Transmembranal Action Potentials From Pregnant Uterus

1956 ◽  
Vol 187 (2) ◽  
pp. 338-340 ◽  
Author(s):  
J. Walter Woodbury ◽  
Donald M. McIntyre

For the first time overshooting action potentials of pregnant guinea pig uterus have been recorded intracellularly. Flexibly mounted ultramicroelectrodes were used. The largest action potential (AP) seen was 48 mv with an associated resting potential (RP) of 38 mv. The mean of 129 measurements of RP in four guinea pigs was 32.6 mv. The mean of 86 AP's was 21.9 mv. Although overshoot was seen only occasionally, the action potentials were always of the same order of magnitude as the resting potentials. It seems probable that the excitable mechanisms of uterine muscle though labile and variable are closely similar to those of other tissues.

1995 ◽  
Vol 74 (2) ◽  
pp. 673-683 ◽  
Author(s):  
A. A. Oyelese ◽  
D. L. Eng ◽  
G. B. Richerson ◽  
J. D. Kocsis

1. The effects of axotomy on the electrophysiologic properties of adult rat dorsal root ganglion (DRG) neurons were studied to understand the changes in excitability induced by traumatic nerve injury. Nerve injury was induced in vivo by sciatic nerve ligation with distal nerve transection. Two to four weeks after nerve ligation, a time when a neuroma forms, lumbar (L4 and L5) DRG neurons were removed and placed in short-term tissue culture. Whole cell patch-clamp recordings were made 5–24 h after plating. 2. DRG neurons were grouped into large (43–65 microns)-, medium (34–42 microns)-, and small (20–32 microns)- sized classes. Large neurons had short duration action potentials with approximately 60% having inflections on the falling phase of their action potentials. In contrast, action potentials of medium and small neurons were longer in duration and approximately 68% had inflections. 3. Pressure microejection of gamma-aminobutyric acid (GABA, 100 microM) or muscimol (100 microM) onto voltage-clamped DRG neurons elicited a rapidly desensitizing inward current that was blocked by 200 microM bicuculline. To measure the peak conductance induced by GABA or muscimol, neurons were voltage-clamped at a holding potential of -60 mV, and pulses to -80 mV and -100 mV were applied at a rate of 2.5 or 5 Hz during drug application. Slope conductances were calculated from plots of whole cell current measured at each of these potentials. 4. GABA-induced currents and conductances of control DRG neurons increased progressively with cell diameter. The mean GABA conductance was 36 +/- 10 nS (mean +/- SE) in small neurons, 124 +/- 21 nS in medium neurons, and 527 +/- 65 nS in large neurons. 5. After axotomy, medium neurons had significantly larger GABA-induced conductances compared with medium control neurons (390 +/- 50 vs. 124 +/- 21; P < 0.001). The increase in GABA conductance of medium neurons was associated with a decrease in duration of action potentials. In contrast, small neurons had no change in GABA conductance or action potential duration after ligation. The GABA conductance of large control neurons was highly variable, and ligation resulted in an increase that was significant only for neurons > 50 microns. The mean action potential duration in large neurons was not significantly changed, but neurons with inflections on the falling phase of the action potential were less common after ligation. There was no difference in resting potential or input resistance between control and ligated groups, except that the resting potential was less negative in small cells after axotomy.(ABSTRACT TRUNCATED AT 400 WORDS)


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.


1994 ◽  
Vol 72 (4) ◽  
pp. 382-393 ◽  
Author(s):  
Qi-Ying Liu ◽  
Mario Vassalle

The effects of some components of ischemia on the oscillatory (Vos) and nonoscillatory (Vex) potentials and respective currents (Ios and Iex), as well as their mechanisms, were studied in guinea pig isolated ventricular myocytes by means of a single-microelectrode, discontinuous voltage clamp method. Repetitive activations induced not only Vos and Ios, but also Vex and Iex. A small decrease in resting potential caused an immediate increase in Vos followed by a gradual increase due to the longer action potential. Immediate and gradual increases in Ios also occurred during voltage clamp steps. A small depolarization increased Vos and Vex, and facilitated the induction of spontaneous discharge by fast drive. At Vh where INa is inactivated, depolarizing steps induced larger Ios and Iex, indicating the importance of the Na-independent Ca loading. High [K]odecreased the resting potential, but also Vos, Vex, Ios, Iex, and ICa. In high [K]o, depolarization still increased Vos and Vex. Norepinephrine (NE) enhanced Vos and Vex, and also Ios and Iex, during voltage clamp steps. High [K]o antagonized NE effects, and NE those of high [K]o. In conclusion, on depolarization, Vos and Ios immediately increase through a voltage-dependent mechanism; and then Vos and Ios gradually increase, apparently through an increased Ca load related to the longer action potentials and the Na–Ca exchange. The depolarization induced by Vex may contribute to increase Vos size. Vos and Vex are similarly influenced by different procedures that modify Ca load. The arrhythmogenic events are enhanced by the simultaneous presence of depolarization, faster rate, or NE. Instead, high [K]o decreases Vos and Vex by decreasing ICa and opposes the effects of NE. The voltage clamp results show that potentiation and antagonism between different components of ischemia are due primarily to changes in Ca loading and not to changes in action potential configuration.Key words: ischemia, arrhythmias, oscillatory and nonoscillatory potentials and currents, norepinephrine, potassium.


1992 ◽  
Vol 70 (9) ◽  
pp. 1236-1246 ◽  
Author(s):  
Jean Marc Renaud ◽  
Peter Light

The effects of increasing the extracellular K+ concentration on the capacity to generate action potentials and to contract were tested on unfatigued muscle fibers isolated from frog sartorius muscle. The goal of this study was to investigate further the role of K+ in muscle fatigue by testing whether an increased extracellular K+ concentration in unfatigued muscle fibers causes a decrease in force similar to the decrease observed during fatigue. Resting and action potentials were measured with conventional microelectrodes. Twitch and tetanic force was elicited by field stimulation. At pHo (extracellular pH) 7.8 and 3 mmol K+∙L−1 (control), the mean resting potential was −86.6 ± 1.7 mV (mean ± SEM) and the mean overshoot of the action potential was 5.6 ± 2.5 mV. An increased K+ concentration from 3 to 8.0 mmol∙L−1 depolarized the sarcolemma to −72.2 ± 1.4 mV, abolished the overshoot as the peak potential during an action potential was −12.0 ± 3.9 mV, potentiated the twitch force by 48.0 ± 5.7%, but did not affect the tetanic force (maximum force) and the ability to maintain a constant force during the plateau phase of a tetanus. An increase to 10 mmol K+∙L−1 depolarized the sarcolemma to −70.1 ± 1.7 mV and caused large decreases in twitch (31.6 ± 26.1%) and tetanic (74.6 ± 12.1%) force. Between 3 and 9 mmol K+∙L−1, the effects of K+ at pHo 7.2 (a pHo mimicking the change in interstitial pH during fatigue) and 6.4 (a pHo known to inhibit force recovery following fatigue) on resting and action potentials as well as on the twitch and tetanic force were similar to those at pHo 7.8. Above 9 mmol K+∙L−1 significant differences were found in the effect of K+ between pHo 7.8 and 7.2 or 6.4. In general, the decrease in peak action potential and twitch and tetanic force occurred at higher K+ concentrations as the pHo was more acidic. The results obtained in this study do not support the hypothesis that an accumulation of K+ at the surface of the sarcolemma is sufficiently large to suppress force development during fatigue. The possibility that the K+ concentration in the T tubules reaches the critical K+ concentration necessary to cause a failure of the excitation–contraction coupling mechanism is discussed.Key words: excitation–contraction coupling, fatigue, potassium, tetanus, twitch.


1964 ◽  
Vol 206 (2) ◽  
pp. 270-282 ◽  
Author(s):  
William Sleator ◽  
Robert F. Furchgott ◽  
Taisija De Gubareff ◽  
Vivian Krespi

Simultaneous recordings were made of action potential ( AP) and contractile strength ( CS) of electrically driven isolated left atria of guinea pigs at 25–27 C under various experimental conditions which alter CS. Reduction of CS produced by decreasing frequency from 1/sec to 0.1/sec, or by spontaneous failure, was associated with only small changes, if any, in AP configuration. The increased CS produced by strophanthin-K or high calcium was associated with shortening of the AP plateau duration; treatment with ryanodine increased AP plateau duration, and decreased CS. The first beat following a 3- to 10-sec rest interval (postrest ( PR) beat) exhibited greater CS, and an AP with shorter plateau and more pronounced "tailing off" than steady-state controls. With high calcium or strophanthin present, PR beats and steady-state beats were nearly identical in both CS and AP. After ryanodine, PR beats were markedly reduced in CS and had prolonged AP plateaus; these changes could be reversed by high calcium or strophanthin. A hypothesis is introduced which accounts for changes in CS under these conditions.


1985 ◽  
Vol 119 (1) ◽  
pp. 287-300 ◽  
Author(s):  
M.J. O'DONNELL

1. Action potentials (APs) have been recorded for the first time from the oocytes of an arthropod, the haematophagous insect Rhodnius prolixus. In saline containing 2mmol l−1 calcium, APs could be evoked by depolarizing the oocyte membrane from its resting potential of −50mV to a threshold between −35 and −40mV. The mean duration and overshoot of the APs were 2.6s and +16mV, respectively. 2. APs could not be evoked by depolarization of follicular epithelia that had been separated from the oocyte. It is concluded that the APs are generated at the oocyte cell membrane. 3. The overshoot of the APs was unaffected by the addition of tetrodotoxin (3 μmol l−1) or the removal of Na+ (choline replacement) from the bathing saline. 4. APs could be reversibly blocked by 1 mmol l−1 La3+ or 10 mmol l−1 Co2+. Verapamil at 50 μmol l−1 and l00 μmol l−1 reduced AP duration by 30% and 50%, respectively. The overshoot increased by 30 mV when bathing saline Ca2+ concentration was increased from 2 to 20 mmol l−1. These results suggested the occurrence of a Ca2+ influx during the rising phase of the AP. 5. Addition of Ba2+ increased the overshoot and duration of APs. In Ca2+-free saline, addition of 2 mmol l−1 Ba2+ resulted in the spontaneous production of a series of action potentials. The duration of APs was as long as 120 s in 20 mmol l−1 Ba2+ saline. It is suggested that Ba2+ may block a voltage-sensitive potassium conductance. 6. Possible functions of action potentials during fertilization and early development are discussed.


1962 ◽  
Vol 202 (5) ◽  
pp. 950-956 ◽  
Author(s):  
Nancy S. Peterson ◽  
George A. Feigen

Transmembrane potentials and contractility were measured in driven guinea pig atria according to conventional methods. The effects of nitrate were studied by substituting 40, 60, 80, and 100% of the chlorides with nitrates, and the influence of Ca and Na was determined by varying their ratio in the presence of 40% nitrate. The magnitudes of the resting potential, action potential, and overshoot were reversibly reduced; the rate of depolarization slowed; and the amplitude of contraction decreased as the proportion of nitrate to chloride was increased in the nutrient medium. In general, the initial phase of the repolarization was shortened, but the terminal phase was slowed. The duration of irresponsiveness was prolonged, and the maximum following frequency was reduced by nitrate. Calcium appeared to antagonize the deleterious effects of nitrate on all of the parameters except the resting potential, the negative afterpotential, and the irresponsive period.


1956 ◽  
Vol 40 (1) ◽  
pp. 1-17 ◽  
Author(s):  
F. H. Shaw ◽  
Shirley E. Simon ◽  
B. M. Johnstone

The sartorius muscles of 320 toads have been analyzed for Na+ and K+. There is a wide variation in the Na+ content which when calculated intracellularly varied from 0 m.eq./kg. to 58 m.eq./kg. In particular it was found that the distribution of internal Na+ in the intact animal was such that only 17 per cent of the muscles should give from the Nernst equation the observed overshoot of 37 mv. In contrast to this wide variation the K+ content is comparatively constant, the range being 71 to 112 m.eq./kg. The mean observed resting potential of 87 mv. agreed well with the potential calculated from the mean intracellular K+ by the Nernst equation. Analyses of plasma show that the Na+ content is constant at 130 m.eq./liter, and the K+ is 3.0 m.eq./liter. The resting and action potentials of 77 muscles have been recorded and then the muscles have been analyzed. The results have shown that there is no correlation between the level of intracellular Na+ and the overshoot. Furthermore the apparent correlation between the average K+ content and the average resting potential has been shown to be fortuitous, when the correlation in individual muscles is considered. When a muscle is soaked in Ringer solution for several hours there is a gain of Na+ and a loss of K+. These shifts should result in changes in the respective potentials, but such changes were not found. The above findings have been discussed in the light of the present theories that the resting potential and the action potential are directly related to the ionic ratio across the membrane. Our results very definitely do not support the theory that the overshoot is related to the Na+ gradient, and this also applies with respect to the K+ gradient and the resting potential.


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.


1999 ◽  
Vol 277 (2) ◽  
pp. H826-H833 ◽  
Author(s):  
Seiko Tanabe ◽  
Toshio Hata ◽  
Masayasu Hiraoka

To explore a possible ionic basis for the prolonged Q-T interval in women compared with that in men, we investigated the electrophysiological effects of estrogen in isolated guinea pig ventricular myocytes. Action potentials and membrane currents were recorded using the whole cell configuration of the patch-clamp technique. Application of 17β-estradiol (10–30 μM) significantly prolonged the action potential duration (APD) at 20% (APD20) and 90% repolarization (APD90) at stimulation rates of 0.1–2.0 Hz. In the presence of 30 μM 17β-estradiol, APD20 and APD90 at 0.1 Hz were prolonged by 46.2 ± 17.1 and 63.4 ± 11.7% of the control ( n = 5), respectively. In the presence of 30 μM 17β-estradiol the peak inward Ca2+ current ( I CaL) was decreased to 80.1 ± 2.5% of the control ( n = 4) without a shift in its voltage dependence. Application of 30 μM 17β-estradiol decreased the rapidly activating component of the delayed outward K+ current ( I Kr) to 63.4 ± 8% and the slowly activating component ( I Ks) to 65.8 ± 8.7% with respect to the control; the inward rectifier K+ current was barely affected. The results suggest that 17β-estradiol prolonged APD mainly by inhibiting the I Kcomponents I Krand I Ks.


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