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

We show that microinjecting cyclic GMP (cGMP) into unfertilized sea urchin eggs activates them by stimulating a rise in the intracellular free calcium ion concentration ([Ca2+]i). The increase in [Ca2+]i is similar in both magnitude and duration to the transient that activates the egg at fertilization. It is due to mobilization of calcium from intracellular stores but is not prevented by the inositol trisphosphate (InsP3) antagonist heparin. Furthermore, cGMP does not stimulate the eggs Na+/H+ antiport when the [Ca2+]i transient is blocked by the calcium chelator bis-(O-aminophenoxy)-N,N,N',N'-tetraacetic acid (BAPTA), suggesting that cGMP does not activate eggs by interacting with the their phosphoinositide signaling pathway. However, the [Ca2+]i increase and activation are prevented in eggs in which the InsP3-sensitive calcium stores have been emptied by the prior microinjection of the InsP3 analogue inositol 1,4,5-trisphosphorothioate. These data indicate that cGMP activates eggs by stimulating the release of calcium from an InsP3-sensitive calcium store via a novel, though unidentified, route independent of the InsP3 receptor.

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Electrotaxis of tumor-initiating cells of H1975 lung adenocarcinoma cells is associated with both activation of stretch-activated cation channels (SACCs) and internal calcium release

Bioelectrochemistry ◽

10.1016/j.bioelechem.2018.03.013 ◽

2018 ◽

Vol 124 ◽

pp. 80-92 ◽

Cited By ~ 4

Author(s):

Yaping Li ◽

Wai-Kin Yu ◽

Likun Chen ◽

Yuen-san Chan ◽

Dandan Liu ◽

...

Keyword(s):

Lung Adenocarcinoma ◽

Calcium Release ◽

Cation Channels ◽

Tumor Initiating Cells ◽

Adenocarcinoma Cells ◽

Lung Adenocarcinoma Cells ◽

Internal Calcium

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Injection of inositol trisphosphorothioate into Limulus ventral photoreceptors causes oscillations of free cytosolic calcium.

The Journal of General Physiology ◽

10.1085/jgp.97.6.1165 ◽

1991 ◽

Vol 97 (6) ◽

pp. 1165-1186 ◽

Cited By ~ 13

Author(s):

R Payne ◽

B V Potter

Keyword(s):

Membrane Potential ◽

Calcium Release ◽

Feedback Inhibition ◽

Initial Response ◽

Periodic Variation ◽

Cytosolic Calcium ◽

Ion Concentration ◽

Free Calcium ◽

Calcium Stores ◽

Calcium Ion Concentration

Limulus ventral photoreceptors contain calcium stores sensitive to release by D-myo-inositol 1,4,5 trisphosphate (InsP3) and a calcium-activated conductance that depolarizes the cell. Mechanisms that terminate the response to InsP3 were investigated using nonmetabolizable DL-myo-inositol 1,4,5 trisphosphorothioate (InsPS3). An injection of 1 mM InsPS3 into a photoreceptor's light-sensitive lobe caused an initial elevation of cytosolic free calcium ion concentration (Cai) and a depolarization lasting only 1-2 s. A period of densensitization followed, during which injections of InsPS3 were ineffective. As sensitivity recovered, oscillations of membrane potential began, continuing for many minutes with a frequency of 0.07-0.3 Hz. The activity of InsPS3 probably results from the D-stereoisomer, since L-InsP3 was much less effective than InsP3. Injections of 1 mM InsP3 caused an initial depolarization and a period of densensitization similar to that caused by 1 mM InsPS3, but no sustained oscillations of membrane potential. The initial response to InsPS3 or InsP3 may therefore be terminated by densensitization, rather than by metabolism. Metabolism of InsP3 may prevent oscillations of membrane potential after sensitivity has recovered. The InsPS3-induced oscillations of membrane potential accompanied oscillations of Cai and were abolished by injection of ethyleneglycol-bis (beta-aminoethyl ether)-N,N'-tetraacetic acid. Removal of extracellular calcium reduced the frequency of oscillation but not its amplitude. Under voltage clamp, oscillations of inward current were observed. These results indicate that periodic bursts of calcium release underly the oscillations of membrane potential. After each burst, the sensitivity of the cell to injected InsP3 was greatly reduced, recovering during the interburst interval. The oscillations may, therefore, result in part from a periodic variation in sensitivity to a constant concentration of InsPS3. Prior injection of calcium inhibited depolarization by InsPS3, suggesting that feedback inhibition of InsPS3-induced calcium release by elevated Cai may mediate desensitization between bursts and after injections of InsPS3.

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Calcium beat: internal calcium stores regulating the rhythm of spontaneous neurotransmitter release

Proceedings of the 9th International Conference on Neural Information Processing, 2002. ICONIP '02. ◽

10.1109/iconip.2002.1202888 ◽

2004 ◽

Author(s):

R.N. Leao ◽

S. Oleskevich ◽

B. Walmsey

Keyword(s):

Neurotransmitter Release ◽

Calcium Stores ◽

Internal Calcium

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Potassium Channels and Internal Calcium Release: Relevance for Memory Storage and Alzheimer’s Disease

Pharmacological Control of Calcium and Potassium Homeostasis - Medical Science Symposia Series ◽

10.1007/978-94-011-0117-2_26 ◽

1995 ◽

pp. 227-235

Author(s):

René Etcheberrigaray ◽

Daniel L. Alkon

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Potassium Channels ◽

Calcium Release ◽

Memory Storage ◽

Internal Calcium

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Heterologous expression of polycystin-1 inhibits endoplasmic reticulum calcium leak in stably transfected MDCK cells

AJP Renal Physiology ◽

10.1152/ajprenal.00348.2007 ◽

2008 ◽

Vol 294 (6) ◽

pp. F1279-F1286 ◽

Cited By ~ 18

Author(s):

Kimberly H. Weber ◽

Eun Kyung Lee ◽

Uma Basavanna ◽

Sabina Lindley ◽

Roy C. Ziegelstein ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Calcium Release ◽

Mdck Cells ◽

Calcium Ionophore ◽

Calcium Flux ◽

Calcium Stores ◽

Endoplasmic Reticulum Calcium ◽

Calcium Indicator ◽

Luminal Calcium ◽

Er Membrane

We previously found that polycystin-1 accelerated the decay of ligand-activated cytoplasmic calcium transients through enhanced reuptake of calcium into the endoplasmic reticulum (ER; Hooper KM, Boletta A, Germino GG, Hu Q, Ziegelstein RC, Sutters M. Am J Physiol Renal Physiol 289: F521–F530, 2005). Calcium flux across the ER membrane is determined by the balance of active uptake and passive leak. In the present study, we show that polycystin-1 inhibited calcium leak across the ER membrane, an effect that would explain the capacity of this protein to accelerate clearance of calcium from the cytoplasm following a calcium release response. Calcium leak was detected by measurement of the accumulation of calcium in the cytoplasm following treatment with thapsigargin. Heterologous polycystin-1, stably expressed in Madin-Darby canine kidney cells, attenuated the thapsigargin-induced calcium peak with no effect on basal calcium stores, mitochondrial calcium uptake, or extrusion of calcium across the plasma membrane. The capacity of polycystin-1 to limit the rate of decay of ER luminal calcium following inhibition of the pump was shown indirectly using the calcium ionophore ionomycin, and directly by loading the ER with a low-affinity calcium indicator. We conclude that disruption of ER luminal calcium homeostasis may contribute to the cyst phenotype in autosomal dominant polycystic kidney disease.

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Inositol 1,4,5-trisphosphate–induced Calcium Release Is Necessary for Generating the Entire Light Response of Limulus Ventral Photoreceptors

The Journal of General Physiology ◽

10.1085/jgp.200208778 ◽

2003 ◽

Vol 121 (5) ◽

pp. 441-449 ◽

Cited By ~ 8

Author(s):

Alan Fein

Keyword(s):

Calcium Release ◽

Cyclopiazonic Acid ◽

Light Response ◽

Calcium Stores ◽

Ip3 Receptor ◽

Treatment Results ◽

Light Responses ◽

Calcium Buffer ◽

Pressure Injection ◽

Inositol 1,4,5 Trisphosphate

The experiments reported here were designed to answer the question of whether inositol 1,4,5-trisphosphate (IP3)-induced calcium release is necessary for generating the entire light response of Limulus ventral photoreceptors. For this purpose the membrane-permeable IP3 receptor antagonist 2-aminoethoxydiphenyl borate (2APB) (Maruyama, T., T. Kanaji, S. Nakade, T. Kanno, and K. Mikoshiba. 1997. J. Biochem. (Tokyo). 122:498–505) was used. Previously, 2APB was found to inhibit the light activated current of Limulus ventral photoreceptors and reversibly inhibit both light and IP3 induced calcium release as well as the current activated by pressure injection of calcium into the light sensitive lobe of the photoreceptor (Wang, Y., M. Deshpande, and R. Payne. 2002. Cell Calcium. 32:209). In this study 2APB was found to inhibit the response to a flash of light at all light intensities and to inhibit the entire light response to a step of light, that is, both the initial transient and the steady-state components of the response to a step of light were inhibited. The light response in cells injected with the calcium buffer 1,2-bis(o-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (BAPTA) was reversibly inhibited by 2APB, indicating that these light responses result from IP3-mediated calcium release giving rise to an increase in Cai. The light response obtained from cells after treatment with 100 μM cyclopiazonic acid (CPA), which acts to empty intracellular calcium stores, was reversibly inhibited by 2APB, indicating that the light response after CPA treatment results from IP3-mediated calcium release and a consequent rise in Cai. Together these findings imply that IP3-induced calcium release is necessary for generating the entire light response of Limulus ventral photoreceptors.

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