Effect of glutamate and some other amino acids on the membrane potential of muscle cells in the pharynx-levator muscle of Helix pomatia

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

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β-Catenin regulates membrane potential in muscle cells by regulating the α2 subunit of Na,K-ATPase

European Journal of Neuroscience ◽

10.1111/ejn.12564 ◽

2014 ◽

Vol 40 (1) ◽

pp. 2216-2224 ◽

Cited By ~ 3

Author(s):

Congying Zhao ◽

Jing Zhang ◽

Kexin Li ◽

Jianming Yang ◽

Huimin Yu ◽

...

Keyword(s):

Membrane Potential ◽

Muscle Cells

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Role of HERG-like K+ currents in opossum esophageal circular smooth muscle

AJP Cell Physiology ◽

10.1152/ajpcell.1999.277.6.c1284 ◽

1999 ◽

Vol 277 (6) ◽

pp. C1284-C1290 ◽

Cited By ~ 55

Author(s):

Hamid I. Akbarali ◽

Hemant Thatte ◽

Xue Dao He ◽

Wayne R. Giles ◽

Raj K. Goyal

Keyword(s):

Smooth Muscle ◽

Membrane Potential ◽

Smooth Muscle Cells ◽

Single Cells ◽

Circular Muscle ◽

Muscle Cells ◽

Resting Membrane Potential ◽

Channel Blockers ◽

Circular Smooth Muscle ◽

Inward Currents

An inwardly rectifying K+ conductance closely resembling the human ether-a-go-go-related gene (HERG) current was identified in single smooth muscle cells of opossum esophageal circular muscle. When cells were voltage clamped at 0 mV, in isotonic K+ solution (140 mM), step hyperpolarizations to −120 mV in 10-mV increments resulted in large inward currents that activated rapidly and then declined slowly (inactivated) during the test pulse in a time- and voltage- dependent fashion. The HERG K+ channel blockers E-4031 (1 μM), cisapride (1 μM), and La3+ (100 μM) strongly inhibited these currents as did millimolar concentrations of Ba2+. Immunoflourescence staining with anti-HERG antibody in single cells resulted in punctate staining at the sarcolemma. At membrane potentials near the resting membrane potential (−50 to −70 mV), this K+ conductance did not inactivate completely. In conventional microelectrode recordings, both E-4031 and cisapride depolarized tissue strips by 10 mV and also induced phasic contractions. In combination, these results provide direct experimental evidence for expression of HERG-like K+ currents in gastrointestinal smooth muscle cells and suggest that HERG plays an important role in modulating the resting membrane potential.

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The Ionic Basis of the Resting Potential in a Cross-Striated Muscle of the Aquatic Snail Lymnaea Stagnalis

Journal of Experimental Biology ◽

10.1242/jeb.108.1.305 ◽

1984 ◽

Vol 108 (1) ◽

pp. 305-314

Author(s):

B. L. BREZDEN ◽

D. R. GARDNER

Keyword(s):

Membrane Potential ◽

Lymnaea Stagnalis ◽

Striated Muscle ◽

Potassium Concentration ◽

Muscle Cells ◽

Resting Potential ◽

Extracellular Potassium ◽

Heart Ventricle ◽

Sodium Permeability ◽

Ionic Basis

The mean resting potential in the heart ventricle muscle cells of the freshwater snail Lymnaea stagnalis was found to be −61.2±3.5 (˙˙) mV (ranging from −56mV to −68mV). The average intracellular potassium concentration was estimated to be 51.5±14.6(˙˙) m (ranging from 27.8 m to 77.3 m). The membrane of the heart ventricle muscle cells appears to be permeable to both potassium and chloride, as changes in the extracellular concentration of either of these ions resulted in a change in the membrane potential. A ten-fold change in the extracellular potassium concentration was associated with a 50.4±3.8(˙˙) mV slope when the potassium concentration was above about 6 m. Deviations from the straight-line relation predicted for a potassium electrode could be accounted for by introducing a term for sodium permeability. The ionic basis of the membrane potential in these cells can be described by a modified form of the Goldman-Hodgkin- Katz equation.

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Effect of nicotine and acetylcholine on crustacean muscle membrane potential

Journal of Applied Physiology ◽

10.1152/jappl.1986.61.2.807 ◽

1986 ◽

Vol 61 (2) ◽

pp. 807-809

Author(s):

R. F. Taylor ◽

D. T. Frazier

Keyword(s):

Membrane Potential ◽

Muscle Tension ◽

Muscle Cells ◽

Abdominal Muscle ◽

Muscle Membrane ◽

Resting Membrane Potential ◽

Crustacean Muscle ◽

Standard Glass ◽

Before And After ◽

Receptor Organ

We have investigated the effect of nicotine and acetylcholine on the resting membrane potential of the crayfish extensor muscle in order to determine whether crustacean muscle can be activated by cholinergic compounds. Intracellular recordings from individual deep extensor abdominal muscle cells were made using standard glass microelectrode techniques. The resting membrane potential was measured before and after treatment with glutamate, nicotine, and acetylcholine. Glutamate, which is a known activator of crayfish muscle, was used to determine whether the muscle cell preparation was viable and capable of responding to any of the test substances. Our results confirm that application of glutamate is associated with a depolarization of the muscle membrane. However, muscle cells showed no depolarization after treatment with nicotine (50 microM) or acetylcholine (66 microM). These results argue against the notion that increases in muscle tension may be responsible for the increased receptor organ discharge observed in the presence of nicotine. Rather, it supports the hypothesis that nicotine is acting directly on the mechanoreceptor membrane to change its sensitivity.

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Effect of isosmotic removal of extracellular Ca2+ and of membrane potential on cell volume in muscle cells

AJP Cell Physiology ◽

10.1152/ajpcell.1994.267.3.c768 ◽

1994 ◽

Vol 267 (3) ◽

pp. C768-C775 ◽

Cited By ~ 5

Author(s):

C. Pena-Rasgado ◽

K. D. McGruder ◽

J. C. Summers ◽

H. Rasgado-Flores

Keyword(s):

Membrane Potential ◽

Sarcoplasmic Reticulum ◽

Cell Volume ◽

Muscle Cells ◽

Membrane Depolarization ◽

Volume Reduction ◽

Sensitive Volume ◽

Volume Increase ◽

Dependent Cell ◽

In Cells

Isosmotic removal of extracellular Ca2+ (Cao) and changes in membrane potential (Vm) are frequently performed manipulations. Using isolated voltage-clamped barnacle muscle cells, we studied the effect of these manipulations on isosmotic cell volume. Replacing Cao by Mg2+ induced 1) verapamil-sensitive extracellular Na(+)-dependent membrane depolarization, 2) membrane depolarization-dependent cell volume reduction in cells whose sarcoplasmic reticulum (SR) was presumably loaded with Ca2+ [intracellular Ca2+ (Cai)-loaded cells], and 3) cell volume increase in cells whose SR was presumably depleted of Ca2+ (Cai-depleted cells) or in Cai-loaded cells whose Vm was held constant. Membrane depolarization induced 1) volume reduction in Cai-loaded cells or 2) verapamil-sensitive volume increase in Cai-depleted cells. This suggests tha, in Cai-loaded cells, membrane depolarization induces SR Ca2+ release, which in turn promotes volume reduction. Conversely, in Cai-depleted cells, the depolarization activates Na+ influx through a verapamil-sensitive pathway leading to the volume increase. This pathway is also revealed when Cao is removed in either Cai-depleted cells or in cells whose Vm is held constant.

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