Axonal Adaptations to Osmotic and Ionic Stress in an Invertebrate Osmoconformer (Mercierella Enigmatica Fauvel): II. Effects of Ionic Dilution on the Resting and Action Potentials

1978 ◽  
Vol 76 (1) ◽  
pp. 205-219
Author(s):  
J. A. BENSON ◽  
J. E. TREHERNE

The giant axon of this extreme euryhaline osmoconformer possess an unusual ability to produce action potentials of large amplitude over a wide range of ionic dilution when constant osmotic concentration is maintained by the addition of mannitol to the bathing medium. Ionic dilution under these circumstances causes a decline in the overshoot of the action potential (resulting largely from reduction in [Na+]0) and an appreciable axonal hyperpolarization (primarily as a result of decrease in [K+]0). This hyperpolarization tends to compensate for the reduction in the extent of the overshoot and so maintains the amplitude of the sodium-mediated action potentials during isosmotic dilution of the bathing medium. The axonal hyperpolarization also appears to reduce sodium inactivation so as to maintain a rapid rate of rise of the action potential despite drastic reduction in the ionic concentration of the bathing medium. Prolonged exposure to reduced ionic concentrations appears to induce a ouabain sensitive reduction in intracellular sodium concentration which increases the sodium gradient across the axon membrane during isosmotic dilution of the external medium.

1978 ◽  
Vol 75 (1) ◽  
pp. 237-251
Author(s):  
A. D. CARLSON ◽  
Y. PICHON ◽  
J. E. TREHERNE

Reprint requests should be addressed to Dr Treherne. The giant axons of the polychaete, Sabella penicillus, can withstand, in vitro, abrupt changes in osmotic and ionic concentration of the bathing medium in the range measured in the blood of this osmoconformer (543–1236 m-osmol) at different external salinities. Isosmotic dilution of the external ions (i.e. when osmotic concentration was maintained by sucrose) induced a modest hyperpolarization of the axonal membrane and a rapid decline in the overshoot of the action potential. In contrast, abrupt hyposmotic dilution resulted in a relatively slow and complex decline in overshoot in the absence of axonal hyperpolarization. A slow potassium depolarization and rate of decrease in overshoot in sodium-free conditions suggests that there is a reduced intercellular access to the axon surfaces following exposure to hyposmotic media. It is suggested that this restricted access could provide short-term protection from fluctuations in blood osmotic concentration.


1974 ◽  
Vol 60 (3) ◽  
pp. 653-671
Author(s):  
D. B. SATTELLE

1. A mean resting potential of -53.3 (S.D. ±2.7) mV has been obtained for 23 neurones of the parietal and visceral ganglia of Limnaea stagnalis (L.). Changes in the resting potential of between 28 and 43 mV accompany tenfold changes in [K+0]. A modified constant-field equation accounts for the behaviour of most cells over the range of external potassium concentrations from 0-5 to 10.o mM/1. Mean values have been estimated for [K+1, 56.2 (S.D.± 9-0) mM/1 and PNa/PK, 0-117 (S.D.±0-028). 2. Investigations on the ionic basis of action potential generation have revealed two cell types which can be distinguished according to the behaviour of their action potentials in sodium-free Ringer. Sodium-sensitive cells are unable to support action potentials for more than 8-10 min in the absence of sodium. Sodium slopes of between 29 and 37 mV per decade change in [Na+0] have been found for these cells. Tetrodotoxin (5 x 10-5 M) usually blocks action potentials in these neurones. Calcium-free inger produces a marked reduction in the overshoot potential and calcium slopes of about 18 mV per decade change in [Ca2+o] are found. Manganous chloride only partially reduces the action potential overshoot in these cells at concentrations of 10 mM/l. 3. Sodium-insensitive neurones maintain action potentials in the absence of external sodium. Stimulation only slightly reduces the amplitude of the action potential under these conditions and such cells are readily accessible to potassium ions in the bathing medium. A calcium-slope of 29 mV per decade change in [Ca2+o] has been observed in these cells in the absence of external sodium. 4. It is concluded that both sodium and calcium ions can be involved in the generation of the action potential in neurones of Limnaea stagnate, their relative contribution varying in different cells.


1978 ◽  
Vol 76 (1) ◽  
pp. 221-235
Author(s):  
J. A. BENSON ◽  
J. E. TREHERNE

The giant axons of this extreme osmoconformer were adapted, in vitro, to progressive hyposmotic dilution of the bathing medium (from 1024 m-Osmol to concentrations as low as 76.8 m-Osmol). Hyposmotic adaptation is associated with reductions in the intracellular concentrations of both sodium and potassium ions. These reductions do not appear to result from appreciable axonal swelling. The different electrical responses to isosmotic and hyposmotic dilution suggest that reduction in [Na+]1 results from ouabain-dependent sodium extrusion, in response to ionic dilution, and that reduction in [K+]1 is induced by a combination of ionic and osmotic dilution. The reduced level of intracellular potassium achieved during hyposmotic adaptation represents a balance between the necessity to contribute to osmotic equilibration and to maintain a potassium gradient across the axon membrane sufficient to produce appreciable axonal hyperpolarization during dilution of the bathing medium. This hyperpolarization tends to maintain the amplitude of the action potential, by compensating for reduction in overshoot (with decline in ENa), and by reducing sodium inactivation. This, together with the reduction in [Na+]1, enables overshooting action potentials of relatively large amplitude and rapid rise time to be maintained during more than tenfold dilution of the ionic and osmotic concentration of the bathing medium.


1964 ◽  
Vol 47 (4) ◽  
pp. 719-733 ◽  
Author(s):  
W. H. Herzog ◽  
R. M. Feibel ◽  
S. H. Bryant

In the giant axon of Loligo pealii, "aconitine potent" Merck added to the bath (10-7 to 1.25 x 10-6 gm/ml) (a) had no effect on resting membrane potential, membrane resistance and rectification, membrane response to subthreshold currents, critical depolarization, or action potential, but (b) on repetitive stimulation produced oscillations of membrane potential after the spike, depolarization, and decrease of membrane resistance. The effect sums with successive action potentials; it increases with concentration of aconitine, time of exposure, and frequency of stimulation. When the oscillations are large enough and the membrane potential is 51.6 ± SD 1.5 mv a burst of self-sustained activity begins; it usually lasts 20 to 70 sec. and at its end the membrane potential is 41.5 ± SD 1.9 mv. Repolarization occurs with a time constant of 2.5 to 11.1 min. Substitution of choline for external sodium after a burst hyperpolarizes the membrane to -70 mv, and return to normal external sodium depolarizes again beyond the resting membrane potential. The effect of aconitine on the membrane is attributed to an increase of sodium and potassium or chloride conductances following the action potential.


1993 ◽  
Vol 71 (3-4) ◽  
pp. 254-262 ◽  
Author(s):  
Jean-Pierre Bourreau ◽  
Hamid S. Banijamali ◽  
Cyril E. Challice

Damage to endocardial endothelium (denudation of the superficial tissue) by brief exposure to a 100-μL bolus of detergent (Triton X-100, 1% by volume stock) decreased the twitch force of papillary muscle (and trabeculae) by ~ 30% to a new but steady level without changes in resting tension. The decline in twitch force was evident immediately after the addition of Triton. Modification of the action potential measured from the contracting tissue appeared only later, when the change in contraction was already well established (i.e., after ~ 2 min). Action potential shortened in duration at 50% repolarization by ~ 100 ms and increased in plateau amplitude, although the latter increase was not always observed. A similar treatment procedure applied to strips of ventricular wall with the endocardium exposed to the superfusion solution resulted in a substantial decrease in action potential duration (~ 110 ms). In contrast, treatment of strips of epicardial layers of ventricular walls (with epicardial side facing the superfusion solution) did not produce a similar result. In β-stimulated (1 μM isoproterenol) and partially depolarized preparations (with 20 mM KCl), with intact endocardium, electrically evoked contractions were followed by aftercontractions, which were suppressed following Triton treatment. Action potentials in a depolarizing medium also shortened in duration (~ 50 ms), although following a delay (2–3 min). The decay to steady state of postextrasystolic potentiated beat was slower after endocardial damage than under control conditions. This suggested an increased Ca2+ recirculation through the sarcoplasmic reticulum between two consecutive beats (35% before Triton vs. 45% after Triton). Finally, in a medium containing 3 μM ryanodine, Triton treatment of the endocardial endothelium failed to induce any effect on either twitch force or action potential. Prolonged exposure to Triton X-100 (by a slow flow or high concentration) induced only deteriorating effects leading to substantial rise in the resting tension and generation of contractures and abbreviated action potentials with depressed plateau. These observations are consistent with the hypothesis that a modification in the sarcoplasmic reticulum function may, at least in part, be responsible for the observed changes in contractile function of the myocardium following endocardial damage with Triton treatment.Key words: endocardial endothelium, sarcoplasmic reticulum, ventricle, myocardial contraction.


1967 ◽  
Vol 47 (2) ◽  
pp. 357-373
Author(s):  
Y. PICHON ◽  
J. BOISTEL

1. The use of very fine-tipped and mechanically strong microelectrodes has allowed reliable recordings of resting and action potentials to be made in cockroach giant axons in sheathed and desheathed nerve cords. 2. When the microelectrode was withdrawn from a giant axon in an intact connective the first positive change in the potential from the resting level, was in most cases followed by a negative deflexion to the original zero level, the ‘sheath potential’. The values of this ‘sheath potential’ together with the resting potential, the action potential, the maximum rate of rise and maximum rate of fall of the action potential have been measured in three different salines. 3. In normal saline, resting potentials were lower in sheathed preparations (58·1 ± 55·4 mV.) than in desheathed ones (67·4 ± 6·2 mV.), whereas action potentials were higher in the former (103±5·9 mV.) than in the latter (85·9±4·6 mV.). 4. Elevation of K+ and Ca2+ concentrations in the saline to the haemolymph level resulted in a decrease of resting and action potentials in desheathed cords, to 57·3±5·3 mV. and 36·5±7·6 mV. respectively. No alterations in the membrane potentials were recorded in intact connectives bathed in this saline, the mean resting potential being 55·6±4·2 mV. and the mean action potential 107·9±6·0 mV. Local desheathing of the nerve cord led only to local disturbance of the resting and action potentials, thus indicating that diffusion processes along the extracellular spaces were very slow. 5. The use of a saline in which cation concentrations have been elevated to the extracellular level resulted in normal resting potentials (64·6±3·3 mV.) and action potentials (90·9±7·2 mV.) in desheathed cords, despite the relatively high potassium concentration (17·1 mM./l.). 6. Recordings of the maximum rates of rise and rates of fall showed that there was no significant modification in the shape of the action potential in these different experimental conditions. 7. The values of the ‘sheath potential’ were very variable from one impalement to another and it is suggested that this potential might be related to variations of the microelectrode tip potential bathed in different ionic solutions. 8. The low resting potentials and high action potentials of giant axons in intact nerve cords may result from an excess of inorganic cations in the extracellular fluid.


1987 ◽  
Vol 128 (1) ◽  
pp. 1-17
Author(s):  
L. A. Orr ◽  
E. M. Lieberman

A lightly platinized tungsten (Pt-W) wire electrode, axially inserted into a crayfish giant axon, causes the development of cardiac-like action potentials with durations of up to 4 s. The plateau in membrane potential typically occurs within 10 min of the start of action potential elongation. The effect occurs without passing current through the Pt-W electrode and is temporally related to a dramatic decrease in intracellular pH (pHi). Such an effect cannot be induced by a decrease in pHi produced by equilibrating the axon with HCO3(−)-CO2 solution (pH6), and NH4Cl rebound or direct intracellular injection of PO4(3-) buffer (pH 4 X 5). Action potential elongation is accompanied by a block of delayed rectification and the possibility that inward rectification also develops cannot be ruled out. Plateau generation requires Na+ and Ca2+ inward currents as demonstrated by abolition of the plateau by [Na+]o or [Ca2+]o depletion or treatment with tetrodotoxin (TTX) or verapamil. The block of outward rectification by Pt-W requires external Na+ or Ca2+. Action potential elongation produced by 3,4-diaminopyridine is not sensitive to verapamil and the waveform is different from that produced by Pt-W. The data support the possibility that different classes of excitable membranes have similar channel populations and that the functional differences between them reside in the inhibitory or masking influences that are present in the microenvironments of the various membrane channels.


1967 ◽  
Vol 50 (3) ◽  
pp. 505-517 ◽  
Author(s):  
Issei Seyama ◽  
Hiroshi Irisawa

It already has been well documented that the maximum rate of depolarization and amplitude of action potentials are directly dependent on [Na+]o in the vertebrate myocardium. Almost all studies have been carried out at low sodium concentration ranges by substituting NaCl for other substances. Action potentials should be demonstrable in higher sodium concentrations, but cells are inevitably damaged by osmotic changes. The blood of elasmobranchs is nearly isosmotic with sea water, but NaCl accounts for 54.5% of the osmotic pressure and 38.7% of it is maintained by urea molecules. Utilizing this special situation in elasmobranchs, the effect of high sodium concentration was studied up to 170% of normal sodium concentration, while still retaining isosmotic condition. The rate of depolarization, amplitude, and duration of the myocardial action potential all increased in direct proportion to [Na+]o, and no depressant effect on transmembrane action potentials was observed in solutions of high sodium concentration. With regard to depolarization rate, the regression curve fitted by the least squares method passed through zero within two standard errors. At high sodium levels, the overshoot changed as expected theoretically, but at lower ranges it deviated from the theoretical values. [Na+]i, and [K+]i, in this tissue have been determined, and these data are explained on the basis of the Na theory.


1958 ◽  
Vol 36 (9) ◽  
pp. 959-975 ◽  
Author(s):  
E. E. Daniel ◽  
H. Singh

In myometrium from pregnant cat, repetitive action potentials have been recorded during contraction. Using intracellular electrodes the depolarizations averaged 35 mv. Maximum rate of depolarization was 1–2 v/sec and the action potential duration varied from 250 milliseconds to much longer periods. Membrane reversal of up to 10 mv sometimes occurred. Total resistance decreased during depolarization and recovered during repolarization. Typical biphasic potentials were also recorded with extracellular electrodes. Their amplitude (peak to peak) varied from 0.3 to several millivolts and their duration (peak to peak) from 10–40 milliseconds. Reduction of external sodium concentration to as little as one-ninth normal (choline chloride or sucrose replacement) did not reduce the amplitudes of the resting or action potentials measured intracellularly or extracellularly, but decreased the action potential frequency. Membrane reversal still occurred with intracellular electrodes and the maximum rate of depolarization was unchanged. The rate of repolarization was increased so that the total duration of the action potential was 150 to 200 milliseconds. With extracellular electrodes, the peak to peak amplitudes were increased and the durations were unchanged. Further reduction of external sodium concentration to less than 15–20 meq/liter caused a contraction without further change in action potential configuration. Gradual relaxation and slowing of the repetition rate of action potentials occurred and resulted eventually in complete mechanical and electrical inactivity.Rabbit taenia coli were also studied and their electrical properties contrasted to those of cat myometrium. The conclusions were reached that: (1) the available evidence opposes the hypotheses that an inward sodium current accounts for depolarization in smooth muscle and (2) smooth muscles differed in their electrical properties and mechanisms of ion distribution not only from striate muscles but also from one another.


1958 ◽  
Vol 36 (1) ◽  
pp. 959-975 ◽  
Author(s):  
E. E. Daniel ◽  
H. Singh

In myometrium from pregnant cat, repetitive action potentials have been recorded during contraction. Using intracellular electrodes the depolarizations averaged 35 mv. Maximum rate of depolarization was 1–2 v/sec and the action potential duration varied from 250 milliseconds to much longer periods. Membrane reversal of up to 10 mv sometimes occurred. Total resistance decreased during depolarization and recovered during repolarization. Typical biphasic potentials were also recorded with extracellular electrodes. Their amplitude (peak to peak) varied from 0.3 to several millivolts and their duration (peak to peak) from 10–40 milliseconds. Reduction of external sodium concentration to as little as one-ninth normal (choline chloride or sucrose replacement) did not reduce the amplitudes of the resting or action potentials measured intracellularly or extracellularly, but decreased the action potential frequency. Membrane reversal still occurred with intracellular electrodes and the maximum rate of depolarization was unchanged. The rate of repolarization was increased so that the total duration of the action potential was 150 to 200 milliseconds. With extracellular electrodes, the peak to peak amplitudes were increased and the durations were unchanged. Further reduction of external sodium concentration to less than 15–20 meq/liter caused a contraction without further change in action potential configuration. Gradual relaxation and slowing of the repetition rate of action potentials occurred and resulted eventually in complete mechanical and electrical inactivity.Rabbit taenia coli were also studied and their electrical properties contrasted to those of cat myometrium. The conclusions were reached that: (1) the available evidence opposes the hypotheses that an inward sodium current accounts for depolarization in smooth muscle and (2) smooth muscles differed in their electrical properties and mechanisms of ion distribution not only from striate muscles but also from one another.


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