scholarly journals Changes in intra- and extracellular potassium and intracellular sodium activities induced by repetitive stimulation and their relation to membrane potential in guinea-pig papillary muscle.

1987 ◽  
Vol 37 (5) ◽  
pp. 797-819 ◽  
Author(s):  
Nobuo HOTOKEBUCHI ◽  
Toshiyuki YANO ◽  
Yasufumi NISHIZONO ◽  
Katsuhide NISHI
Keyword(s):  
Membrane Potential ◽  
Guinea Pig ◽  
Papillary Muscle ◽  
Repetitive Stimulation ◽  
Intracellular Sodium ◽  
Extracellular Potassium

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.

Role of aiNa in positive force-frequency staircase in guinea pig papillary muscle

1988 ◽  
Vol 255 (6) ◽  
pp. C798-C807 ◽  
Author(s):  
D. Y. Wang ◽  
S. W. Chae ◽  
Q. Y. Gong ◽  
C. O. Lee
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Papillary Muscle ◽  
Time Course ◽  
Hysteresis Phenomenon ◽  
Force Frequency ◽  
Guinea Pig Heart ◽  
Stimulation Rate ◽  
Twitch Force

In the ventricular papillary muscle of guinea pig heart, membrane potential, intracellular sodium activity (aiNa), and twitch force were measured simultaneously and continuously for many hours at stimulation rates of 0, 0.5, 1, 2, 3, 4, 5, and 6 Hz to investigate the relation of aiNa to twitch force and membrane potential both in the steady state and during the changes in these variables. After an increase in stimulation rate, both aiNa and twitch force increased progressively, reaching steady-state levels. The relation between twitch force and aiNa in the steady state was generally sigmoidal over the range of 0.5-5 Hz and steep in the 1- to 4-Hz range. After either increase or decrease in stimulation rate, the time course of change in aiNa was exponential and similar to that of change in twitch force. Moreover, the force-aiNa relation observed after increase in stimulation rate from 0.5 to 3 Hz resembled that observed after decrease in the rate from 3 to 0.5 Hz, indicating an absence of hysteresis in the relation. The results suggest that an increase in aiNa is an important factor involved in the force staircase. As stimulation rate was increased from 0.5 to higher rates (5 or 6 Hz) and then decreased back to 0.5 Hz, a hysteresis phenomenon was observed in the relation between twitch force and aiNa. This suggests that some secondary factor may alter the relation between twitch force and aiNa. As stimulation rate increased and aiNa rose, the steady-state diastolic membrane potential hyperpolarized. This result is consistent with the view that an increase in aiNa enhances the electrogenic Na+-K+ pump and hyperpolarizes the cell membrane.

Use-dependent depression of IPSPs in rat hippocampal pyramidal cells in vitro

1985 ◽  
Vol 53 (2) ◽  
pp. 557-571 ◽  
Author(s):  
M. McCarren ◽  
B. E. Alger
Keyword(s):  
Membrane Potential ◽  
Conditioning Stimulus ◽  
Pyramidal Cells ◽  
Repetitive Stimulation ◽  
Stratum Radiatum ◽  
Resting Potential ◽  
Masking Effect ◽  
Extracellular Potassium ◽  
Gamma Aminobutyric Acid ◽  
Hippocampal Pyramidal Cells

We have used intracellular recording techniques to study the use-dependence of evoked inhibitory postsynaptic potentials (IPSPs) in rat CA1 hippocampal pyramidal cells. We determined reversal potentials and conductance changes associated with IPSPs and responses to directly applied gamma-aminobutyric acid (GABA). The IPSP depression could be seen after a single conditioning stimulus. This depression appeared to be due primarily to a 50% decrease in IPSP conductance (gIPSP). Trains of stimulating pulses (50 pulses at 5 or 10 Hz) produced more pronounced effects than a single conditioning pulse. Suprathreshold repetitive stimulation of stratum radiatum (SR) produced epileptiform burst firing and greater depression of IPSPs than did alvear (ALV) or subthreshold SR stimulation. During suprathreshold SR stimulation the IPSP was nearly abolished and the membrane potential could become less negative than the resting potential. A masking effect of facilitated depolarizing potentials on IPSPs was unlikely since IPSPs accompanied by little or no depolarizing potential were also depressed by SR trains. The 75% reduction in IPSP conductance found after repetitive stimulation confirmed that an overlapping conductance was not responsible for the depression of the IPSP. The GABA-induced conductance increase was not depressed by identical trains. Trains of stimulation induced depolarizing shifts in equilibrium potentials for the IPSP (EIPSP) and GABA (EGABA) of approximately 10 mV. These shifts were always greater after SR trains than after ALV trains. Simultaneous recordings of membrane potential and extracellular potassium concentration ([K+]o) with K+-sensitive microelectrodes revealed a direct correlation between the two during a stimulus train. Membrane potential depolarized as much as 18 mV from the peak of the IPSP and [K+]o could increase to a maximum of 10 mM during some trains. A depressant effect (of approximately 50%) of K+ on IPSPs was demonstrated by brief pressure ejection of K+ near the soma. We conclude that repetitive stimulation depresses gIPSP and shifts EIPSP in the depolarizing direction. Whereas gIPSP began to decline after a single conditioning pulse, the additional depression of IPSPs produced by stimulus trains was due in large part to shifts in EIPSP. Depression of gIPSP was not due to desensitization or block of ionic conductances, since gGABA was not reduced. The EIPSP may change as a result of increases in [K+]o.

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