Electrophysiology of the Giant Nerve Cell Bodies of Limnaea Stagnalis (L.) (Gastropoda: Pulmonata)

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.

2001 ◽  
Vol 86 (6) ◽  
pp. 2998-3010 ◽  
Author(s):  
Nace L. Golding ◽  
William L. Kath ◽  
Nelson Spruston

In hippocampal CA1 pyramidal neurons, action potentials are typically initiated in the axon and backpropagate into the dendrites, shaping the integration of synaptic activity and influencing the induction of synaptic plasticity. Despite previous reports describing action-potential propagation in the proximal apical dendrites, the extent to which action potentials invade the distal dendrites of CA1 pyramidal neurons remains controversial. Using paired somatic and dendritic whole cell recordings, we find that in the dendrites proximal to 280 μm from the soma, single backpropagating action potentials exhibit <50% attenuation from their amplitude in the soma. However, in dendritic recordings distal to 300 μm from the soma, action potentials in most cells backpropagated either strongly (26–42% attenuation; n = 9/20) or weakly (71–87% attenuation; n = 10/20) with only one cell exhibiting an intermediate value (45% attenuation). In experiments combining dual somatic and dendritic whole cell recordings with calcium imaging, the amount of calcium influx triggered by backpropagating action potentials was correlated with the extent of action-potential invasion of the distal dendrites. Quantitative morphometric analyses revealed that the dichotomy in action-potential backpropagation occurred in the presence of only subtle differences in either the diameter of the primary apical dendrite or branching pattern. In addition, action-potential backpropagation was not dependent on a number of electrophysiological parameters (input resistance, resting potential, voltage sensitivity of dendritic spike amplitude). There was, however, a striking correlation of the shape of the action potential at the soma with its amplitude in the dendrite; larger, faster-rising, and narrower somatic action potentials exhibited more attenuation in the distal dendrites (300–410 μm from the soma). Simple compartmental models of CA1 pyramidal neurons revealed that a dichotomy in action-potential backpropagation could be generated in response to subtle manipulations of the distribution of either sodium or potassium channels in the dendrites. Backpropagation efficacy could also be influenced by local alterations in dendritic side branches, but these effects were highly sensitive to model parameters. Based on these findings, we hypothesize that the observed dichotomy in dendritic action-potential amplitude is conferred primarily by differences in the distribution, density, or modulatory state of voltage-gated channels along the somatodendritic axis.


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 50 (7) ◽  
pp. 1929-1953 ◽  
Author(s):  
Alfred Strickholm ◽  
B. Gunnar Wallin

The changes in membrane potential of isolated, single crayfish giant axons following rapid shifts in external ion concentrations have been studied. At normal resting potential the immediate change in membrane potential after a variation in external potassium concentration is quite marked compared to the effect of an equivalent chloride change. If the membrane is depolarized by a maintained potassium elevation, the immediate potential change due to a chloride variation becomes comparable to that of an equivalent potassium change. There is no appreciable effect on membrane potential when external sodium is varied, at normal or at a depolarized membrane potential. Starting from the constant field equation, expressions for the permeability ratios PCl/PK, PNa/PK, and for intracellular potassium and chloride concentrations are derived. At normal resting membrane potential, PCl/PK is 0.13 but at a membrane potential of -53 mv (external potassium level increased about five times) it is 0.85. The intracellular concentrations of potassium and chloride are estimated to be 233 and 34 mM, respectively, and it is pointed out that this is not compatible with ions distributed in a Nernst equilibrium across the membrane. It is also stressed that the information given by a plot of membrane potential vs. the logarithm of external potassium concentrations is very limited and rests upon several important assumptions.


1993 ◽  
Vol 70 (5) ◽  
pp. 1874-1884 ◽  
Author(s):  
K. Morita ◽  
G. David ◽  
J. N. Barrett ◽  
E. F. Barrett

1. The hyperpolarization that follows tetanic stimulation was recorded intra-axonally from the internodal region of intramuscular myelinated motor axons. 2. The peak amplitude of the posttetanic hyperpolarization (PTH) that followed stimulation at 20-100 Hz for < or = 35 s increased with increasing train duration, reaching a maximum of 22 mV. PTH decayed over a time course that increased from tens to hundreds of seconds with increasing train duration. For a given frequency of stimulation the time integral of PTH was proportional to the number of stimuli in the train, averaging 3-4 mV.s per action potential. 3. Ouabain (0.1-1 mM) and cyanide (1 mM) depolarized the resting potential and abolished PTH. Tetanic stimulation in ouabain was followed by a slowly decaying depolarization (probably due to extra-axonal K+ accumulation) whose magnitude and duration increased as the duration of the train increased. 4. Axonal input resistance showed no consistent change during PTH in normal solution but increased during PTH in the presence of 3 mM Cs+ (which blocks axonal inward rectifier currents). 5. PTH was abolished when bath Na+ was replaced by Li+ or choline. PTH persisted after removal of bath Ca2+ and addition of 2 mM Mn2+. 6. Removal of bath K+ abolished the PTH recorded after brief stimulus trains and greatly reduced the duration of PTH recorded after longer stimulus trains. 7. A brief application of 10 mM K+, which normally depolarizes axons, produced a ouabain-sensitive hyperpolarization in axons bathed in K(+)-free solution. 8. These observations suggest that in these myelinated axons PTH is produced mainly by activation of an electrogenic Na(+)-K(+)-ATPase, rather than by changes in K+ permeability or transmembrane [K+] gradients. This conclusion is supported by calculations showing agreement between estimates of Na+ efflux/impulse based on PTH measurements and estimates of Na+ influx/impulse based on nodal voltage-clamp measurements. Pump activity also appears to contribute to the resting potential. 9. The stimulus intensity required to initiate a propagating action potential increased during PTH but decreased during the posttetanic depolarization recorded in ouabain. Thus changes in axonal excitability after tetanic stimulation correlate with changes in the posttetanic membrane potential. 10. Action potentials that propagated during PTH had a larger peak amplitude and were followed by a larger and longer depolarizing afterpotential than action potentials elicited at the resting potential. This enhancement of the depolarizing afterpotential is consistent with previous reports of an increased superexcitable period after action potentials evoked during PTH.


1964 ◽  
Vol 206 (1) ◽  
pp. 205-210 ◽  
Author(s):  
Makoto Kobayashi ◽  
Hiroshi Irisawa

Action potentials of the smooth muscle of cat ureter were studied by using ultramicroelectrodes. Among 193 penetrations, the resting potential averaged 45 mv and the amplitude of action potential 32 mv. In four instances a slight overshoot was recorded. Action potential consisted of a relatively rapid rising phase followed by a slow repolarization phase, and its duration was about 0.3 sec. Effects of sodium deficiency on action potential were studied by using three different sodium substitutes. Both the height and the rising rate of action potential decreased as the concentration of extracellular sodium was reduced, indicating that the action potential of ureter muscle can be explained on the basis of sodium theory. The duration of the action potential was prolonged when sucrose or choline chloride was used as a sodium substitute; on the other hand, it shortened when tris chloride was employed. The essential role of sodium ions in the development of the action potential in ureter muscle is discussed.


1984 ◽  
Vol 62 (5) ◽  
pp. 596-599
Author(s):  
Julio Alvarez ◽  
Francisco Dorticós ◽  
Jesús Morlans

Experiments were performed to study the effects of hypoxia on the characteristics of premature action potentials of rabbit papillary muscles. At normal resting potential, the duration of the premature action potential at the shortest coupling intervals was always greater than that of the control response. As the coupling interval was increased beyond 150 ms, the duration of the premature action potential regained control values. In cells depolarized to −70 mV by KCl, early lengthening of the premature response was attenuated. After 60 min of hypoxia, recovery of action potential duration at normal and reduced resting potentials was accelerated. The maximum rate of depolarization and its reactivation time constant were not affected by 60 min of hypoxia. It is suggested that intracellular free Ca is important in the control of action potential duration via the outward background potassium current.


1988 ◽  
Vol 254 (5) ◽  
pp. C675-C683 ◽  
Author(s):  
V. Nassar-Gentina ◽  
H. B. Pollard ◽  
E. Rojas

Membrane potentials of medullary chromaffin cells of the adrenal gland of the mouse were measured in situ. Resting potential (-54.3 +/- 8.8 mV) depended on extracellular [K+] as predicted by the constant-field equation with a permeability ratio, PNa/PK, of 0.09. Current-voltage (I-V) relationships showed that the current is rectified across the chromaffin cell membrane. A rectification ratio of 0.4 was calculated from the slopes of the I-V curves for positive (41 +/- 26 M omega) and negative (103 +/- M omega) currents. Because input resistance for a resting chromaffin cell in isolation is approximately 5 G omega, the chromaffin cells in situ behave as if they were electrically coupled. Most cells responded to depolarizing current pulses with repetitive action potentials, but only 50% of them showed spontaneous electrical activity. Spontaneous activity was often seen in the presence of tetrodotoxin (3 microM). Although the application of the K+-channel blockers tetraethylammonium and Ba2+ greatly increased the amplitude of the action potentials, only Ba2+ induced continuous electrical activity. Application of acetylcholine (ACh) always depolarized the cell membrane. This effect was blocked by atropine but not by D-tubocurarine, suggesting that ACh stimulation of chromaffin cells in the mouse involves activation of muscarinic receptors.


1978 ◽  
Vol 71 (1) ◽  
pp. 47-67 ◽  
Author(s):  
D J Miller ◽  
A Mörchen

Resting and action potentials were recorded from superfused strips of frog ventricle. Reducing the bathing calcium concentration ([Ca2+]0) with or without ethylene glycol-bis(beta-aminoethyl ether)N,N,N',N'-tetraacetate (EGTA) prolongs the action potential (AP). The change in the duration of the AP extends over many minutes, but is rapidly reversed by restoring calcium ions. Other changes (e.g., in resting potential and overshoot) are, however, only more slowly reversed. Reducing [Ca2+]0 with 0.2, 2, or 5 mM EGTA produces progressively greater prolongation of AP; maximum values were well in excess of 1 min. This prolongation can be reversed by other divalent cations in EGTA (Mg2+, Sr2+) or Ca-free (Mn2+) solutions, or by acetylcholine. Barium ions increase AP duration in keeping with their known effect on potassium conductance. D600, which blocks the slow inward current in cardiac muscle, is without effect on the action potentials recorded in EGTA solutions, or on the time course and extent of the recovery to normal duration upon restoring calcium ions. It is concluded that divalent cations exert an influence on membrane potassium conductance extracellularly in frog heart. The cell membrane does not become excessively "leaky" in EGTA solutions.


1973 ◽  
Vol 58 (1) ◽  
pp. 15-28
Author(s):  
D. B. SATTELLE

1. Resting potentials and action potentials recorded from in situ, intact and desheathed giant neurones of the right parietal ganglion of Limnaea stagnalis are of similar magnitude. Ganglionic potential profiles reveal the absence of a sheath potential. It is concluded that the extra-neuronal fluid has a similar ionic composition to the blood (bathing medium). 2. A 34 mV decade potassium slope is obtained for both intact and de-sheathed neurones. Depolarization of the neuronal membrane takes place rapidly in intact preparations, and the de-sheathing procedure significantly increases the rate of depolarization. 3. A reduction in temperature from 23 to 8°C only slightly prolongs the time-course of depolarization of an intact neurone. When the concentration of potassium in the fluid bathing the surface of an intact ganglion is elevated, the concentration of this cation at the neuronal surface changes exponentially with time. It is suggested therefore that diffusion along the extracellular channels is the mechanism and pathway for the movement of potassium ions through the right parietal ganglion of Limnaea stagnalis.


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.


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