scholarly journals Effects of anions and cations on the resting membrane potential of internally perfused barnacle muscle fibres

1973 ◽  
Vol 233 (3) ◽  
pp. 613-634 ◽  
Author(s):  
N. Lakshminarayanaiah ◽  
E. Rojas
Keyword(s):  
Membrane Potential ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Barnacle Muscle ◽  
Anions And Cations

The resting membrane potential of white muscle from brown trout (Salmo trutta) exposed to copper in soft, acidic water

2000 ◽  
Vol 203 (14) ◽  
pp. 2229-2236 ◽  
Author(s):  
M.W. Beaumont ◽  
E.W. Taylor ◽  
P.J. Butler
Keyword(s):  
Membrane Potential ◽  
Brown Trout ◽  
Salmo Trutta ◽  
White Muscle ◽  
Low Ph ◽  
Ammonium Ion ◽  
Muscle Membrane ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Brown Trout Salmo Trutta

Previously, the distribution of ammonia between the intracellular and extracellular compartments has been used to predict a significant depolarisation of the resting membrane potential (E(M)) of white muscle from brown trout (Salmo trutta) exposed to a sub-lethal combination of copper and low pH. However, this prediction is based upon two assumptions (i) a relatively high membrane permeability for the ammonium ion with respect to that for ammonia gas and (ii) that this is unaltered by exposure to copper and low pH. Since there is conflicting evidence in the literature of the validity of these assumptions, in the present study E(M) was directly measured in white muscle fibres of trout exposed to copper and low pH (E(M)=−52.2+/−4.9 mV) and compared with that of unexposed, control animals (E(M)=−86.5+/−2.9 mV) (means +/− s.e.m., N=6). In confirming the predicted depolarisation, these data support the hypothesis of electrophysiological impairment as a factor in the reduction in the swimming performance of trout exposed to these pollutants. In addition, the results of this study support the role of a significant permeability of the muscle membrane to NH(4)(+) in determining the distribution of ammonia in fish.

The effect of diazepam on potassium contractures, contraction threshold, and resting tension in rat skeletal muscles

1988 ◽  
Vol 66 (5) ◽  
pp. 573-579 ◽  
Author(s):  
Michael Chua ◽  
Angela F. Dulhunty
Keyword(s):  
Membrane Potential ◽  
Type Equation ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
High Potassium ◽  
Fourfold Increase ◽  
Maximum Tension ◽  
Potassium Contracture ◽  
Negative Shift ◽  
Resting Tension

The effects of diazepam on potassium contractures, contraction threshold, and resting tension have been examined in rat soleus muscle fibres. Two actions of the drug were defined that could not be attributed to changes in the resting membrane potential or depolarization in high potassium solutions. The major effect was an increase in the amplitude of submaximal tension during either twitches or potassium contractures and an increase in resting tension. At 400 μM diazepam, there was (a) a fourfold increase in 40 mM potassium contracture tension, (b) a negative shift of 8 mV in the membrane potential for half maximum tension estimated from the best fit of a Boltzmann-type equation to average potassium contracture data, (c) a negative shift of 8 mV in the threshold for contraction measured under voltage clamp conditions, and (d) a contracture of variable amplitude to a level that was occasionally equivalent to maximum tetanic tension. These potentiating actions of diazepam depended on drag concentration within the range of 100–800 μM. In contrast, the second effect of diazepam, depression of maximum tension by 10–15%, was independent of drug concentration between 100 and 400 μM. The results support the idea that diazepam produces an increase in resting myoplasmic calcium concentrations.

The nature of the monosynaptic excitatory and inhibitory processes in the spinal cord

1952 ◽  
Vol 140 (899) ◽  
pp. 169-176 ◽  
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Glass Tube ◽  
Giant Axon ◽  
Resting Membrane Potential ◽  
Muscle Fibres ◽  
Spike Potential ◽  
Inhibitory Processes ◽  
Fine Glass

Recently it has been possible to record electrically from motoneurones in the spinal cord of the anaesthetized cat by means of an intracellular electrode (Brock, Coombs & Eccles 1951, 1952). As with investigations on isolated nerve and muscle fibres (Ling & Gerard 1949; Nastuk & Hodgkin 1950; Weidmann 1951; Fatt & Katz 1951) the micro-electrode is a fine glass tube filled with 3 m-KCI and with a tip diameter of about 0-5 µ .Necessarily it has to be inserted ‘blindly’ into a motoneurone lying some 2 mm deep in the spinal cord. However, the position of a pool of motoneurones belonging to any one muscle is now fairly well known (Romanes 1951), and the motoneurones are made to signal their position electrically during the process of insertion by firing impulses into them antidromically and also by monosynaptically activating them. The entry of a micro-electrode into a motoneurone is immediately and unambiguously signalled by two events: the recording of the resting membrane potential (about 70 mV); the inversion and large increase in the antidromic spike potential, which gives a reversal of membrane potential of as much as 35 mV. In general, both during rest and in the propagation of impulses, the electrical properties of the motoneurone closely resemble those of the isolated giant axon.

Changes in Membrane Properties of the Drosophila Dorsal Longitudinal Flight Muscle Induced by Sodium Pump Inhibitors

1981 ◽  
Vol 90 (1) ◽  
pp. 175-183 ◽  
Author(s):  
BARBARA K. HENON ◽  
KAZUO IKEDA
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Sodium Pump ◽  
Flight Muscle ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Slow Phase ◽  
Muscle Fibres ◽  
Fast Phase ◽  
In Cells

1. Drosophila dorsal longitudinal flight muscle fibres made anoxic by passing nitrogen through the tracheal system or treated with 10−5M ouabain or strophanthidin show a reversible fall in resting membrane potential of 16·5 mV (S.E. 0·96), 1·37 mV (S.E. 0·87), and 1·70 mV (S.E. 2·8), respectively. The reversible depolarization obtained with these sodium pump blockers occurred within 10–15 min. 2. The depolarization of the muscle fibres was accompanied by a decrease in input resistance of 21·2% (S.E. 3·8) in anoxia, 21·4% in ouabain, and 25·6% (S.E. 6·7) in strophanthidin. The resistance decrease in strophanthidin and ouabain was transient and returned to above the resting level while the muscle fibres were still exposed to these agents. 3. Recovery of membrane potential in cells exposed to anoxia is biphasic. An initial ‘fast’ phase of recovery occurs within 15 s upon return to air followed by a late ‘slow’ phase lasting several minutes. Recovery of input resistance in cells exposed to N2 coincided with the ‘fast’ phase of the recovery of resting membrane potential. 4. Recovery of membrane potential following exposure to strophanthidin is a long, slow process which occurs at conductance values at the resting level or below. 5. The tendency towards spontaneous action potentials was increased by anoxia and the action potentials occurring in anoxia were elongated into plateau potentials of about 18s duration. 6. These results are consistent with the hypothesis that anoxia and cardioactive steroids inhibit a metabolic process, possibly an electrogenic ion pump, that is essential for maintenance of the resting membrane potential in Drosophila flight muscle. Exposure to these agents also results in changes in input resistance. Both of these effects could contribute to the depolarization and affect the excitable properties of the muscle fibre membrane.

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