Large extracellular space leads to neuronal susceptibility to ischemic injury in a Na+/K + pumps–dependent manner
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Homeostasis
Extracellular electric fields have been proposed as a mechanism for electrical coupling between excitable cells. This study deals with the extracellular potential produced by an isolated excitable spherical cell due to a traveling depolarization wave on the cell's surface. Both uniform and nonuniform propagation velocity profiles are considered. Using boundary element methods, the extracellular potential was computed. The polarity of the extracellular potential was found to be space-dependent. The peak extracellular potential increased when a) the propagation velocity decreased, b) the rise time of the depolarization decreased, and c) the extracellular resistivity increased.< >
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The membrane potential responses of Paramecium caudatum to Na+ ions were examined to understand the mechanisms underlying the sensation of external inorganic ions in the ciliate by comparing the responses of the wild type and the behavioral mutant. Wild-type cells exhibited initial continuous backward swimming followed by repeated transient backward swimming in the Na+-containing test solution. A wild-type cell impaled by a microelectrode produced initial action potentials and a sustained depolarization to an application of the test solution. The prolonged depolarization, the depolarizing afterpotential, took place subsequently after stimulation. The ciliary reversal of the cell was closely associated with the depolarizing responses. When the application of the test solution was prolonged, the wild-type cell produced sustained depolarization overlapped by repeated transient depolarization. A behavioral mutant defective in the Ca2+ channel, CNR (caudatum non reversal), produced a sustained depolarization but no action potential or depolarizing afterpotential. The mutant cell responded to prolonged stimulation with sustained depolarization overlapped by transient depolarization, although it did not show backward swimming. The results suggest that Paramecium shows at least two kinds of membrane potential responses to Na+ ions: a depolarizing afterpotential mediating initial backward swimming and repeated transient depolarization responsible for the repeated transient backward swimming.
Paramecium caudatum
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Paramecium caudatum
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Wounding electrical responses were studied in Chara corallina. Specimens comprising two adjoining internodal cells were prepared. When one cell (victim cell) was cut, the other cell (receptor cell) generated four kinds of depolarization: (i) rapid depolarization; (ii) long-lasting depolarization; (iii) action potentials; and (iv) small spikes. In the present study, attention was focused on the long-lasting depolarization. A decrease in the electrical resistance suggested activation of ion channel(s). The duration of the depolarization was sensitive to the external ions. K+ significantly prolonged the depolarization. On the other hand, Ca2+, Mg2+ and Na+ had a tendency to shorten the duration prolonged by K+. When a nodal end was continuously flushed with a medium lacking K+, the depolarization was significantly shortened. Treatment of the nodal end with artificial cell sap for 2 min induced a long-lasting depolarization similar to that induced by cutting the victim cell. These findings suggested the involvement of K+ released from the victim cell in generating the long-lasting depolarization by the receptor cell.
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Squid giant axon
Tetrodotoxin
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The cytotoxic action of adriamycin is influenced by its intracellular accumulation. Therefore, it is important to clarify the mechanisms of adriamycin influx and efflux. In the present study, the influence of the extracellular KCl and Ca2+ concentration, the extracellular pH and the presence of NaHC03 on the ADR accumulation was investigated in order to study the mechanisms in ADR accumulation influenced by ions. The extracellular KCl concentration did not affect the intracellular ADR accumulation. This suggests the cell membrane potential does not affect the ADR accumulation since it is influenced by the KCl concentration. The intracellular intensity of fluorescence of Fluo3, an indicator of Ca2+, increased between 0 and 20 mM of the extracellular concentration of Ca2+ ion. However, the ADR accumulation did not change between 0 and 20 mM of the extracellular concentration of Ca2+. This indicates that the extracellular concentration of Ca2+ does not affect the ADR accumulation under physiological conditions since 20 mM of Ca2+ is beyond normal physiological conditions. Further, the intracellular fluorescence of Fluo3 decreased as increasing the extracellular pH. In contrast, the ADR accumulation increased as increasing the extracellular pH. These suggest that the ADR accumulation increases as decreasing the intracellular Ca2+ as changing the extracellular pH. In wild type strain, the ADR accumulation did not change by the extracellular pH in the absence of NaHCO3, but increased as increasing the extracellular pH in the presence of NaHCO3. This suggests that the ADR accumulation in the wild type strain is influenced by NaHCO3 but the extracellular pH. In the ADR-resistant strain, the ADR accumulation decreased as increasing the extracellular pH regardless of NaHCO3. However, the accumulation of ADR increased as increasing the extracellular pH when the adjustment of pH was carried out with 1N HCl. This suggests that Cl- may play an important role in the ADR influx in the ADR-resistant strain.
Intracellular pH
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Background and aims: In experiments designed to dissect the signalling pathways in beta cells, the depolarizing effect of glucose metabolism is often replaced by a strong K+ depolarization. Recent observations raised doubt that high K+ is an appropriate experimental substitute for the physiologically induced depolarization.
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Instability of the inner mitochondrial membrane potential (ΔΨm) has been implicated in electrical dysfunction, including arrhythmogenesis during ischemia-reperfusion. Monitoring ΔΨm has led to conflicting results, where depolarization has been reported as sporadic and as a propagating wave. The present study was designed to resolve the aforementioned difference and determine the unknown relationship between ΔΨm and electrophysiology. We developed a novel imaging modality for simultaneous optical mapping of ΔΨm and transmembrane potential (Vm). Optical mapping was performed using potentiometric dyes on preparations from 4 mouse hearts, 14 rabbit hearts, and 7 human hearts. Our data showed that during ischemia, ΔΨm depolarization is sporadic and changes asynchronously with electrophysiological changes. Spatially, ΔΨm depolarization was associated with action potential duration shortening but not conduction slowing. Analysis of focal activity indicated that ΔΨm is not different within the myocardium where the focus originates compared with normal ventricular tissue. Overall, our data suggest that during ischemia, mitochondria maintain their function at the expense of sarcolemmal electrophysiology, but ΔΨm depolarization does not have a direct association to ischemia-induced arrhythmias.
Cardiac Electrophysiology
Voltage-sensitive dye
Optical mapping
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