scholarly journals Time Course of TEA+-Induced Anomalous Rectification in Squid Giant Axons

1966 ◽  
Vol 50 (2) ◽  
pp. 491-503 ◽  
Author(s):  
Clay M. Armstrong
Keyword(s):  
Time Course ◽  
Sea Water ◽  
Resting Potential ◽  
Tetraethylammonium Chloride ◽  
Giant Axons ◽  
Interesting Conclusion ◽  
Simple Kinetic Model ◽  
K Current ◽  
Current Record ◽  
External K

Changes in the voltage clamp currents of squid giant axons wrought by low axoplasmic TEA+ (tetraethylammonium chloride) concentrations (0.3 mM and above) are described. They are: (a) For positive steps from the resting potential in sea water, the K+ current increases, decreases, then increases, instead of increasing monotonically. (b) For positive steps from the resting potential in 440 mM external K+, the current has an exponentially decaying component, whose decay rate increases with axoplasmic [TEA+]. The control currents increase monotonically. (c) For negative steps from the resting potential in 440 mM external K+, the current record has a peak followed by a decay that is slow relative to the control. The control record decreases monotonically. Qualitatively these findings can be described by a simple kinetic model, from which, with one assumption, it is possible to calculate the rate at which K+ ions move through the K+ channels. An interesting conclusion from (c) is that the channels cannot be closed by the normal voltage-sensitive mechanism (described by Hodgkin and Huxley) until they are free of TEA+.

Long-term Adaptations of Sabella Giant Axons to Hyposmotic Stress

1978 ◽  
Vol 75 (1) ◽  
pp. 253-263
Author(s):  
J. E. TREHERNE ◽  
Y. PICHON
Keyword(s):  
Sea Water ◽  
Potassium Concentration ◽  
Resting Potential ◽  
Sodium Permeability ◽  
Bathing Medium ◽  
Appreciable Change ◽  
Axon Membrane ◽  
Giant Axons

Reprint requests should be addressed to Dr Treherne. Sabella is a euryhaline osmoconformer which is killed by direct transfer to 50% sea water, but can adapt to this salinity with progressive dilution of the sea water. The giant axons were adapted to progressive dilution of the bathing medium (both in vivo and in vitro) and were able to function at hyposmotic dilutions (down to 50%) sufficient to induce conduction block in unadapted axons. Hyposmotic adaptation of the giant axon involves a decrease in intracellular potassium concentration which tends to maintain a relatively constant resting potential during adaptation despite the reduction in external potassium concentration. There is no appreciable change in the intracellular sodium concentration, but the relative sodium permeability of the active membrane increases during hyposmotic adaptation. This increase partially compensates for the reduction in sodium gradient across the axon membrane, during dilution of the bathing media, by increasing the overshoot of the action potentials recorded in hyposmotically adapted axons.

Existence of a transient outward K+ current in guinea pig cardiac myocytes

2000 ◽  
Vol 279 (1) ◽  
pp. H130-H138 ◽  
Author(s):  
Gui-Rong Li ◽  
Baofeng Yang ◽  
Haiying Sun ◽  
Clive M. Baumgarten
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Outward Current ◽  
Resting Potential ◽  
Transient Outward Current ◽  
Time Constants ◽  
Zero Current ◽  
Steady State Inactivation ◽  
K Current ◽  
External K

A novel transient outward K+current that exhibits inward-going rectification ( I to.ir) was identified in guinea pig atrial and ventricular myocytes. I to.ir was insensitive to 4-aminopyridine (4-AP) but was blocked by 200 μmol/l Ba2+or removal of external K+. The zero current potential shifted 51–53 mV/decade change in external K+. I to.ir density was twofold greater in ventricular than in atrial myocytes, and biexponential inactivation occurs in both types of myocytes. At −20 mV, the fast inactivation time constants were 7.7 ± 1.8 and 6.1 ± 1.2 ms and the slow inactivation time constants were 85.1 ± 14.8 and 77.3 ± 10.4 ms in ventricular and atrial cells, respectively. The midpoints for steady-state inactivation were −36.4 ± 0.3 and −51.6 ± 0.4 mV, and recovery from inactivation was rapid near the resting potential (time constants = 7.9 ± 1.9 and 8.8 ± 2.1 ms, respectively). I to.ir was detected in Na+-containing and Na+-free solutions and was not blocked by 20 nmol/l saxitoxin. Action potential clamp revealed that I to.ir contributed an outward current that activated rapidly on depolarization and inactivated by early phase 2 in both tissues. Although it is well known that 4-AP-sensitive transient outward current is absent in guinea pig, this Ba2+-sensitive and 4-AP-insensitive K+ current has been overlooked.

Recurrent Inhibition in the Giant-Fibre System of the Crayfish and Its Effect on the Excitability of the Escape Response

1968 ◽  
Vol 48 (3) ◽  
pp. 545-567
Author(s):  
ALAN ROBERTS
Keyword(s):  
Escape Response ◽  
Time Course ◽  
Excitatory Input ◽  
Recurrent Inhibition ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Giant Fibre ◽  
Impulse Generation ◽  
Giant Axons ◽  
Slow Potentials

1. A single impulse in any one of the central giant fibres of the crayfish is sufficient to evoke a full escape response. 2. Following such a single impulse a search was made for inhibitory processes of similar duration to the driving movement of the escape response. 3. There is no inhibition of flexor motoneurones or muscles to prevent response to impulses in the central giant axons during the escape response. However, following an impulse in any central giant, intracellular recording showed that there is inhibition of excitatory input to the lateral giants in the abdomen. This inhibition suppresses impulse generation for the duration of the escape response. 4. The inhibition coincides with slow, depolarizing potentials in the lateral giants. These have an equilibrium potential between the normal resting potential and the threshold for spike initiation in the lateral giants. During these slow potentials there is a postsynaptic resistance decrease coinciding very closely in time course with the inhibition of excitatory input. The slow potentials are therefore identified as IPSPs (inhibitory postsynaptic potentials) because of their close association with a postsynaptic inhibitory process. This conclusion is endorsed: (a) by the absence of similar slow potentials in the abdominal medial giants which have no excitatory input at this location, and (b) by the diminution of the slow potentials by picrotoxin, a drug known to block inhibition at many crustacean synapses. 5. When evoked repetitively, even at low frequencies like 0.25 per sec, the IPSPs decrease in amplitude. No other ‘after effects’ of repeated activity were found. 6. Attempts to localize the inhibitory synapses are frustrated by the large space constant of the lateral giants. However, the evidence is compatible with the notion that inhibition originates within each abdominal ganglion. There is occlusion and crossed response decrement between the central giant axons evoking lateral giant inhibition. This suggests that the different presynaptic fibres excite some common inhibitory pathway in each ganglion. Further experiments showed that pathways producing inhibition in one ganglion can be excited in others. Interneuronal arrangements to explain properties of the inhibitory pathways are discussed. 7. Two functions are suggested for the recurrent inhibition in the crayfish lateral giants. First, it may limit the number of impulses that are evoked by a single afferent excitatory volley. Secondly, it may coordinate successive escape responses by suppressing impulse generation in the lateral giants during such responses.

scholarly journals Rapid recovery from K current inactivation on membrane hyperpolarization in molluscan neurons.

1984 ◽  
Vol 84 (6) ◽  
pp. 861-875 ◽  
Author(s):  
P Ruben ◽  
S Thompson
Keyword(s):  
Time Course ◽  
Outward Current ◽  
Rapid Recovery ◽  
Resting Potential ◽  
Molluscan Neurons ◽  
Membrane Hyperpolarization ◽  
Time Constants ◽  
Recovery From Inactivation ◽  
Voltage Dependent ◽  
K Current

Recovery from K current inactivation was studied in molluscan neurons using two-microelectrode and internal perfusion voltage clamps. Experiments were designed to study the voltage-dependent delayed outward current (IK) without contamination from other K currents. The amount of recovery from inactivation and the rate of recovery increase dramatically when the membrane potential is made more negative. The time course of recovery at the resting potential, -40 mV, is well fit by a single exponential with a time constant of 24.5 s (n = 7). At more negative voltages, the time course is best fit by the sum of two exponentials with time constants at -90 mV of 1.7 and 9.8 s (n = 7). In unclamped cells, a short hyperpolarization can cause rapid recovery from inactivation that results in a shortening of the action potential duration. We conclude that there are two inactivated states of the channel and that the time constants for recovery from both states are voltage dependent. The results are discussed in terms of the multistate model for K channel gating that was developed by R. N. Aldrich (1981, Biophys. J., 36:519-532).

scholarly journals Canine Myocytes Represent a Good Model for Human Ventricular Cells Regarding Their Electrophysiological Properties

2021 ◽  
Vol 14 (8) ◽  
pp. 748
Author(s):  
Péter P. Nánási ◽  
Balázs Horváth ◽  
Fábián Tar ◽  
János Almássy ◽  
Norbert Szentandrássy ◽  
...  
Keyword(s):  
Action Potential ◽  
Time Course ◽  
Laboratory Animals ◽  
Delayed Rectifier ◽  
Ion Currents ◽  
Human Cardiomyocytes ◽  
Ventricular Cells ◽  
Repolarization Reserve ◽  
Electrophysiological Studies ◽  
K Current

Due to the limited availability of healthy human ventricular tissues, the most suitable animal model has to be applied for electrophysiological and pharmacological studies. This can be best identified by studying the properties of ion currents shaping the action potential in the frequently used laboratory animals, such as dogs, rabbits, guinea pigs, or rats, and comparing them to those of human cardiomyocytes. The authors of this article with the experience of three decades of electrophysiological studies, performed in mammalian and human ventricular tissues and isolated cardiomyocytes, summarize their results obtained regarding the major canine and human cardiac ion currents. Accordingly, L-type Ca2+ current (ICa), late Na+ current (INa-late), rapid and slow components of the delayed rectifier K+ current (IKr and IKs, respectively), inward rectifier K+ current (IK1), transient outward K+ current (Ito1), and Na+/Ca2+ exchange current (INCX) were characterized and compared. Importantly, many of these measurements were performed using the action potential voltage clamp technique allowing for visualization of the actual current profiles flowing during the ventricular action potential. Densities and shapes of these ion currents, as well as the action potential configuration, were similar in human and canine ventricular cells, except for the density of IK1 and the recovery kinetics of Ito. IK1 displayed a largely four-fold larger density in canine than human myocytes, and Ito recovery from inactivation displayed a somewhat different time course in the two species. On the basis of these results, it is concluded that canine ventricular cells represent a reasonably good model for human myocytes for electrophysiological studies, however, it must be borne in mind that due to their stronger IK1, the repolarization reserve is more pronounced in canine cells, and moderate differences in the frequency-dependent repolarization patterns can also be anticipated.

Is cyclic guanosine monophosphate the internal 'second messenger' for cholinergic actions on central neurons?

1976 ◽  
Vol 54 (2) ◽  
pp. 172-176 ◽  
Author(s):  
K. Krnjević ◽  
E. Puil ◽  
R. Werman
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Resting Potential ◽  
Electrical Excitability ◽  
Spinal Motoneurons ◽  
Central Neurons ◽  
Intracellular Cgmp ◽  
Post Synaptic Potential

The most consistent effects produced by intracellular injections of guanosine 3′,5′-cyclic monophosphate (cGMP) (but not 5′-guanosine 5′-monophosphate in spinal motoneurons of cats are a rise in membrane conductance, acceleration in time course of spike potentials, and accentuation of the post-spike hyperpolarization. Associated changes in resting potential are smaller, less constant, and more often in the depolarizing than hyperpolarizing direction. cGMP tends to increase electrical excitability but reduces excitatory post-synaptic potential amplitudes. Most of the effects of intracellular cGMP are quite different from, or indeed opposite to, those of either extra- or intracellular applications of acetylcholine and therefore not consistent with the proposal that cGMP is the internal mediator of muscarinic actions.

Inward rectification in rat nucleus accumbens neurons

1989 ◽  
Vol 62 (6) ◽  
pp. 1280-1286 ◽  
Author(s):  
N. Uchimura ◽  
E. Cherubini ◽  
R. A. North
Keyword(s):  
Steady State ◽  
Nucleus Accumbens ◽  
Time Course ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Inward Rectification ◽  
Resting Membrane Potential ◽  
Potential Range ◽  
Inward Current ◽  
Rat Nucleus Accumbens

1. Intracellular recordings were made from neurons in slices cut from the rat nucleus accumbens septi. Membrane currents were measured with a single-electrode voltage-clamp amplifier in the potential range -50 to -140 mV. 2. In control conditions (2.5 mM potassium), the resting membrane potential of the neurons was -83.4 +/- 1.1 (SE) mV (n = 157). Steady state membrane conductance was voltage dependent, being 34.8 +/- 1.7 nS (n = 25) at -100 mV and 8.0 +/- 0.7 nS (n = 25) at -60 mV. 3. Barium (1 microM) markedly reduced the inward rectification and caused a small inward current (40.6 +/- 8.7 pA, n = 8) at the resting potential. These effects became larger with higher barium concentrations, and, in 100 microM barium, the current-voltage relation was straight. 4. The block of the inward current by barium (at -130 mV) occurred with an exponential time course; the time constant was approximately 1 s at 1 microM barium and less than 90 ms with 100 microM. Strontium had effects similar to those of barium, but 1000-fold higher concentrations were required. Cesium chloride (2 mM) and rubidium chloride (2 mM) also blocked the inward rectification; their action reached steady state within 50 ms. 5. It is concluded that the nucleus accumbens neurons have a potassium conductance with many features of a typical inward rectifier and that this contributes to the potassium conductance at the resting potential.

scholarly journals A novel inward-rectifying K+ current with a cell-cycle dependence governs the resting potential of mammalian neuroblastoma cells.

1995 ◽  
Vol 489 (2) ◽  
pp. 455-471 ◽  
Author(s):  
A Arcangeli ◽  
L Bianchi ◽  
A Becchetti ◽  
L Faravelli ◽  
M Coronnello ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Neuroblastoma Cells ◽  
Resting Potential ◽  
K Current ◽  
A Cell ◽  
Cell Cycle Dependence ◽  
Cycle Dependence

scholarly journals Gonadotropin-Releasing Hormone Inhibits Ether-à-Go-Go-Related Gene K+ Currents in Mouse Gonadotropes

Endocrinology ◽  
2010 ◽  
Vol 151 (3) ◽  
pp. 1079-1088 ◽  
Author(s):  
Wiebke Hirdes ◽  
Crenguta Dinu ◽  
Christiane K. Bauer ◽  
Ulrich Boehm ◽  
Jürgen R. Schwarz
Keyword(s):  
Resting Potential ◽  
Related Gene ◽  
Activation Curve ◽  
Signal Cascade ◽  
Primary Mouse ◽  
Voltage Dependent ◽  
K Current ◽  
Unknown Signal ◽  
Ca2 Channels ◽  
K Currents

Secretion of LH from gonadotropes is initiated by a GnRH-induced increase in intracellular Ca2+ concentration ([Ca2+]i). This increase in [Ca2+]i is the result of Ca2+ release from intracellular stores and Ca2+ influx through voltage-dependent Ca2+ channels. Here we describe an ether-à-go-go-related gene (erg) K+ current in primary mouse gonadotropes and its possible function in the control of Ca2+ influx. To detect gonadotropes, we used a knock-in mouse strain, in which GnRH receptor-expressing cells are fluorescently labeled. Erg K+ currents were recorded in 80–90% of gonadotropes. Blockage of erg currents by E-4031 depolarized the resting potential by 5–8 mV and led to an increase in [Ca2+]i, which was abolished by nifedipine. GnRH inhibited erg currents by a reduction of the maximal erg current and in some cells additionally by a shift of the activation curve to more positive potentials. In conclusion, the erg current contributes to the maintenance of the resting potential in gonadotropes, thereby securing a low [Ca2+]i by restricting Ca2+ influx. In addition, the erg channels are modulated by GnRH by an as-yet unknown signal cascade.

Transmembrane Activity Gradients of K and cl in the Muscle Fibres of Osmoconforming Marine Decapod Crustaceans

1978 ◽  
Vol 72 (1) ◽  
pp. 127-140
Author(s):  
ROBERT W. FREEL
Keyword(s):  
Sea Water ◽  
Membrane Potentials ◽  
Resting Potential ◽  
Muscle Fibres ◽  
Salinity Adaptation ◽  
Decapod Crustaceans ◽  
Marine Crustaceans ◽  
Equilibrium Distributions

1. The resting membrane potentials (Em) and the transmembrane activity gradients for K and Cl were measured in the muscle fibres of osmoconforming (Callianassa and Cancer) and weakly osmoregulating (Pachygrapsus) marine crustaceans acclimated to various osmotic conditions. 2. The muscle membranes of sea water acclimated crabs behave as good K electrodes. However, a slight contribution of Na to the resting potential was demonstrated in all species. The ratio PNa/PK was about 0.01. Equilibrium potentials (measured with ion-selective microelectrodes) for Cl were equal to Em, while EK was always more negative than Em as a result of the slight Na contribution. 3. Acclimation to dilute or concentrated sea water had little effect on the K electrode properties or Na permeabilities of these fibres. The muscle fibres were depolarized in crabs acclimated to concentrated sea water and were hyperpolarized in crabs adapted to dilute sea water. These changes resulted solely from alterations in (aK)i/ (aK)O which were in turn brought about by changes in cellular and haemolymph hydration. 4. Since the Na contribution to Em was so small in all conditions, it was concluded that the distributions of K and Cl are best considered in terms of Donnan equilibria, and that the cellular K and Cl adjustments observed during salinity adaptation reflect the passive re-establishment of new equilibrium distributions for these ions.

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