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R H Adrian

Publications and source records attributed to R H Adrian.

32 records · Page 2Linked to original sources
PubMed1973

Reconstruction of the action potential of frog sartorius muscle.

1. Propagated action potentials of striated muscle are calculated using an equivalent circuit that represents the transverse tubular system as a radial cable of sixteen elements. The membrane of the transverse tubules is assumed to have activatable ionic currents similar to those in the fibre surface.2. The configuration of the after-potential and the conduction velocity are best accounted for by postulating a resistance of about 150Omega cm(2) separating the extracellular fluid from the lumen of the transverse tubules at the edge of the fibre, and a density of sodium channels in the tubular wall about a twentieth of that in the fibre surface.3. Calculations with imposed voltage steps at the fibre surface suggest that the potential across the tubular membrane at the centre of the fibre is very far from clamped.4. Currents providing charge for the tubular capacity can give rise to substantial errors in estimating the zero-current potential of the ionic currents.

Action Potentials↗
PubMed1970

Voltage clamp experiments in striated muscle fibres.

1. Membrane currents during step depolarizations were determined by a method in which three electrodes were inserted near the end of a fibre in the frog's sartorius muscle. The theoretical basis and limitations of the method are discussed.2. Measurements of the membrane capacity (C(M)) and resting resistance (R(M)) derived from the current during a step change in membrane potential are consistent with values found by other methods.3. In fibres made mechanically inactive with hypertonic solutions (Ringer solution plus 350 mM sucrose) step depolarizations produced ionic currents which resembled those of nerve in showing (a) an early transient inward current, abolished by tetrodotoxin, which reversed when the depolarization was carried beyond an internal potential of about +20 mV, (b) a delayed outward current, with a linear instantaneous current-voltage relation, and a mean equilibrium potential with a normal potassium concentration (2.5 mM) of -85 mV.4. The reversal potential for the early current appears to be consistent with the sodium equilibrium potential expected in hypertonic solutions.5. The variation of the equilibrium potential for the delayed current (V'(K)) with external potassium concentration suggests that the channel for delayed current has a ratio of potassium to sodium permeability of 30:1; this is less than the resting membrane where the ratio appears to be 100:1. V'(K) corresponds well with the membrane potential at the beginning of the negative after-potential observed under similar conditions.6. The variation of V'(K) with the amount of current which has passed through the delayed channel suggests that potassium ions accumulate in a space of between (1/3) and (1/6) of the fibre volume. If potassium accumulates in the transverse tubular system (T system) much greater variation in V'(K) would be expected.7. The delayed current is not maintained but is inactivated like the early current. The inactivation is approximately exponential with a time constant of 0.5 to 1 sec at 20 degrees C. The steady-state inactivation of the potassium current is similar to that for the sodium current, but its voltage dependence is less steep and the potential for half inactivation is 20 mV rate more positive.8. Reconstructions of ionic currents were made in terms of the parameters (m, n, h) of the Hodgkin-Huxley model for the squid axon, using constants which showed a similar dependence on voltage.9. Propagated action potentials and conduction velocities were computed for various conditions on the assumption that the T system behaves as if it were a series resistance and capacity in parallel with surface capacity and the channels for sodium, potassium and leak current. There was reasonable agreement with observed values, the main difference being that the calculated velocities and rates of rise were somewhat less than those observed experimentally.

Action Potentials↗
PubMed1970

Slow changes in potassium permeability in skeletal muscle.

1. Voltage clamp experiments on sartorius muscle fibres at 3 degrees C showed that the potassium current is divisible into three components, namely:(a) Current in the delayed rectifier channel, which reached a maximum in about 0.1 sec at -30 mV, and declined with a time constant of about 4 msec when the fibre was repolarized to -100 mV; this component had an approximately linear instantaneous current-voltage relation and an equilibrium potential E(1) at 10-15 mV positive to the resting potential.(b) A slow component which reached a maximum in about 3 sec at -30 mV, and declined with a time constant of about 0.5 sec when the fibre was repolarized to -100 mV; this component had an approximately linear instantaneous current-voltage relation and a mean equilibrium potential E(2) at -83 mV in fibres where E(1) averaged -75 mV.(c) Current in the inward rectifier channel which decreased with a time constant of about 0.25 sec when the fibre was hyperpolarized to -150 mV. This component had an equilibrium potential close to the resting potential and an instantaneous current-voltage relation which was that of an inward rectifier.2. The general characteristics of the late after-potential in muscles in hypertonic solutions at 3 degrees C are consistent with those of the slow conductance change. The sign of the late after-potentials was reversed by depolarizing below -80 mV.3. The decline of current during a maintained hyperpolarization cannot be attributed solely to a decrease in tubular potassium concentration, since there may be a large decrease in current without much alteration of equilibrium potential. The negative slope conductance often seen at -150 mV is also difficult to reconcile with the tubular depletion hypothesis.4. Replacement of 10 mM-K by 10 mM-Rb abolished inward rectification but had less effect on the fast and slow components of the potassium conductance.

Action Potentials↗
PubMed1969

The kinetics of mechanical activation in frog muscle.

1. The kinetics of mechanical activation were examined in muscle fibres of the frog's sartorius muscle, using a voltage clamp to control membrane potential, tetrodotoxin to eliminate electrical activity and microscopic observations to determine the mechanical threshold.2. The strength-duration curve was determined over a range of membrane potentials varying between -52 mV (rheobase) and +90 mV. At 4 degrees C the critical duration was about 11 msec at -30 mV, 4 msec at 0 mV and 2 msec at +40 mV.3. For pulses where V > -10 mV the threshold criterion at 4 degrees C was that the ;area above -30 mV' must exceed about 120 mV msec.4. The effect of a brief subthreshold pulse declines with a time constant of about 3 msec at -100 mV and about 8 msec at -85 mV at 4 degrees C.5. Although the strength-duration curve is well fitted by assuming a first-order mechanism in which the rate of release of activator increases with membrane potential, other experiments show that the over-all mechanism is probably second order in time.6. A short pulse must be at least 50% threshold if it is to give a visible contraction when added to a long pulse which is just below rheobase.7. Delayed rectification was conspicuous with medium or long pulses which were just below the mechanical threshold, but short pulses could give contraction without turning on any appreciable potassium conductance.8. The Appendix extends Falk's (1968) treatment of the charging of the tubular system under a voltage clamp.

Animals↗
PubMed1969

Radial spread of contraction in frog muscle fibres.

1. The membrane potential of isolated muscle fibres in solutions containing tetrodotoxin (TTX) was controlled with a two-electrode voltage clamp. The striation pattern in the region of the electrodes was observed microscopically.2. With square steps of depolarization of increasing magnitude, contraction occurs first in the myofibrils just beneath the surface membrane, and then spreads inwards towards the axis of the fibre as the depolarization is increased.3. From the depolarizations which make the superficial and axial myofibrils contract it is possible to estimate a space constant (lambda(T)) for electrotonic spread in a transverse tubular network.4. lambda(T) was found to vary with fibre radius; for a 50 mu fibre it was about 60 mu. lambda(T) was not greatly affected by tetraethylammonium (TEA) chloride (111 mM), or by sucrose substitution of most of the sodium chloride in the Ringer solution.5. The ratio of the depolarization threshold for contraction of surface myofibrils and of central myofibrils was smaller for short (3 msec) than for long depolarization.6. Action potentials, recorded from a sartorius fibre, were used as the command signal for the voltage-clamped fibre in tetrodotoxin. The central myofibrils of this fibre did not appear to contract unless the imposed ;action potentials' were of normal size.7. The passive electrical characteristics of the transverse tubular system will just allow an action potential, at room temperature, to activate the myofibrils at the centre of a frog muscle fibre. An active potential change would be required to achieve a safety factor appreciably greater than one for this process.

Action Potentials↗
PubMed1966

Membrane potential and conductance during transport of sodium, potassium and rubidium in frog muscle.

1. Muscles with high intracellular sodium concentrations can extrude sodium into solutions which contain 10 m-equiv/l. of either potassium or rubidium. Potassium or rubidium replaces the extruded intracellular sodium. These cation movements take place equally well when the external anion is chloride or sulphate, though muscles deteriorate if left for long periods in sulphate solutions.2. Measurements of intracellular potentials during extrusion of sodium into solutions containing potassium show:(a) an internal potential more negative than the potassium equilibrium potential (E(K)); at 20 degrees C the difference is nearly 20 mV.(b) that a difference between the membrane potential and E(K) is dependent on temperature and is abolished by 10(-5)M ouabain.(c) an internal potential which becomes more negative in the presence of 0.1% cocaine, a concentration of cocaine which substantially increases the membrane resistance to potassium movement. In the absence of potassium or rubidium no such hyperpolarization occurs.3. When muscles extrude into solutions which contain rubidium they have internal potentials which are 10-20 mV more negative than when extruding sodium into corresponding solutions containing potassium.4. Measurements of electrical conductance in the potassium solution suggest that the electrochemical potential difference for potassium ions may be large enough to account for the measured inward potassium movements during sodium extrusion. The reliability of the measurements does not, however, exclude the possibility that some part of the inward potassium movement is chemically linked to outward movement.5. Measurements of membrane conductance in solutions containing rubidium, and of net movements of rubidium in the presence and absence of ouabain, lead to the conclusion that at least 90% of the inward rubidium movement during sodium extrusion must be chemically linked to the sodium movement.6. The hyperpolarization during extrusion of sodium could be explained on the basis of a fall of the potassium or rubidium concentration in a region of the extracellular space immediately external to the membrane. It is argued that certain characteristics of the hyperpolarization make it difficult to explain the hyperpolarization on this basis alone, though some part of it may be due to extracellular depletion of either potassium or rubidium.The main conclusion is that the sodium pump is capable of transferring electric charge across the membrane in which it is operating, but that, in a given time, the net charge transferred is less than the charge on the sodium ions that the pump has transported, by an amount that corresponds to the charge on the potassium or rubidium ions chemically transported by the pump.

Animals↗