scholarly journals Fast calcium transients in neuronal spines driven by extreme statistics

2018 ◽  
Author(s):  
Kanishka Basnayake ◽  
Eduard Korkotian ◽  
David Holcman
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Ions ◽  
Calcium Release ◽  
Calcium Transients ◽  
Forward Rate ◽  
Rate Theory ◽  
Asymmetric Distribution ◽  
Small Target ◽  
Extreme Statistics ◽  
Spine Apparatus

AbstractExtreme statistics describe the distribution of rare events that can define the timescales of transduction within cellular microdomains. We combine biophysical modeling and analysis of live-cell calcium imaging to explain the fast calcium transient in spines. We show that in the presence of a spine apparatus (SA), which is an extension of the smooth endoplasmic reticulum (ER), calcium transients during synaptic inputs rely on rare and extreme calcium ion trajectories. Using numerical simulations, we predicted the asymmetrical distributions of Ryanodine receptors and SERCA pumps that we confirmed experimentally. When calcium ions are released in the spine head, the fastest ions arriving at the base determine the transient timescale through a calcium-induced calcium release mechanism. In general, the fastest particles arriving at a small target are likely to be a generic mechanism that determines the timescale of molecular transduction in cellular neuroscience.Significance statementIntrigued by fast calcium transients of few milliseconds in dendritic spines, we investigated its underlying biophysical mechanism. We show here that it is generated by the diffusion of the fastest calcium ions when the spine contains a Spine Apparatus, an extension of the endoplasmic reticulum. This timescale is modulated by the initial number of released calcium ions and the asymmetric distribution of its associated calcium release associated Ryanodyne receptors, present only at the base of a spine. This novel mechanism of calcium signaling that we have unraveled here is driven by the fastest particles. To conclude, the rate of arrival of the fastest particles (ions) to a small target receptor defines the timescale of activation instead of the classical forward rate of chemical reactions introduced by von Smoluchowski in 1916. Applying this new rate theory to transduction should refine our understanding of the biophysical mechanisms underlying molecular signaling.

scholarly journals STRUCTURES LINKING THE MYONEMES, ENDOPLASMIC RETICULUM, AND SURFACE MEMBRANES IN THE CONTRACTILE CILIATE VORTICELLA

1973 ◽  
Vol 56 (2) ◽  
pp. 559-579 ◽  
Author(s):  
Richard D. Allen
Keyword(s):  
Endoplasmic Reticulum ◽  
Electron Microscope ◽  
Calcium Ions ◽  
Calcium Release ◽  
Basal Bodies ◽  
Membrane Systems ◽  
Electron Microscope Investigation ◽  
Complex Morphology ◽  
Pass Through ◽  
Er Membrane

An electron microscope investigation of the interface between the myonemes of Vorticella convallaria and their associated endoplasmic reticulum (ER) has revealed structures of a complex morphology linking these two organelles. These structures are named "linkage complexes". Each complex contains a spindle-shaped midpiece which lies in a groove of the ER membrane. Microfilaments splay out from the tips of the midpiece and may come in contact with the inner alveolar sac membrane. Three to six raillike structures lie on each side of the midpiece and parallel it. The ER membrane appears to pass through the sides of the rails. In the lumen of the ER these rails are associated with a meshwork of filaments. A cradle of five rods lies within the groove under the midpiece. The ER membrane also passes through these rods which contact the same meshwork. In the scopular region and in the stalk the microfilaments from the midpiece form a bundle which passes into the lumen of modified basal bodies. These basal bodies are connected to the alveolar sac which, in the stalk, passes as a flattened tube along its length. The parts of the dissociated linkage complex are scattered throughout the spasmoneme of the stalk along membranes of the intraspasmonemal tubules. Thus, both stalk and body contractile bundles have linkage complexes that link their associated membrane systems to the microfibrils and, in turn, connect this membrane-microfibrillar interface to the pellicular membranes. The arrangement of the linkage complex suggests an involvement in the control of the transport of calcium ions between ER and microfibrils, and possibly the transfer of a message from the surface membranes to the sites of calcium release to trigger myonemal contraction.

scholarly journals Off-target effect of the cPLA2α inhibitor pyrrophenone: Inhibition of calcium release from the endoplasmic reticulum

2016 ◽  
Vol 479 (1) ◽  
pp. 61-66 ◽  
Author(s):  
Bogeon Yun ◽  
HeeJung Lee ◽  
Heather Ewing ◽  
Michael H. Gelb ◽  
Christina C. Leslie
Keyword(s):  
Endoplasmic Reticulum ◽  
Calcium Release ◽  
Target Effect

Caffeine attenuates contraction-induced diminutions of the intracellular calcium transient in mouse lumbrical muscle ex vivo

2019 ◽  
Vol 97 (5) ◽  
pp. 429-435 ◽  
Author(s):  
Ian C. Smith ◽  
Rene Vandenboom ◽  
A. Russell Tupling
Keyword(s):  
Skeletal Muscle ◽  
Intracellular Calcium ◽  
Calcium Release ◽  
Ex Vivo ◽  
Calcium Transient ◽  
Calcium Transients ◽  
Inotropic Effects ◽  
Intracellular Calcium Transient ◽  
Lumbrical Muscle ◽  
Lumbrical Muscles

The amount of calcium released from the sarcoplasmic reticulum in skeletal muscle rapidly declines during repeated twitch contractions. In this study, we test the hypothesis that caffeine can mitigate these contraction-induced declines in calcium release. Lumbrical muscles were isolated from male C57BL/6 mice and loaded with the calcium-sensitive indicator, AM-furaptra. Muscles were then stimulated at 8 Hz for 2.0 s in the presence or absence of 0.5 mM caffeine, at either 30 °C or 37 °C. The amplitude and area of the furaptra-based intracellular calcium transients and force produced during twitch contractions were calculated. For each of these measures, the values for twitch 16 relative to twitch 1 were higher in the presence of caffeine than in the absence of caffeine at both temperatures. We conclude that caffeine can attenuate contraction-induced diminutions of calcium release during repeated twitch contractions, thereby contributing to the inotropic effects of caffeine.

cADP-ribose releases Ca2+ from cardiac sarcoplasmic reticulum independently of ryanodine receptor

1997 ◽  
Vol 273 (3) ◽  
pp. H1082-H1089 ◽  
Author(s):  
P. Lahouratate ◽  
J. Guibert ◽  
J. F. Faivre
Keyword(s):  
Endoplasmic Reticulum ◽  
Sarcoplasmic Reticulum ◽  
Ryanodine Receptor ◽  
Sea Urchin ◽  
Calcium Release ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Cardiac Sarcoplasmic Reticulum ◽  
Consistent Effect ◽  
Cyclic Adp Ribose

Cyclic ADP-ribose (cADPR), an endogenous metabolite of beta-NAD+, activates Ca2+ release from endoplasmic reticulum in sea urchin eggs via the ryanodine receptor (RyR) pathway. A similar role has been proposed in cardiac sarcoplasmic reticulum (SR), although this remains controversial. We therefore investigated the ability of cADPR to induce Ca2+ release from canine cardiac SR microsomes using fluo 3 to monitor extravesicular Ca2+ concentration. We found that cADPR induced Ca2+ release in a concentration-dependent manner, whereas neither its precursor, NAD+, nor its metabolite, ADP-ribose, elicited a consistent effect. In addition, an additive effect on calcium release between cADPR and 9-Me-7-Br-eudistomin-D (MBED), an activator of RyR, was found as well as no cross-desensitization between cADPR and MBED. Specific blockers of the RyR did not abolish the cADPR-induced Ca2+ release. These results provide evidence for cADPR-induced Ca2+ release from dog cardiac SR via a novel mechanism which is independent of RyR activation.

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