THE RELATIONSHIP BETWEEN MEMBRANE POTENTIAL AND Ca2+ FLUXES IN SARCOPLASMIC RETICULUM

1981 ◽  
pp. 207-218
Author(s):  
Anthony N. Martonosi
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
The Relationship

Contribution of a voltage-sensitive calcium release mechanism to contraction in cardiac ventricular myocytes

1998 ◽  
Vol 274 (1) ◽  
pp. H155-H170 ◽  
Author(s):  
Susan E. Howlett ◽  
Jie-Quan Zhu ◽  
Gregory R. Ferrier
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Calcium Release ◽  
Ventricular Myocytes ◽  
Cardiac Contraction ◽  
Release Mechanism ◽  
Steady State Inactivation ◽  
Slope Factor ◽  
The Relationship

The contribution of a voltage-sensitive release mechanism (VSRM) for sarcoplasmic reticulum (SR) Ca2+ to contraction was investigated in voltage-clamped ventricular myocytes at 37°C. Na+ current was blocked with lidocaine. The VSRM exhibited steady-state inactivation (half-inactivation voltage: −47.6 mV; slope factor: 4.37 mV). When the VSRM was inactivated, contraction-voltage relationships were proportional to L-type Ca2+current ( I Ca-L). When the VSRM was available, the relationship was sigmoidal, with contractions independent of voltage positive to −20 mV. VSRM and I Ca-Lcontractions could be separated by activation-inactivation properties. VSRM contractions were extremely sensitive to ryanodine, thapsigargin, and conditioning protocols to reduce SR Ca2+ load. I Ca-Lcontractions were less sensitive. When both VSRM and I Ca-L were available, sigmoidal contraction-voltage relationships became bell-shaped with protocols to reduce SR Ca2+ load. Myocytes demonstrated restitution of contraction that was slower than restitution of I Ca-L. Restitution was a property of the VSRM. Thus activation and recovery of the VSRM are important in coupling cardiac contraction to membrane potential, SR Ca2+ load, and activation interval.

Calcium channels and excitation–contraction coupling in cardiac cells. I. Two components of contraction in guinea-pig papillary muscle

1987 ◽  
Vol 65 (9) ◽  
pp. 1821-1831 ◽  
Author(s):  
E. Honoré ◽  
M. M. Adamantidis ◽  
B. A. Dupuis ◽  
C. E. Challice ◽  
P. Guilbault
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Papillary Muscle ◽  
Cardiac Cells ◽  
Resting Membrane Potential ◽  
Tonic Component ◽  
Contraction Coupling ◽  
Rich Solution ◽  
The Relationship ◽  
Guinea Pig Atria

Biphasic contractions have been obtained in guinea-pig papillary muscle by inducing partial depolarization in K+-rich solution (17 mM) containing 0.3 μM isoproterenol; whereas in guinea-pig atria, the same conditions led to monophasic contractions corresponding to the first component of contraction in papillary muscle. The relationships between the amplitude of the two components of the biphasic contraction and the resting membrane potential were sigmoidal curves. The first component of contraction was inactivated for membrane potentials less positive than those for the second component. In Na+-low solution (25 mM), biphasic contraction became monophasic subsequent to the loss of the second component, but tetraethylammonium unmasked the second component of contraction. The relationship between the amplitude of the first component of contraction and the logarithm of extracellular Ca2+ concentration was complex, whereas for the second component it was linear. When Ca2+ ions were replaced by Sr2+ ions, only the second component of contraction was observed. It is suggested that the first component of contraction may be triggered by a Ca2+ release from sarcoplasmic reticulum, induced by the fast inward Ca2+ current and (or) by the depolarization. The second component of contraction may be due to a direct activation of contractile proteins by Ca2+ entering the cell along with the slow inward Ca2+ current and diffusing through the sarcoplasm. These results do not exclude the existence of a third "tonic" component, which could possibly be mixed with the second component of contraction.

Effect of aminophylline on the contraction threshold of rat diaphragm fibers

1991 ◽  
Vol 71 (4) ◽  
pp. 1409-1414 ◽  
Author(s):  
A. S. Losavio ◽  
B. A. Kotsias
Keyword(s):  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Resting Membrane Potential ◽  
Dependent Manner ◽  
Direct Visualization ◽  
Rat Diaphragm ◽  
Current Clamp ◽  
Cyclic Monophosphate ◽  
Dose Dependent

We studied the effect of aminophylline (0.1–1 mM) on the contraction threshold (CT) of rat diaphragm fibers (25 degrees C). The CT was measured by direct visualization (x200) of the fiber under current-clamp conditions. The main findings are the following: 1) Aminophylline lowers the CT, in a dose-dependent manner, toward more negative values of the resting membrane potential (Vm). 2) Dibutyryl adenosine 3′,5′-cyclic monophosphate (2 mM) shifts the CT, although this change is smaller than in the presence of xanthine. 3) Tetracaine (1 mM), a drug that diminishes Ca release from the sarcoplasmic reticulum, reduces the shift induced by 1 mM aminophylline; this is partially overcome by increasing aminophylline concentration to 5 mM. 4) Hyperpolarization of the fibers shifts the CT to more negative Vm. We suggest that the displacement in the CT to more negative Vm plays an important role in the potentiating effect of aminophylline. This could be the result of an enhancement of Ca release from the sarcoplasmic reticulum.

Effect of a spider toxin (JSTX) on excitatory postsynaptic current at neuromuscular synapse of spiny lobster

1987 ◽  
Vol 58 (2) ◽  
pp. 319-326 ◽  
Author(s):  
A. Miwa ◽  
N. Kawai ◽  
M. Saito ◽  
H. Pan-Hou ◽  
M. Yoshioka
Keyword(s):  
Membrane Potential ◽  
Neuromuscular Junction ◽  
Time Constant ◽  
Spiny Lobster ◽  
Neuromuscular Synapse ◽  
Ionic Channel ◽  
Excitatory Postsynaptic Potential ◽  
Excitatory Postsynaptic Current ◽  
Steady Level ◽  
The Relationship

1. We studied the blocking properties of a spider (Nephila clavata) toxin (JSTX) purified from venom on the spiny lobster neuromuscular junction. 2. When a small amount of JSTX was applied to the neuromuscular junction, the excitatory postsynaptic potential (EPSP) was partially suppressed. The amplitude of EPSPs remained at a steady level for several hours during the washing of the preparation, showing that the action of JSTX is irreversible. 3. We recorded the excitatory postsynaptic current (EPSC) from synaptic site using a macro-patch electrode. The amplitude of EPSC increased linearly with hyperpolarization of the membrane potential in the presence and absence of JSTX. 4. The decay phase time constant of EPSC and spontaneous EPSC was decreased by hyperpolarizing the membrane potential both in the absence and in the presence of JSTX. The relationship between the decay time constant and the membrane potential was not modified by JSTX. 5. It is suggested that JSTX irreversibly blocks EPSC by acting on the site that is apart from the ionic channel of the glutamate receptor molecule.

Synaptic and intrinsic control of membrane excitability of neostriatal neurons. II. An in vitro analysis

1990 ◽  
Vol 63 (4) ◽  
pp. 663-675 ◽  
Author(s):  
P. Calabresi ◽  
N. B. Mercuri ◽  
G. Bernardi
Keyword(s):  
Membrane Potential ◽  
Tetanus Toxin ◽  
Reversal Potential ◽  
Membrane Potentials ◽  
Synaptic Activity ◽  
Membrane Properties ◽  
Membrane Excitability ◽  
Epsp Amplitude ◽  
The Relationship

1. The effects of intrinsic membrane properties on the spontaneous and synaptically evoked activity of neostriatal neurons were studied in an in vitro slice preparation with the use of intracellular recordings. The recorded neurons did not show spontaneous action potentials at rest; depolarizing current pulses triggered a tonic firing pattern. 2. Subthreshold spontaneous depolarizing potentials (SDPs) were observed in 52% of the recorded neurons. The amplitude of these potentials at rest ranged between 2 and 15 mV, and their duration between 4 and 100 ms. The frequency and the amplitude of the SDPs were functions of the membrane potential: membrane depolarization by constant positive current increased the frequency of the SDPs and reduced their amplitude; hyperpolarization of the membrane decreased their frequency and increased their amplitude. Often, at membrane potentials more negative than -90 mV, SDPs were completely suppressed. 3. SDPs were blocked by low calcium-cobalt containing solutions. In the presence of tetrodotoxin (TTX, 1-3 microM), SDPs were completely abolished in 50% of the tested neurons; in the remaining neurons, small (1-4 mV) TTX-resistant SDPs were observed. In most of the neurons, bicuculline (BIC, 10-100 microM) and low concentrations of tetanus toxin (5-10 micrograms/ml) did not clearly affect the SDPs. Higher concentrations of tetanus toxin (100 micrograms/ml) blocked the SDPs as well as the synaptic potentials evoked by intrastriatal stimulation. 4. At resting membrane potential, intrastriatal stimulation produced a fast depolarizing postsynaptic potential (EPSP) that was reduced by BIC (10-100 microM). The relationship between EPSP amplitude and membrane potential was studied either by utilizing K(+)-chloride electrodes or by the use of cesium-chloride electrodes. In both these cases, the reversal potential for the EPSPs was between 0 and -14 mV. In cesium-loaded neurons, the decrease of the EPSP, usually observed at negative membrane potentials (below -85 mV), was clearly reduced. Internal cesium prolonged the duration of the SDPs and the EPSPs evoked by intrastriatal stimulation. 5. The relationship between spontaneous and evoked synaptic activity and membrane potential was studied in the presence of different external potassium blockers. 4-Aminopyridine (4AP, 0.1-1 mM) increased the EPSP amplitude and the frequency of the SDPs, but did not decrease membrane rectification and the shunt of the EPSPs present at negative membrane potentials. On the contrary, rectification of the membrane and the shunt of the EPSPs below -85 mV were clearly reduced by tetraethylammonium (TEA, 10-20 mM).(ABSTRACT TRUNCATED AT 400 WORDS)

The function of the sarcoplasmic reticulum is not inhibited by low temperatures in trout atrial myocytes

2001 ◽  
Vol 281 (6) ◽  
pp. R1902-R1906 ◽  
Author(s):  
Leif Hove-Madsen ◽  
Anna Llach ◽  
Lluis Tort
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Low Temperatures ◽  
Experimental Temperature ◽  
Effect Of Temperature ◽  
Fast Time ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Two Temperatures ◽  
Perforated Patch Clamp ◽  
The Relationship

The effect of temperature on sarcoplasmic reticulum (SR) Ca2+ uptake and release was measured in trout atrial myocytes using the perforated patch-clamp technique. Depolarization of the myocyte for 10 s to different membrane potentials ( V m) induced SR Ca2+ uptake. The relationship between V m and SR Ca2+ uptake was not significantly changed by lowering the experimental temperature from 21 to 7°C, and the relationship between total cytosolic Ca2+and SR Ca2+ uptake was similar at the two temperatures with a pooled Vmax = 66 amol/pF and K 0.5 = 4 amol/pF. Quantification of the Ca2+ release from the SR elicited by 10-ms depolarizations to different V m showed an increasing SR Ca2+ release at more positive V mbetween −50 and +10 mV, whereas SR Ca2+ release stagnated between +10 and +50 mV. Lowering of the temperature did not affect this relationship significantly, giving an SR Ca2+ release of 1.71 and 1.54 amol/pF at 21 and 7°C, respectively. Furthermore, clearance of the SR Ca2+ content slowed down inactivation of the L-type Ca2+ current at both temperatures (the fast time constant increased significantly from 10.4 ± 1.9 to 15.0 ± 2.0 ms at 21°C and from 38 ± 15 to 73 ± 24 ms at 7°C). Thus the SR has the capacity to remove the entire Ca2+ transient at physiologically relevant stimulation frequencies at both 21 and 7°C, although it is estimated that ∼40% of the total Ca2+ transient is liberated from and reuptaken by the SR with continuous stimulation at 0.5 Hz independently of the experimental temperature.

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