K+-induced twitch potentiation is not due to longer action potential

2002 ◽  
Vol 283 (1) ◽  
pp. C169-C177 ◽  
Author(s):  
Craig Yensen ◽  
Wadih Matar ◽  
Jean-Marc Renaud
Keyword(s):  
Action Potential ◽  
Soleus Muscle ◽  
Action Potentials ◽  
Muscle Twitch ◽  
Similar Action ◽  
Twitch Force ◽  
Relaxation Phase ◽  
Time To Peak ◽  
Twitch Potentiation ◽  
Edl Muscle

The objective of this study was to determine whether an increased duration of the action potential contributes to the K+-induced twitch potentiation at 37°C. Twitch contractions were elicited by field stimulation, and action potentials were measured with conventional microelectrodes. For mouse extensor digitorum longus (EDL) muscle, twitch force was greater at 7–13 mM K+ than at 4.7 mM (control). For soleus muscle, twitch force potentiation was observed between 7 and 11 mM K+. Time to peak and half-relaxation time were not affected by the increase in extracellular K+ concentration in EDL muscle, whereas both parameters became significantly longer in soleus muscle. Decrease in overshoot and prolongation of the action potential duration observed at 9 and 11 mM K+ were mimicked when muscles were respectively exposed to 25 and 50 nM tetrodotoxin (TTX; used to partially block Na+ channels). Despite similar action potentials, twitch force was not potentiated by TTX. It is therefore suggested that the K+-induced potentiation of the twitch in EDL muscle is not due to a prolongation of the action potential and contraction time, whereas a longer contraction, especially the relaxation phase, may contribute to the potentiation in soleus muscle.

Stimulation pulse characteristics and electrode configuration determine site of excitation in isolated mammalian skeletal muscle: implications for fatigue

2007 ◽  
Vol 103 (1) ◽  
pp. 359-368 ◽  
Author(s):  
Simeon P. Cairns ◽  
Eva R. Chin ◽  
Jean-Marc Renaud
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Soleus Muscle ◽  
Action Potentials ◽  
Surface Membrane ◽  
Electrical Field Stimulation ◽  
Mammalian Skeletal Muscle ◽  
Voltage Dependent ◽  
Flexor Digitorum Brevis ◽  
Edl Muscle

We examined whether electrical field stimulation with varying characteristics could excite isolated mammalian skeletal muscle through different sites. Supramaximal (20-V, 0.1-ms) pulse stimulation with transverse wire or parallel plate electrodes evoked similar forces in nonfatigued slow-twitch soleus and fast-twitch extensor digitorum longus (EDL) muscles from mice. d-tubocurarine shifted the twitch force-stimulation strength relationship toward higher pulse strengths with both electrode configurations in soleus muscle, suggesting that weaker pulses excite muscle via neuromuscular transmission. With wire stimulation, movement of the recording electrode along the muscle caused a delay between the stimulus artifact and the peak of the action potential, consistent with action potential propagation along the sarcolemma. TTX abolished all contractions evoked with 20-V, 0.1-ms pulses, suggesting that excitation occurred via voltage-dependent Na+ channels and, hence, muscle action potentials. TTX did not prevent force development with ≥0.4-ms pulses in soleus or 1-ms pulses in EDL muscle. Furthermore, myoplasmic Ca2+ (i.e., the fura 2 ratio) and sarcomere shortening were greater during tetanic stimulation with 2.0-ms than with 0.5-ms pulses in flexor digitorum brevis fibers from rats. TTX prevented all shortening and Ca2+ release with 0.5-ms, but not 2.0-ms, pulses, indicating that longer pulses can directly trigger Ca2+ release. Hence, proper interpretation of mechanistic studies requires precise understanding of how muscles are excited; otherwise, incorrect conclusions can be made. Using this new understanding, we showed that disrupted propagation of action potentials along the surface membrane is a major cause of fatigue in soleus muscle that is focally and continuously stimulated at 125 Hz.

Resting and Active Properties of Pyramidal Neurons in Subiculum and CA1 of Rat Hippocampus

2000 ◽  
Vol 84 (5) ◽  
pp. 2398-2408 ◽  
Author(s):  
Nathan P. Staff ◽  
Hae-Yoon Jung ◽  
Tara Thiagarajan ◽  
Michael Yao ◽  
Nelson Spruston
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Pyramidal Neurons ◽  
Current Injection ◽  
Synaptic Integration ◽  
Membrane Properties ◽  
Neuronal Membrane ◽  
Similar Action ◽  
Ca1 Neurons ◽  
Ca1 Pyramidal Neurons

Action potentials are the end product of synaptic integration, a process influenced by resting and active neuronal membrane properties. Diversity in these properties contributes to specialized mechanisms of synaptic integration and action potential firing, which are likely to be of functional significance within neural circuits. In the hippocampus, the majority of subicular pyramidal neurons fire high-frequency bursts of action potentials, whereas CA1 pyramidal neurons exhibit regular spiking behavior when subjected to direct somatic current injection. Using patch-clamp recordings from morphologically identified neurons in hippocampal slices, we analyzed and compared the resting and active membrane properties of pyramidal neurons in the subiculum and CA1 regions of the hippocampus. In response to direct somatic current injection, three subicular firing types were identified (regular spiking, weak bursting, and strong bursting), while all CA1 neurons were regular spiking. Within subiculum strong bursting neurons were found preferentially further away from the CA1 subregion. Input resistance ( R N), membrane time constant (τm), and depolarizing “sag” in response to hyperpolarizing current pulses were similar in all subicular neurons, while R N and τm were significantly larger in CA1 neurons. The first spike of all subicular neurons exhibited similar action potential properties; CA1 action potentials exhibited faster rising rates, greater amplitudes, and wider half-widths than subicular action potentials. Therefore both the resting and active properties of CA1 pyramidal neurons are distinct from those of subicular neurons, which form a related class of neurons, differing in their propensity to burst. We also found that both regular spiking subicular and CA1 neurons could be transformed into a burst firing mode by application of a low concentration of 4-aminopyridine, suggesting that in both hippocampal subfields, firing properties are regulated by a slowly inactivating, D-type potassium current. The ability of all subicular pyramidal neurons to burst strengthens the notion that they form a single neuronal class, sharing a burst generating mechanism that is stronger in some cells than others.

Changes in cytosolic calcium monitored by inward currents during action potentials in guinea-pig ventricular cells

1989 ◽  
Vol 238 (1291) ◽  
pp. 171-188 ◽  
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Voltage Clamp ◽  
Action Potentials ◽  
Single Cells ◽  
Calcium Transient ◽  
Cytosolic Calcium ◽  
Time To Peak ◽  
Ventricular Cells ◽  
In Cells

Action potentials were recorded from single cells isolated from guinea-pig ventricular muscle. Contraction was measured with an optical technique. Tail currents thought to be activated by cytosolic calcium were recorded when action potentials were interrupted by application of a voltage-clamp. A family of tail currents was recorded by interrupting the action potential at various times after the upstroke. The envelope of tail current amplitudes was taken as an index of changes in cytosoli calcium. Con­sistent with this interpretation, tail currents were negligible following intracellular loading with the calcium chelator BAPTA to suppress calcium transients. The cytosolic calcium transient estimated from the envelope of tails reached a peak approximately 50 ms after the upstroke of the action potential, and fell close to diastolic levels before repolarization was com­plete; 10 mM caffeine delayed the time to peak contraction, and caused a prolongation of the cytosolic calcium transient estimated from the envelope of tail currents. Caffeine also induced the appearance of a distinct late plateau phase of the action potential. Intracellular BAPTA suppressed the late plateau, contraction and tail currents in cells exposed to caffeine. Exposure to caffeine increased the time constant for decay of tail currents (from approximately 35 to 70 ms). When action potentials were greatly abbreviated by interruption with a voltage-clamp, a pro­gressive decline occurred in the subsequent three contractions and tail currents. There was a progressive reversal of these effects over four responses when the full action potential duration was restored. None of these effects was observed in cells exposed to caffeine. Calcium-activated tail currents appear to be a useful qualitative index of changes in cytosolic calcium. The observations are consistent with the suggestion that cytosolic calcium is reduced during the plateau by a combination of calcium extrusion through Na–Ca exchange and calcium uptake into caffeine-sensitive stores. It also appears that reduction of stores loading during abbreviated action potentials reduces subsequent contraction in cells not exposed to caffeine.

Modification of excitation–contraction coupling in cat ventricular myocardium following endocardial damage

1993 ◽  
Vol 71 (3-4) ◽  
pp. 254-262 ◽  
Author(s):  
Jean-Pierre Bourreau ◽  
Hamid S. Banijamali ◽  
Cyril E. Challice
Keyword(s):  
Sarcoplasmic Reticulum ◽  
Action Potential ◽  
Action Potentials ◽  
Prolonged Exposure ◽  
Contractile Function ◽  
Similar Treatment ◽  
Twitch Force ◽  
Resting Tension ◽  
Triton X ◽  
Endocardial Endothelium

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.

Changes of action potentials and force at lowered [Na+]o in mouse skeletal muscle: implications for fatigue

2003 ◽  
Vol 285 (5) ◽  
pp. C1131-C1141 ◽  
Author(s):  
Simeon P. Cairns ◽  
Sarah J. Buller ◽  
Denis S. Loiselle ◽  
Jean-Marc Renaud
Keyword(s):  
Skeletal Muscle ◽  
Action Potential ◽  
Soleus Muscle ◽  
Action Potentials ◽  
Extensor Digitorum Longus ◽  
Large Range ◽  
Action Potential Amplitude ◽  
Mouse Skeletal Muscle ◽  
Fatigued Muscle ◽  
Slow Twitch

We examined 1) whether the effects of lowered trans-sarcolemmal Na+ gradient on force differed between nonfatigued fast- and slow-twitch muscles of mice and 2) whether effects on action potentials could explain the decrease of force. The Na+ gradient was reduced by lowering the extracellular [Na+] ([Na+]o). The peak force-[Na+]o relationships for the twitch and tetanus were the same in nonfatigued extensor digitorum longus and soleus muscles: force was maintained over a large range of [Na+]o and then decreased abruptly over a much smaller range. However, fatigue was significantly exacerbated at a lowered [Na+]o that had little effect in nonfatigued soleus muscle. This finding suggests that substantial differences exist in the Na+ effect on force between nonfatigued and fatigued muscle. The reduced contractility in nonfatigued muscles at lowered [Na+]o was largely due to 1) an increased number of inexcitable fibers and threshold for action potentials, 2) a reduction of action potential amplitude, and 3) a reduced capacity to generate action potentials throughout trains.

Calcium Dynamics and Compartmentalization in Leech Neurons

2005 ◽  
Vol 94 (6) ◽  
pp. 4430-4440 ◽  
Author(s):  
Sofija Andjelic ◽  
Vincent Torre
Keyword(s):  
Information Processing ◽  
Action Potential ◽  
Action Potentials ◽  
Time Course ◽  
Ccd Camera ◽  
Calcium Dynamics ◽  
Single Action ◽  
Single Action Potential ◽  
Calcium Indicator ◽  
Mechanosensory Neurons

Calcium dynamics in leech neurons were studied using a fast CCD camera. Fluorescence changes (Δ F/ F) of the membrane impermeable calcium indicator Oregon Green were measured. The dye was pressure injected into the soma of neurons under investigation. Δ F/ F caused by a single action potential (AP) in mechanosensory neurons had approximately the same amplitude and time course in the soma and in distal processes. By contrast, in other neurons such as the Anterior Pagoda neuron, the Annulus Erector motoneuron, the L motoneuron, and other motoneurons, APs evoked by passing depolarizing current in the soma produced much larger fluorescence changes in distal processes than in the soma. When APs were evoked by stimulating one distal axon through the root, Δ F/ F was large in all distal processes but very small in the soma. Our results show a clear compartmentalization of calcium dynamics in most leech neurons in which the soma does not give propagating action potentials. In such cells, the soma, while not excitable, can affect information processing by modulating the sites of origin and conduction of AP propagation in distal excitable processes.

scholarly journals Zinc Enhances the Inhibitory Effects of Strychnine-Sensitive Glycine Receptors in Mouse Hippocampal Neurons

2007 ◽  
Vol 98 (6) ◽  
pp. 3666-3676 ◽  
Author(s):  
Hai Xia Zhang ◽  
Liu Lin Thio
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Hippocampal Neurons ◽  
Neuronal Excitability ◽  
Hippocampal Slices ◽  
Glycine Receptors ◽  
Inhibitory Effects ◽  
Action Potential Firing ◽  
Embryonic Mouse ◽  
Potential Firing

Although extracellular Zn2+ is an endogenous biphasic modulator of strychnine-sensitive glycine receptors (GlyRs), the physiological significance of this modulation remains poorly understood. Zn2+ modulation of GlyR may be especially important in the hippocampus where presynaptic Zn2+ is abundant. Using cultured embryonic mouse hippocampal neurons, we examined whether 1 μM Zn2+, a potentiating concentration, enhances the inhibitory effects of GlyRs activated by sustained glycine applications. Sustained 20 μM glycine (EC25) applications alone did not decrease the number of action potentials evoked by depolarizing steps, but they did in 1 μM Zn2+. At least part of this effect resulted from Zn2+ enhancing the GlyR-induced decrease in input resistance. Sustained 20 μM glycine applications alone did not alter neuronal bursting, a form of hyperexcitability induced by omitting extracellular Mg2+. However, sustained 20 μM glycine applications depressed neuronal bursting in 1 μM Zn2+. Zn2+ did not enhance the inhibitory effects of sustained 60 μM glycine (EC70) applications in these paradigms. These results suggest that tonic GlyR activation could decrease neuronal excitability. To test this possibility, we examined the effect of the GlyR antagonist strychnine and the Zn2+ chelator tricine on action potential firing by CA1 pyramidal neurons in mouse hippocampal slices. Co-applying strychnine and tricine slightly but significantly increased the number of action potentials fired during a depolarizing current step and decreased the rheobase for action potential firing. Thus Zn2+ may modulate neuronal excitability normally and in pathological conditions such as seizures by potentiating GlyRs tonically activated by low agonist concentrations.

Outward current and repolarization in hypoxic rat myocardium

1983 ◽  
Vol 244 (3) ◽  
pp. H341-H350
Author(s):  
C. H. Conrad ◽  
R. G. Mark ◽  
O. H. Bing
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Outward Current ◽  
Iodoacetic Acid ◽  
Mechanical Activity ◽  
Potential Range ◽  
Papillary Muscles ◽  
Rat Myocardium ◽  
Cable Properties ◽  
Sucrose Gap

We studied the effects of brief periods (20-30 min) of hypoxia in the presence of 5 and 50 mM glucose and of glycolytic blockade (10(-4) M iodoacetic acid, IAA) on action potentials, membrane currents, and mechanical activity in rat ventricular papillary muscles using a single sucrose gap voltage-clamp technique. Steady-state outward current (iss) was determined at the end of a 500-ms clamp to the test potential following a 600-ms clamp to a holding potential of -50 mV. In the presence of 5 mM glucose, hypoxia resulted in a decrease in action potential duration (APD) and an increase in iss (on the order of 60% at 0 mV) over the potential range studied. The increase in iss did not appear to be due to an increase in leakage current or to a change in the cable properties of the preparation. Addition of 50 mM glucose prevented the change in both APD and iss with hypoxia. In addition, glycolytic blockade with IAA did not alter iss in the presence of oxygen. We conclude that an increase in iss appears to be a major factor in the abbreviation of rat ventricular action potential seen with hypoxia. Glycolysis appears to be a sufficient (with 50 mM glucose) but not necessary source of energy for the maintenance of normal iss.

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
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Cell Types ◽  
Resting Potential ◽  
Constant Field ◽  
Bathing Medium ◽  
Mean Values ◽  
Relative Contribution ◽  
External Potassium ◽  
Limnaea Stagnalis

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.

Neuromodulation of Dendritic Action Potentials

1999 ◽  
Vol 81 (1) ◽  
pp. 408-411 ◽  
Author(s):  
Dax A. Hoffman ◽  
Daniel Johnston
Keyword(s):  
Protein Kinase ◽  
Action Potential ◽  
Action Potentials ◽  
Acetylcholine Receptors ◽  
Muscarinic Acetylcholine Receptors ◽  
Action Potential Amplitude ◽  
Neurotransmitter System ◽  
Potential Amplitude ◽  
Hippocampal Ca1 ◽  
Dopaminergic Neurotransmitter

Hoffman, Dax A. and Daniel Johnston. Neuromodulation of dendritic action potentials. J. Neurophysiol. 81: 408–411, 1999. The extent to which regenerative action potentials invade hippocampal CA1 pyramidal dendrites is dependent on both recent activity and distance from the soma. Previously, we have shown that the amplitude of back-propagating dendritic action potentials can be increased by activating either protein kinase A (PKA) or protein kinase C (PKC) and a subsequent depolarizing shift in the activation curve for dendritic K+ channels. Physiologically, an increase in intracellular PKA and PKC would be expected upon activation of β-adrenergic and muscarinic acetylcholine receptors, respectively. Accordingly, we report here that activation of either of these neurotransmitter systems results in an increase in dendritic action-potential amplitude. Activation of the dopaminergic neurotransmitter system, which is also expected to raise intracellular adenosine 3′,5′-cyclic monophosphate (cAMP) and PKA levels, increased action-potential amplitude in only a subpopulation of neurons tested.

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