up neurotransmitters, buffer extracellular K+ and generate Ca2+ signals that release molecular regulators of neural circuitry. The underlying machinery remains enigmatic, mainly because the sponge-like astrocyte morphology has been difficult to access experimentally or explore theoretically. Here, we systematically incorporate multi-scale, tri-dimensional astroglial architecture into a realistic multi-compartmental cell model, which we constrain by empirical tests and integrate into the NEURON computational biophysical environment. This approach is implemented as a flexible astrocyte-model builder ASTRO. As a proof-of-concept, we explore an in silico astrocyte to evaluate basic cell physiology features inaccessible experimentally. Our simulations suggest that currents generated by glutamate transporters or K+ channels have negligible distant effects on membrane voltage and that individual astrocytes can successfully handle extracellular K+ hotspots. We show how intracellular Ca2+ buffers affect Ca2+ waves and why the classical Ca2+ sparks-and-puffs mechanism is theoretically compatible with common readouts of astroglial Ca2+ imaging.

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Section: Resultsmentioning

confidence: 99%

Disentangling astroglial physiology with a realistic cell model in silico

et al. 2018

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“…Gap junctions generally permit passive diffusion of small solutes, such as calcium and IP 3 . Interestingly, the diffusion of calcium within a cell is limited to small domains by the buffering effects of calcium-binding proteins [82], [83], while the diffusion rate of IP 3 is much greater, allowing it to act as a global messenger [84]. Given these diffusion rates it seems likely that IP 3 is primarily responsible for synchronization of calcium signaling in the spermatheca.…”

Section: Discussionmentioning

confidence: 99%

Filamin and Phospholipase C-ε Are Required for Calcium Signaling in the Caenorhabditis elegans Spermatheca

2013

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The Caenorhabditis elegans spermatheca is a myoepithelial tube that stores sperm and undergoes cycles of stretching and constriction as oocytes enter, are fertilized, and exit into the uterus. FLN-1/filamin, a stretch-sensitive structural and signaling scaffold, and PLC-1/phospholipase C-ε, an enzyme that generates the second messenger IP3, are required for embryos to exit normally after fertilization. Using GCaMP, a genetically encoded calcium indicator, we show that entry of an oocyte into the spermatheca initiates a distinctive series of IP3-dependent calcium oscillations that propagate across the tissue via gap junctions and lead to constriction of the spermatheca. PLC-1 is required for the calcium release mechanism triggered by oocyte entry, and FLN-1 is required for timely initiation of the calcium oscillations. INX-12, a gap junction subunit, coordinates propagation of the calcium transients across the spermatheca. Gain-of-function mutations in ITR-1/IP3R, an IP3-dependent calcium channel, and loss-of-function mutations in LFE-2, a negative regulator of IP3 signaling, increase calcium release and suppress the exit defect in filamin-deficient animals. We further demonstrate that a regulatory cassette consisting of MEL-11/myosin phosphatase and NMY-1/non-muscle myosin is required for coordinated contraction of the spermatheca. In summary, this study answers long-standing questions concerning calcium signaling dynamics in the C. elegans spermatheca and suggests FLN-1 is needed in response to oocyte entry to trigger calcium release and coordinated contraction of the spermathecal tissue.

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“…Despite the fact that inhibitory or amplifying effects have been demonstrated previously for maprotiline in other types of cells, 2-5 a possible effect of maprotiline on baseline [Ca 2+ ] i has never been considered. A regulated increase in [Ca 2+ ] i is a key signal in all cell types and can trigger many physiopathological events; [7][8][9] however, an unregulated elevation in [Ca 2+ ] i is often cytotoxic. 10 The Ca 2+ homeostasis mechanisms, in which the Ca 2+ entry pathways play a key role, are critically involved in both normal function and the cancerous transformation of prostate epithelial cells.…”

Section: Introductionmentioning

confidence: 99%

EFFECT OF THE ANTIDEPRESSANT MAPROTILINE ON CA²⁺ MOVEMENT AND PROLIFERATION IN HUMAN PROSTATE CANCER CELLS

Hsu

Chen

Lo³

et al. 2004

Clin Exp Pharma Physio

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1. The effect of maprotiline, an antidepressant, on human prostate cells is unclear. In the present study, the effect of maprotiline on [Ca2+]i and growth in PC3 human prostate cancer cells was measured using the fluorescent dyes fura-2 and tetrazolium, respectively. 2. Maprotiline caused a rapid, concentration-dependent increase in [Ca2+]i (EC50 = 200 micromol/L). The maprotiline-induced [Ca2+]i increase was reduced by removal of extracellular Ca2+ or pretreatment with nicardipine. 3. The maprotiline-induced Mn2+ influx-associated fura-2 fluorescence quench directly suggests that maprotiline caused Ca2+ influx. 4. In Ca(2+)-free medium, thapsigargin, an inhibitor of the endoplasmic reticulum Ca(2+)-ATPase, caused a monophasic [Ca2+]i increase, after which the effects of maprotiline of increasing [Ca2+]i were abolished. In addition, pretreatment with maprotiline reduced a major portion of the thapsigargin-induced increase in [Ca2+]i. 5. U73122, an inhibitor of phospholipase C, abolished the ATP (but not maprotiline)-induced increase in [Ca2+]i. 6. Overnight incubation with 1-10 micromol/L maprotiline did not alter cell proliferation, although incubation with 30-50 micromol/L maprotiline decreased cell proliferation. 7, These findings suggest that maprotiline rapidly increases [Ca2+]i in human prostate cancer cells by stimulating both extracellular Ca2+ influx and intracellular Ca2+ release and that it may modulate cell proliferation in a concentration-dependent manner.

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Inositol Trisphosphate and Calcium Signaling

Cited by 187 publications

References 0 publications

Disentangling astroglial physiology with a realistic cell model in silico

Disentangling astroglial physiology with a realistic cell model in silico

Filamin and Phospholipase C-ε Are Required for Calcium Signaling in the Caenorhabditis elegans Spermatheca

EFFECT OF THE ANTIDEPRESSANT MAPROTILINE ON CA²⁺ MOVEMENT AND PROLIFERATION IN HUMAN PROSTATE CANCER CELLS

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Inositol Trisphosphate and Calcium Signaling

Cited by 187 publications

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Disentangling astroglial physiology with a realistic cell model in silico

Disentangling astroglial physiology with a realistic cell model in silico

Filamin and Phospholipase C-ε Are Required for Calcium Signaling in the Caenorhabditis elegans Spermatheca

EFFECT OF THE ANTIDEPRESSANT MAPROTILINE ON CA2+ MOVEMENT AND PROLIFERATION IN HUMAN PROSTATE CANCER CELLS

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EFFECT OF THE ANTIDEPRESSANT MAPROTILINE ON CA²⁺ MOVEMENT AND PROLIFERATION IN HUMAN PROSTATE CANCER CELLS