Role of calcium oscillations in sperm physiology

Biosystems ◽  
2021 ◽  
Vol 209 ◽  
pp. 104524 ◽  
Author(s):  
Esperanza Mata-Martínez ◽  
Claudia Sánchez-Cárdenas ◽  
Julio C. Chávez ◽  
Adán Guerrero ◽  
Claudia L. Treviño ◽  
...  
Keyword(s):  
2005 ◽  
Vol 184 (2) ◽  
pp. 371-379 ◽  
Author(s):  
M Estrada ◽  
A Espinosa ◽  
C J Gibson ◽  
P Uhlen ◽  
E Jaimovich

Ca2+ oscillations are one of the most important signals within the cell. The mechanism for generation of Ca2+ oscillations is still not yet fully elucidated. We studied the role of capacitative Ca2+ entry (CCE) on intracellular Ca2+ oscillations induced by testosterone at the single-cell level in primary myotubes. Testosterone (100 nM) rapidly induced an intracellular Ca2+ rise, accompanied by Ca2+ oscillations in a majority of myotubes. Spectral analysis of the Ca2+ oscillations revealed a periodicity of 20.3 ± 1.8 s (frequency of 49.3 ± 4.4 mHz). In Ca2+-free medium, an increase in intracellular Ca2+ was still observed, but no oscillations. Neither nifedipine nor ryanodine affected the testosterone-induced Ca2+ response. This intracellular Ca2+ release was previously shown in myotubes to be dependent on inositol-1,4,5-trisphosphate (IP3). Intracellular Ca2+ store depletion in Ca2+-free medium, using a sarcoplasmic/endoplasmic reticulum calcium ATPase-pump inhibitor, followed by re-addition of extracellular Ca2+, gave a fast rise in intracellular Ca2+, indicating that CCE was present in these myotubes. Application of either testosterone or albumin-bound testosterone induced Ca2+ release and led to CCE after re-addition of Ca2+ to Ca2+-free extracellular medium. The CCE blockers 2-aminoethyl diphenylborate and La3+, as well as perturbation of the cytoskeleton by cytochalasin D, inhibited testosterone-induced Ca2+ oscillations and CCE. The steady increase in Ca2+ induced by testosterone was not, however, affected by either La3+ or cytochalasin D. These results demonstrate testosterone-induced Ca2+ oscillations in myotubes, mediated by the interplay of IP3-sensitive Ca2+ stores and Ca2+ influx through CCE.


2005 ◽  
Vol 89 (6) ◽  
pp. 3741-3756 ◽  
Author(s):  
J.M.A.M. Kusters ◽  
M.M. Dernison ◽  
W.P.M. van Meerwijk ◽  
D.L. Ypey ◽  
A.P.R. Theuvenet ◽  
...  

2002 ◽  
Vol 277 (16) ◽  
pp. 13597-13608 ◽  
Author(s):  
Xiaoyan Wu ◽  
György Babnigg ◽  
Tatiana Zagranichnaya ◽  
Mitchel L. Villereal

2003 ◽  
Vol 285 (1) ◽  
pp. E138-E154 ◽  
Author(s):  
Leonid E. Fridlyand ◽  
Natalia Tamarina ◽  
Louis H. Philipson

We have developed a detailed mathematical model of ionic flux in β-cells that includes the most essential channels and pumps in the plasma membrane. This model is coupled to equations describing Ca2+, inositol 1,4,5-trisphosphate (IP3), ATP, and Na+ homeostasis, including the uptake and release of Ca2+ by the endoplasmic reticulum (ER). In our model, metabolically derived ATP activates inward Ca2+ flux by regulation of ATP-sensitive K+ channels and depolarization of the plasma membrane. Results from the simulations support the hypothesis that intracellular Na+ and Ca2+ in the ER can be the main variables driving both fast (2–7 osc/min) and slow intracellular Ca2+ concentration oscillations (0.3–0.9 osc/min) and that the effect of IP3 on Ca2+ leak from the ER contributes to the pattern of slow calcium oscillations. Simulations also show that filling the ER Ca2+ stores leads to faster electrical bursting and Ca2+ oscillations. Specific Ca2+ oscillations in isolated β-cell lines can also be simulated.


2006 ◽  
Vol 100 (1) ◽  
pp. 307-317 ◽  
Author(s):  
Raymond C. Koehler ◽  
Debebe Gebremedhin ◽  
David R. Harder

Astrocytes send processes to synapses and blood vessels, communicate with other astrocytes through gap junctions and by release of ATP, and thus are an integral component of the neurovascular unit. Electrical field stimulations in brain slices demonstrate an increase in intracellular calcium in astrocyte cell bodies transmitted to perivascular end-feet, followed by a decrease in vascular smooth muscle calcium oscillations and arteriolar dilation. The increase in astrocyte calcium after neuronal activation is mediated, in part, by activation of metabotropic glutamate receptors. Calcium signaling in vitro can also be influenced by adenosine acting on A2B receptors and by epoxyeicosatrienoic acids (EETs) shown to be synthesized in astrocytes. Prostaglandins, EETs, arachidonic acid, and potassium ions are candidate mediators of communication between astrocyte end-feet and vascular smooth muscle. In vivo evidence supports a role for cyclooxygenase-2 metabolites, EETs, adenosine, and neuronally derived nitric oxide in the coupling of increased blood flow to increased neuronal activity. Combined inhibition of the EETs, nitric oxide, and adenosine pathways indicates that signaling is not by parallel, independent pathways. Indirect pharmacological results are consistent with astrocytes acting as intermediaries in neurovascular signaling within the neurovascular unit. For specific stimuli, astrocytes are also capable of transmitting signals to pial arterioles on the brain surface for ensuring adequate inflow pressure to parenchymal feeding arterioles. Therefore, evidence from brain slices and indirect evidence in vivo with pharmacological approaches suggest that astrocytes play a pivotal role in regulating the fundamental physiological response coupling dynamic changes in cerebral blood flow to neuronal synaptic activity. Future work using in vivo imaging and genetic manipulation will be required to provide more direct evidence for a role of astrocytes in neurovascular coupling.


2010 ◽  
Vol 20 (11) ◽  
pp. 3709-3715 ◽  
Author(s):  
YUBING GONG ◽  
XIU LIN ◽  
YINGHANG HAO ◽  
XIAOGUANG MA

We have studied the effect of a particular kind of non-Gaussian noise (NGN), mainly of its deviation q from Gaussian noise, on the intercellular calcium (Ca2+) oscillations in an array of bidirectionally coupled cells. It is found that as q is increased, the Ca2+ oscillation becomes the most regular at an intermediate optimal q value, representing the occurrence of coherence resonance (CR). This deviation-induced CR behavior shows that the intercellular Ca2+ oscillations of the coupled cells can be enhanced and even optimized by the appropriate NGN. This result provides a new insight into the constructive role of the NGN on the transmission of Ca2+ signaling in coupled cells.


Biosystems ◽  
2000 ◽  
Vol 57 (2) ◽  
pp. 75-86 ◽  
Author(s):  
Marko Marhl ◽  
Thomas Haberichter ◽  
Milan Brumen ◽  
Reinhart Heinrich

2011 ◽  
Vol 10 (01) ◽  
pp. 31-39 ◽  
Author(s):  
HONGYING LI ◽  
JIANHONG BI

We have studied the role of internal noise for intracellular calcium signaling in coupled biological cell system. It is found that internal noise can induce calcium oscillations and the performance of such oscillations shows two peaks with the variation of the cell size-Ω for any cell chain length-N, indicating the occurrence of system size bi-resonance or internal noise stochastic bi-resonance, which may be very relevant to the canard explosion. We also find that there exists an optimal cell chain length-N for the first peak at which the collective calcium oscillations show the best performance, it is also a phenomenon of "system size resonance". It is interesting to note that one of the optimal cell sizes is present at Ω ~ 103μm3, which is close to a real living cell size in vivo.


2010 ◽  
Vol 7 (3) ◽  
pp. 036009 ◽  
Author(s):  
C Bodenstein ◽  
B Knoke ◽  
M Marhl ◽  
M Perc ◽  
S Schuster

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