scholarly journals Calcium-induced calcium release mechanism in guinea pig taenia caeci.

1989 ◽  
Vol 94 (2) ◽  
pp. 363-383 ◽  
Author(s):  
M Iino
Keyword(s):  
Guinea Pig ◽  
Calcium Release ◽  
Adenine Nucleotide ◽  
Physiological Role ◽  
Release Mechanism ◽  
Smooth Muscle Fiber ◽  
Skinned Smooth Muscle ◽  
Intracellular Ca ◽  
Almost All ◽  
Calcium Induced Calcium Release

Fura-2 was used to measure the amount of Ca released from the intracellular Ca store of a saponin-skinned smooth muscle fiber bundle of the guinea pig taenia caeci (width, 150-250 microns) placed in a capillary cuvette at 20-22 degrees C. The amount of Ca actively loaded into the store was assayed when released by the application of 50 mM caffeine and/or 10 microM inositol 1,4,5-trisphosphate (IP3) in the absence of ATP, and was found to have a biphasic dependence on the loading [Ca2+] with a peak near pCa 6. After Ca loading at pCa 6, IP3 released almost all the releasable Ca, whereas caffeine discharged Ca from only approximately 40% of the store. The maximum amount of Ca in the store was some 220 mumol/liter cell water. Ca in the caffeine-releasable store was released approximately exponentially to zero with time when Ca2+ was applied in the absence of ATP, and the rate constant of the Ca-induced Ca release (CICR) increased steeply with the concentration of Ca2+ applied. Increase in [Mg2+] (0.5-5.0 mM) or decrease in pH (7.3-6.7) shifted the relation between pCa and the rate of CICR roughly in parallel toward the lower pCa. An adenine nucleotide increased the rate of the CICR, but it did not change the range of effective [Ca2+]. 5 mM caffeine greatly enhanced the CICR mechanism, making it approximately 30 times more sensitive to [Ca2+]. However the drug had no Ca-releasing action in the absence of Ca2+. Procaine in millimolar concentrations inhibited the rate of the CICR. These properties are similar to those of the skeletal muscle CICR and ryanodine receptor channels. Rates of the CICR under a physiological ionic milieu were estimated from the results, and a [Ca2+] greater than 1 microM was expected to be necessary for the activation of the Ca release. This Ca sensitivity seems too low for the CICR mechanism to play a primary physiological role in Ca mobilization, unless assisted by other mechanisms.

scholarly journals Intracellular Ca release in skinned smooth muscle.

1982 ◽  
Vol 80 (2) ◽  
pp. 191-202 ◽  
Author(s):  
K Saida
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Release Mechanism ◽  
Bathing Solution ◽  
Storage Site ◽  
Physiological Range ◽  
Skinned Muscle ◽  
Skinned Smooth Muscle ◽  
Intracellular Ca

The release of internal Ca from saponin-treated skinned smooth muscle of guinea pig taenia caecum was studied. The amount of Ca released was estimated by the area under the contraction curve during treatment with 25 mM caffeine in the presence of 0.1 mM EGTA. The magnitude of the caffeine response in skinned muscle, after loading with 10(-6) M Ca for 3 min, was similar to that in the depolarized muscle in the presence of EGTA before treatment with saponin. This suggests that Ca in the skinned muscle was in a physiological range after loading. The release of Ca from the storage site could be facilitated by Ca itself when the skinned muscle was exposed to Ca above 3 x 10(-6) M. An increase in environmental MG concentration suppressed the Ca-induced Ca release mechanism. Sudden replacement of propionate with Cl in the bathing solution made it possible to release Ca from the storage site. This "depolarization"-induced Ca release occurred only immediately after the application of Cl; thereafter, the Ca release mechanism seemed to be inactivated by the prolonged presence of Cl. These results suggest that two mechanisms of Ca release operate in smooth muscle: (a) release induced by Ca itself, and (b) release by "depolarization".

A calcium-induced calcium release mechanism supports luteinizing hormone-induced testosterone secretion in mouse Leydig cells

2010 ◽  
Vol 299 (2) ◽  
pp. C316-C323 ◽  
Author(s):  
Roberta Ribeiro Costa ◽  
Wamberto Antonio Varanda ◽  
Celso Rodrigues Franci
Keyword(s):  
Plasma Membrane ◽  
Luteinizing Hormone ◽  
Leydig Cells ◽  
Calcium Release ◽  
Ryanodine Receptors ◽  
Release Mechanism ◽  
Testosterone Secretion ◽  
Intracellular Ca ◽  
Calcium Induced Calcium Release ◽  
First Time

Leydig cells are responsible for the synthesis and secretion of testosterone, processes controlled by luteinizing hormone (LH). Binding of LH to a G protein-coupled receptor in the plasma membrane results in an increase in cAMP and in intracellular Ca2+ concentration ([Ca2+]i). Here we show, using immunofluorescence, that Leydig cells express ryanodine receptors (RyRs) and inositol 1,4,5-trisphosphate receptors (IP3Rs). Measurements of intracellular calcium changes using the fluorescent calcium-sensitive dye fluo-3 and confocal microscopy show that both types of receptors are involved in a calcium-induced calcium release (CICR) mechanism, which amplifies the initial Ca2+ influx through plasma membrane T-type calcium channels (CaV3). The RyRs and IP3Rs are functional, as judged from both their activation by caffeine and IP3 and block by ryanodine and 2-aminoethoxydiphenyl borate (2-APB), respectively. RyRs are the principal players involved in the release of Ca2+ from the endoplasmic reticulum, as evidenced by the fact that global Ca2+ changes evoked by LH are readily blocked by 100 μM ryanodine but not by 2-APB or xestospongin C. Finally, steroid production by Leydig cells is inhibited by ryanodine but not by 2-APB. These results not only broaden our understanding of the role played by calcium in Leydig cells but also show, for the first time, that RyRs have an important role in determining testosterone secretion by the testis.

Ryanodine-Sensitive Stores Regulate the Excitability of AH Neurons in the Myenteric Plexus of Guinea-Pig Ileum

2000 ◽  
Vol 84 (6) ◽  
pp. 2777-2785 ◽  
Author(s):  
K. Hillsley ◽  
J. L. Kenyon ◽  
T. K. Smith
Keyword(s):  
Sensory Processing ◽  
Calcium Release ◽  
Excitatory Postsynaptic Potential ◽  
Similar Time ◽  
Intracellular Ca ◽  
Time Courses ◽  
High Concentrations ◽  
Calcium Induced Calcium Release ◽  
Activity Dependent

Myenteric afterhyperpolarizing (AH) neurons are primary afferent neurons within the gastrointestinal tract. Stimulation of the intestinal mucosa evokes action potentials (AP) that are followed by a slow afterhyperpolarization (AHPslow) in the soma. The role of intracellular Ca2+ ([Ca2+]i) and ryanodine-sensitive Ca2+ stores in modulating the electrical activity of myenteric AH neurons was investigated by recording membrane potential and bis-fura-2 fluorescence from 34 AH neurons. Mean resting [Ca2+]i was ∼200 nM. Depolarizing current pulses that elicited APs evoked AHPslow and an increase in [Ca2+]i, with similar time courses. The amplitudes and durations of AHPslow and the Ca2+ transient were proportional to the number of evoked APs, with each AP increasing [Ca2+]i by ∼50 nM. Ryanodine (10 μM) significantly reduced both the amplitude and duration (by 60%) of the evoked Ca2+ transient and AHPslow over the range of APs tested (1–15). Calcium-induced calcium release (CICR) was graded and proportional to the number of APs, with each AP triggering a rise in [Ca2+]i of ∼30 nM Ca2+ via CICR. This indicates that CICR amplifies Ca2+ influx. Similar changes in [Ca2+]i and AHPslow were evoked by two APs in control and six APs in ryanodine. Thus, the magnitude of the change in bulk [Ca2+]i and not the source of the Ca2+ is the determinant of the magnitude of AHPslow. Furthermore, lowering of free [Ca2+]i, either by reducing extracellular Ca2+ or injecting high concentrations of Ca2+buffer, induced depolarization, increased excitability, and abolition of AHPslow. In addition, activation of synaptic input to AH neurons elicited a slow excitatory postsynaptic potential (sEPSP) that was completely blocked in ryanodine. These results demonstrate the importance of [Ca2+]i and CICR in sensory processing in AH neurons. Activity-dependent CICR may be a mechanism to grade the output of AH neurons according to the intensity of sensory input.

scholarly journals Somatic ATP release from guinea pig sympathetic neurons does not require calcium-induced calcium release from internal stores

2010 ◽  
Vol 299 (4) ◽  
pp. C836-C843 ◽  
Author(s):  
Laura A. Merriam ◽  
Sarah A. Locknar ◽  
Beatrice M. Girard ◽  
Rodney L. Parsons
Keyword(s):  
Guinea Pig ◽  
Calcium Release ◽  
Sympathetic Neurons ◽  
Atp Release ◽  
P2x Receptor ◽  
Slow Inward Current ◽  
Membrane Excitability ◽  
Sodium Influx ◽  
Intracellular Ca ◽  
Inward Currents

Prior studies indicated that a Ca2+-dependent release of ATP can be initiated from the soma of sympathetic neurons dissociated from guinea pig stellate ganglia. Previous studies also indicated that Ca2+-induced Ca2+ release (CICR) can modulate membrane excitability in these same neurons. As Ca2+ release from internal stores is thought to support somatodendritic transmitter release in other neurons, the present study investigated whether CICR is essential for somatic ATP release from dissociated sympathetic neurons. Caffeine increased intracellular Ca2+ and activated two inward currents: a slow inward current (SIC) in 85% of cells, and multiple faster inward currents [asynchronous transient inward currents (ASTICs)] in 40% of cells voltage-clamped to negative potentials. Caffeine evoked both currents when cells were bathed in a Ca2+-deficient solution, indicating that both were initiated by Ca2+ release from ryanodine-sensitive stores in the endoplasmic reticulum. Sodium influx contributed to generation of both SICs and ASTICs, but only ASTICs were inhibited by the presence of the P2X receptor blocker PPADs. Thus ASTICs, but not SICs, resulted from an ATP activation of P2X receptors. Ionomycin induced ASTICs in a Ca2+-containing solution, but not when it was applied in a Ca2+-deficient solution, demonstrating the key requirement for external Ca2+ in initiating ASTICs by ionomycin. Pretreatment with drugs to deplete the internal stores of Ca2+ did not block the ability of ionomycin or long depolarizing voltage steps to initiate ASTICs. Although a caffeine-induced release of Ca2+ from internal stores can elicit both SICs and ASTICs in dissociated sympathetic neurons, CICR is not required for the somatic release of ATP.

Metabolic syndrome inhibits store-operated Ca2+ entry and calcium-induced calcium-release mechanism in coronary artery smooth muscle

2020 ◽  
Vol 182 ◽  
pp. 114222
Author(s):  
Belén Climent ◽  
Elvira Santiago ◽  
Ana Sánchez ◽  
Mercedes Muñoz-Picos ◽  
Francisco Pérez–Vizcaíno ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Smooth Muscle ◽  
Coronary Artery ◽  
Calcium Release ◽  
Release Mechanism ◽  
Calcium Induced Calcium Release
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