PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Action Potentials”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 379 records · Page 21Linked to original sources
PubMed1993

Effects of monophasic and biphasic shocks on action potentials during ventricular fibrillation in dogs.

This study determined the response of action potentials during ventricular fibrillation (VF) to timed monophasic and biphasic shocks. A floating glass microelectrode was used to record intracellularly from the anterior right ventricle in 10 open-chest dogs. After 10 seconds of electrically induced VF, 5-millisecond monophasic and 2.5/2.5-millisecond biphasic shocks or 16-millisecond monophasic and 8/8-millisecond biphasic shocks were given via mesh electrodes on either side of the microelectrode. Monophasic and biphasic truncated exponential shocks of 5 V/cm were given with coupling intervals timed from the beginning of a VF action potential to the shock ranging from 50 to 70 milliseconds in 5-millisecond increments. Each coupling interval for each waveform was tested during a different VF episode. The interval between successive activations during VF was 86 +/- 15 milliseconds (mean +/- SD). The refractory period during VF was 61 +/- 5 milliseconds for 5-millisecond monophasic shocks and 66 +/- 6 milliseconds for 2.5/2.5-millisecond biphasic shocks (P < .05). At each coupling interval, action potential duration at 50% repolarization (APD50) was significantly prolonged by the shocks compared with the mean preshock APD50 (P < .05). ADP50 duration increased significantly with increases in the coupling interval (P < .05) for both monophasic and biphasic waveforms. For all coupling intervals together, APD50 prolongation as a percent of the mean preshock APD50 was 170 +/- 55%, 192 +/- 45%, 151 +/- 44%, and 175 +/- 45% for 5- and 16-millisecond monophasic and 2.5/2.5- and 8/8-millisecond biphasic waveforms, respectively. This APD50 prolongation was greater for monophasic than biphasic shocks and was greater for longer than shorter waveforms (P < .05). Thus, during VF, (1) the refractory period for 5-V/cm truncated exponential waveforms lasting 5 milliseconds is approximately 75% of the VF activation interval; (2) the refractory period is shorter for monophasic than for comparable biphasic waveforms; (3) both monophasic and biphasic 5-V/cm shock fields cause prolongation of action potential duration; (4) prolongation of action potential duration increases as the coupling interval increases; and (5) prolongation of action potential duration is greater for monophasic shocks and for longer shock waveforms.

Action Potentials↗
PubMed1984

The effects of ryanodine, EGTA and low-sodium on action potentials in rat and guinea-pig ventricular myocytes: evidence for two inward currents during the plateau.

Action potentials were recorded from single cells isolated from rat and guinea-pig ventricular muscle. In rat cells the repolarization showed two distinct phases, referred to as the early and late phases. In guinea-pig cells there was a maintained plateau. Reducing external sodium by replacement with lithium or choline suppressed the late phase of the action potential in rat cells, and shortened the plateau of the action potential in guinea-pig cells. Intracellular EGTA abolished contraction while suppressing the late phase of the action potential in rat cells, and shortening the plateau in guinea-pig cells. Ryanodine (1 microM), which is thought to inhibit the release of calcium from internal stores, suppressed contraction and the late phase of the action potential in rat cells. In guinea-pig cells, there was no substantial effect of ryanodine (1 microM) on either contraction or the time course of the action potential. The late phase of the action potential in rat cells was suppressed by increasing the external potassium concentration to 12 mM, and enhanced by reducing external potassium to 1.2 mM. It is concluded that an inward current activated by internal calcium contributes to the late phase of the action potential in rat cells, and to the plateau in guinea-pig cells. Two possibilities are a current arising from electrogenic sodium-calcium exchange, and a current through ion channels activated by calcium. The effects of reducing external sodium would be consistent with either mechanism. The contribution of such an inward current would be expected to be modified by outward currents through a rectifying potassium conductance which varies with external potassium concentration. In the rat, but not the guinea-pig, the rise in internal calcium which activates the inward current seems to be largely dependent on ryanodine-sensitive release of calcium from internal stores.

Action Potentials↗
PubMed1998

Muscarinic M1 receptor activation reduces maximum upstroke velocity of action potential in mouse right atria.

We investigated whether acetylcholine affects cardiac action potentials through the muscarinic M1 in addition to M2 receptors in spontaneously beating mouse isolated right atria. A conventional glass microelectrode technique was used for the purpose. Acetylcholine (3-10 microM) reduced the maximum upstroke velocity of the action potentials (Vmax), followed by an increase. It shortened action potential duration at 90% repolarization, hyperpolarized the resting membrane and decreased the rate of beating. Atropine (3-100 nM) concentration dependently antagonized these effects of acetylcholine. Pirenzepine (10 and 30 nM), a selective muscarinic M1 receptor antagonist, antagonized acetylcholine (5 microM)-induced reduction of Vmax without affecting other effects of acetylcholine. In addition, pirenzepine (30 nM) induced an immediate and linear acceleration of the VmaX reduced by acetylcholine. In contrast, AF-DX 116 (11(¿2-[(diethylamino)-methyl]-1-piperidyl¿acetyl)-5,11-dihydro-6 H-pyridol[2,3-b][1,4]benzodiazepine-6-one base, 30-300 nM), a selective muscarinic M2 receptor antagonist, failed to antagonize acetylcholine-induced reduction of Vmax, but abolished its increase. It antagonized the shortening of action potential duration, membrane hyperpolarization and decreased the beating rate. McN-A-343 (4-(m-chlorophenyl-carbamoyloxy)-2-butynyltrimethylammonium chloride, 100 and 300 microM), a muscarinic M1 receptor agonist, reduced Vmax and prolonged action potential duration, while oxotremorine (100-300 nM), a muscarinic M2 receptor agonist, evoked reverse effects. These results suggest that acetylcholine exerts a mixed effect on Vmax, consisting of a reduction and a facilitation, possibly mediated by concurrent activation of muscarinic M1 and M2 receptors, respectively, in isolated right atria of mice.

(4-(m-Chlorophenylcarbamoyloxy)-2-butynyl)trimethy↗
PubMed1994

Activation of adenylate cyclase attenuates the hyperpolarization following single action potentials in brain noradrenergic neurons independently of protein kinase A.

Afterhyperpolarizations that follow action potentials are a prominent mechanism for the control of neuronal excitability. Such afterhyperpolarizations in many neurons are modulated by a variety of second messenger systems. Here, we examined the regulation of afterhyperpolarizations in noradrenergic locus coeruleus neurons by the adenylate cyclase system. Although superfusion of the adenylate cyclase activator, forskolin, had no effect on hyperpolarizations following trains of action potentials, both forskolin and a membrane permeable analog of cyclic AMP, 8-bromo-cyclic AMP, attenuated the amplitude of afterhyperpolarizations which followed single action potentials of locus coeruleus neurons recorded intracellularly in brain slices. In contrast, superfusion of 1,9-dideoxyforskolin, the forskolin analog that does not activate adenylate cyclase, had no effect on these single action potential afterhyperpolarizations. Co-application of a protein kinase inhibitor (H8, KT5720, staurosporin or Rp-cAMPS) with either forskolin or 8-bromo-cyclic AMP failed to block the reduction of afterhyperpolarization amplitude, but blocked the cyclic AMP-dependent enhancement of opiate responses in the same locus coeruleus neurons. Furthermore, application of a membrane permeable analog of 5'-AMP, 8-bromo-5'-AMP, the cyclic AMP metabolite that does not activate a protein kinase, potently reduced the amplitudes of single action potential afterhyperpolarizations. The afterhyperpolarization amplitude was also reduced in locus coeruleus neurons taken from chronically morphine-treated rats, a treatment known to increase adenylate cyclase activity. These results indicate that elevation of intracellular cyclic AMP or 5'-AMP reduces the single action potential afterhyperpolarization in locus coeruleus neurons. This action may be mediated through a mechanism independent of protein kinase activation.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

Modeling the dynamics of cardiac action potentials.

The nonlinear dynamics of cardiac action potentials is explained via simple model equations describing the membrane potential and the inward and outward currents through the membrane. The equations approximate ionic models, yet are expressed as polynomial functions, and robustly capture the phase-space dynamics of action potentials.

Action Potentials↗
PubMed1998

The physiological origin of the slow afterwave in muscle action potentials.

OBJECTIVE: Both intramuscularly-recorded motor unit action potentials (MUAPs) and surface recorded MUAPs and compound muscle action potentials (CMAPs) have slow afterwaves which can contribute as much as half their measured duration. This study tested the hypothesis that the slow afterwave has its physiological origin in the negative afterpotential of the muscle fiber intracellular action potential (IAP). METHODS: We investigated the slow afterwave in MUAPs and CMAPs from brachial biceps, tibialis anterior, first dorsal interosseous, thenar and hypothenar muscles in 15 normal subjects, and using computer simulations. RESULTS: The slow afterwaves did not match the time constant of the amplifier's high-pass filter, and so were not filtering artifacts. They lasted long after propagation had terminated at the muscle/tendon junction, and so were not due to the temporal or spatial dispersion of propagating single-fiber potentials. Their amplitude and polarity varied with the recording site as predicted by computer simulations that modeled the IAP as having a negative afterpotential. They also changed with double-pulse stimulation and decreasing temperature in ways consistent with the results of intracellular studies of the IAP negative afterpotential. CONCLUSIONS: The presented results support our hypothesis that the slow afterwave is a manifestation of the IAP negative afterpotential.

Action Potentials↗
PubMed1991

Determinants of action potential duration in neonatal rat ventricle cells.

STUDY OBJECTIVE: The aim was to study the currents that determine the action potential duration in ventricular cells from neonatal rats. DESIGN: Microelectrode measurements of action potentials from ventricle strips were compared with action potentials obtained from isolated myocytes with the whole cell patch clamp method in current clamp mode. Ionic currents were studied in myocytes in voltage clamp mode using recognised modulators of channel activity. EXPERIMENTAL MATERIAL: Neonatal rats (2 d old) were decapitated and myocytes were prepared from the apical third of collagenase treated hearts. MEASUREMENTS AND MAIN RESULTS: Modification of the action potential by 1.8-5.0 mM Ca, 2.0 mM Co, 8 mM 4-aminopyridine, 1.8 mM Sr, and 20 mM tetraethylammonium suggested the presence of the slowly inactivating Ca current ICa,L, an early outward current Ieo, and at least one other K current. Action potentials from myocytes and ventricular strips were comparable. Voltage clamp experiments were confirmatory and revealed currents with the following properties: (1) ICa,L: a Ca current with a current density of 21.7 microA.cm-2, activated between -30 and -20 mV, saturated at 1.8 Cao, inactivated faster at 5 than at 1.8 mM Cao, more permeable to Ba and Sr than to Ca, and with Sr as charge carrier blocked by Ca; (2) Ieo: the peak current had a linear I/V relation between 0 and 70 mV and was abolished by 4 mM 4-aminopyridine; (3) IK1: the current was an inward rectifier that showed a relaxation at potentials negative to -90 mV. CONCLUSIONS: Action potentials obtained from neonatal rat ventricle with microelectrodes are comparable with those measured in myocytes in current clamp mode. The action potential duration is mainly determined by ICa,L, Ieo, and IK1, and there is no evidence for the presence of a delayed rectifier.

Action Potentials↗
PubMed1990

The influence of action potentials on the development of the central visual pathway in mammals.

The development of the mammalian visual system begins prenatally at distributed sites, where cells generated at different embryonic ages are destined to interconnect and form the visual pathways, and ends postnatally with the functional tuning of neuronal receptive-field properties. It is reasonable to assume that the earliest stages in this developmental sequence are completed prior to the onset of neural activity, and also that activity may play only a minor role or even none at all in primary axon outgrowth and pathway finding (Harris, 1981; Harris and Holt, 1990). However, recent evidence indicates that subsequent events in development, such as the sorting of axons at their targets, the cellular differentiation of target cells and the formation of synaptic contacts by developing axons, are all influenced by action potentials. Action potentials in the developing retino-geniculo-cortical pathway can be eliminated by blocking the voltage-gated sodium channel with tetrodotoxin. Prenatal blockade prevents the laminar segregation of retinogeniculate axons. Postnatal blockade interrupts the formation of retinogeniculate synaptogenesis, slows the cytoarchitectonic differentiation of the lateral geniculate nucleus and produces abnormalities in the responses of lateral geniculate neurons. In the visual cortex, the development of cells and synapses is retarded and the eye-specific separation of geniculocortical axons is halted, thereby blocking the formation of ocular dominance columns. While the cellular mechanisms underlying these effects are not understood, a partial restoration of normal development can be produced by stimulating blocked axonal pathways electrically.

Action Potentials↗
PubMed1997

Action-potential propagation gated by an axonal I(A)-like K+ conductance in hippocampus.

Integration of membrane-potential changes is traditionally reserved for neuronal somatodendritic compartments. Axons are typically considered to transmit reliably the result of this integration, the action potential, to nerve terminals. By recording from pairs of pyramidal cells in hippocampal slice cultures, we show here that the propagation of action potentials to nerve terminals is impaired if presynaptic action potentials are preceded by brief or tonic hyperpolarization. Action-potential propagation fails only when the presynaptic action potential is triggered within the first 15-20ms of a depolarizing step from hyperpolarized potentials; action-potential propagation failures are blocked when presynaptic cells are impaled with electrodes containing 4-aminopyridine, indicating that a fast-inactivating, A-type K+ conductance is involved. Propagation failed between some, but not all, of the postsynaptic cells contacted by a single presynaptic cell, suggesting that the presynaptic action potentials failed at axonal branch points. We conclude that the physiological activation of an I(A)-like potassium conductance can locally block propagation of presynaptic action potentials in axons of the central nervous system. Thus axons do not always behave as simple electrical cables: their capacity to transmit action potentials is determined by a time-dependent integration of recent membrane-potential changes.

4-Aminopyridine↗
PubMed1992

The interrelation between the monophasic action potential duration, cycle length and ischaemia in the human left ventricle.

Steady state monophasic action potentials were recorded from a single site in the left ventricular endocardium during incremental atrial pacing to the point of angina in 25 patients. Ischaemic areas of the left ventricle were documented using a perfusion marker (99mTc-MIBI) simultaneously with the action potential recording procedure. Recordings were obtained from an ischaemic area in 13 patients and from a non-ischaemic area in 12. A linear correlation between action potential duration and cycle length changes was demonstrated for both ischaemic and non-ischaemic zone recordings between cycle length changes of 750 and 428 ms. Ischaemia induced a shortening of the action potential duration significantly greater than that produced by cycle length changes (P less than 0.0001). Mean action potential duration shortening corrected for 100 ms change in cycle length for ischaemic zone recordings was 31.4 +/- 4.2 (SD) compared to 23.3 +/- 3.1 ms for non-ischaemic zone recordings. A range of values of action potential duration shortening in unit time was analysed for sensitivity and specificity for the detection of ischaemia. A value of 26.5 ms per 100 ms change in cycle length provided the optimum compromise with 88% sensitivity and specificity. Our data provide a means of employing the monophasic action potential duration to quantify early localized ischaemia in the presence of an alteration in cycle length.

Action Potentials↗
PubMed1996

Effects of potassium channel blockers on the action potentials and contractility of the rat right ventricle.

1. The effects of several potassium channel blockers on the action potentials and contractile force of the electrically driven rat right ventricle have been determined. 2. Glibenclamide, which blocks the ATP-sensitive potassium channels, had no effect on the ventricular action potentials or contractile force responses. 3. 4-Aminopyridine, which blocks the Na(+)-activated potassium channels in ventricles, at 0.3-3 mM increased the amplitude and prolonged the action potentials, and also augmented the force responses to cardiac stimulation and to isoprenaline. 4. Clofilium, a selective blocker of the delayed outward rectifying potassium channel, at 0.1 and 0.3 microM prolonged the action potentials. At 0.1 microM, clofilium augmented the cardiac stimulation responses and, at 0.3 microM, clofilium augmented the maximal responses to isoprenaline. At 1 and 3 microM, clofilium had a lesser ability to prolong action potentials and did not alter force responses. 5. Procaine blocks the Na(+)-activated and the delayed outward rectifying potassium channels and, at higher concentrations, sodium channels. Procaine, at 30 microM, prolonged the action potentials and augmented the force responses to isoprenaline, presumably by blocking potassium channels. Procaine, at 1 mM, had no effect on action potentials but reduced the maximal force responses to isoprenaline, probably by blocking sodium channels. 6. Tetraethylammonium blocks the inward rectifying and delayed outward rectifying potassium channels. Tetraethylammonium, at 1 and 3 mM, prolonged the action potentials and augmented all of the force responses; these effects are likely to be predominantly due to blocking the outward rectifying potassium channel. Thus, in the presence of procaine, the effects of tetraethylammonium are predominantly due to the additional blockade of the inward rectifying potassium channel and there were no effects. 7. None of the potassium channel blockers at any of the concentrations tested had arrhythmogenic effects alone or in the presence of isoprenaline. 8. In summary, this study has shown that blockade of the Na(+)-activated and the delayed outward rectifying, but not the ATP-sensitive or inward rectifying, potassium channel is associated with prolongation of the action potentials, augments the contractile force responses, and is not arrhythmogenic on the rat right ventricle. New drugs that block the Na(+)-activated or delayed outward rectifying potassium channel may have potential as positive inotropes in the treatment of heart failure.

4-Aminopyridine↗
PubMed2003

Regulation of backpropagating action potentials in mitral cell lateral dendrites by A-type potassium currents.

Dendrodendritic synapses, distributed along mitral cell lateral dendrites, provide powerful and extensive inhibition in the olfactory bulb. Activation of inhibition depends on effective penetration of action potentials into dendrites. Although action potentials backpropagate with remarkable fidelity in apical dendrites, this issue is controversial for lateral dendrites. We used paired somatic and dendritic recordings to measure action potentials in proximal dendritic segments (0-200 microm from soma) and action potential-generated calcium transients to monitor activity in distal dendritic segments (200-600 microm from soma). Somatically elicited action potentials were attenuated in proximal lateral dendrites. The attenuation was not due to impaired access resistance in dendrites or to basal synaptic activity. However, a single somatically elicited action potential was sufficient to evoke a calcium transient throughout the lateral dendrite, suggesting that action potentials reach distal dendritic compartments. Block of A-type potassium channels (I(A)) with 4-aminopyridine (10 mM) prevented action potential attenuation in direct recordings and significantly increased dendritic calcium transients, particularly in distal dendritic compartments. Our results suggest that I(A) may regulate inhibition in the olfactory bulb by controlling action potential amplitudes in lateral dendrites.

2-Amino-5-phosphonovalerate↗
PubMed1975

Two mechanisms for the meperidine block of action potential production in frog's skeletal muscle; non-specific and opiate drug receptor mediated blockade.

The effects of meperidine and naloxone, and their interaction effects on action potential production in frog's sartorius muscle fibres, were studied with intracellular micro-electrode techniques. 1. Meperidine, a narcotic analgesic drug, depressed the rate of rise, the rate of fall and the amplitude of the action potentials. 2. At a meperidine concentration of 0-35 mM, the depression in the action potential maximum rate of rise followed a diphasic time course. At first there was a rapid reduction in the maximum rate of rise which was levelling off at about 60% of control 60-90 min after drug application. This was followed by the second phase during which there was an initial rapid decrease in the maximum rate of rise and all surface fibres were inexcitable by 180 min. 3. The addition of naloxone, a narcotic antagonist, in low concentrations (3 X 10(-5) to 3 X 10(-4) mM) at 70-90 min blocked the second phase of the meperidine-induced depression. 4. With lower concentrations of meperidine (0-18 and 0-07 mM) the depression usually developed more slowly (up to 6 hr with the latter dose) and the addition of low naloxone concentrations partially antagonized the effects of meperidine. However, under no conditions was it possible to completely antagonize the effects of meperidine by the addition of naloxone. 5. A linear relation was found between action potential amplitude and the action potential maximum rate of fall. 6. Meperidine caused a shift in the relation of rate of fall against amplitude to higher action potential amplitudes, indicating that the drug inhibited the increase in potassium conductivity (gK) associated with the falling phase of the action potential. 7. When low naloxone concentrations antagonized the effects of meperidine on the rate of rise and restored action potential amplitudes to control levels, the effect of meperidine on the maximum rate of fall was not antagonized. 8. Larger naloxone concentrations (1-5 X 10(-2) mM or more) depressed the action potential rate of rise but did not alter the relation between action potential amplitude and the maximum rate of fall. 9. It is proposed that meperidine blocks action potential production by two mechanisms: (i) a non-specific mechanism in which the increases in both gNa and gK ar depressed and (ii) an opiate drug receptor mediated mechanism causing a specific depression of gNa. 10. The impression gained from the results is that there are opiate drug receptors located on the inner surface of the muscle membrane associated with the 'sodium channels' and that drug activation of these receptors by either meperidine or high naloxone concentrations interferes with the opening of the 'sodium channels' normally produced by membrane depolarization.

Action Potentials↗
PubMed1991

[Clinical value of monophasic action potentials].

The method of monophasic action potential (MAP) recording has experienced a significant surge in interest since the introduction of the contact electrode, which in contrast to the suction electrode, allows the safe and simple use of this technique in the clinical electrophysiology laboratory. MAP recording not only provide for a more precise determination of local activation, but most importantly, permit direct measurement of myocardial repolarization and action potential duration (APD), respectively. This had led to new insights into the cycle-length-dependence of the human APD, both in response to single extrastimuli and to steady-state heart rate changes. An advancement of the contact electrode catheter design now permits simultaneous pacing and MAP recording, and thereby, simultaneous determinations of APD and effective refractory periods (EPP) at the same endocardial site in the human heart. MAP recordings have demonstrated significant usefulness in the direct monitoring of antiarrhythmic drug effects, both in terms of dosage control and in the direct measurement of antiarrhythmic drug effects on the relationship between ERP and APD (ERP/ARD-ratio). Because MAP recordings reflect the local cellular electrophysiology, they also provide a more sensitive and precise index of myocardial ischemia than conventional ECG recordings. This can be utilized to assess the success of revascularizing procedures directly during or after the intervention. Recently, MAP recordings helped to discover early after-depolarizations in patients with "torsade de pointes", providing a possible explanation for the mechanism of polymorphous ventricular tachycardia in man.

Anti-Arrhythmia Agents↗
PubMed1980

Ontogenetically determined changes in the duration of ventricular action potentials of the rabbit heart under various conditions of stimulation.

Using glass microelectrodes, we measured the duration of action potentials of the right ventricular papillary muscles and myocardium of rabbits aged 1--3 (newborn), 7, 10 and 30 days and adult, stimulated in different ways. In the steady state, the duration of action potentials of the myocardium of adult animals was longest on stimulation at 1.5 Hz frequency. Frequencies above and below this value shortened the action potentials. In newborn animals, the duration of action potentials was the same at all the stimulation frequencies used. After a two minutes' break, the first action potential of the myocardium of newborn animals was the longest (and the same length as in the steady state); in older age groups its duration shortened, in inverse proportion to age. After a two minutes' break, a steady state was reattained the soonest in newborn animals (the second action potential in the series was the same length as the first); with advancing age more action potentials were needed before a steady state was attained (in adult animals, at 1 Hz frequency, usually five). The results show that the ventricular myocardium does not acquire the ability to react to different and changing stimulation frequencies by a change in the duration of action potentials until during postnatal ontogenesis (mainly in the first month).

Action Potentials↗
PubMed1993

Ionic basis of the action potential of guinea pig gallbladder smooth muscle cells.

Smooth muscle cells in the intact guinea pig gallbladder had a resting membrane potential of about -45 mV and had spontaneous action potentials that consisted of a rapid depolarization, a transient repolarization, a plateau phase, and a complete repolarization. These action potentials lasted approximately 570 ms and occurred at a frequency of approximately 0.4 Hz. Action potentials were abolished by the dihydropyridine (DHP)-sensitive Ca2+ channel blocker nifedipine (1.0 microM) and were enhanced by the DHP-sensitive Ca2+ channel agonist BAY K 8644 (0.5 microM). The K+ channel blockers tetraethylammonium chloride (5.0 mM) and 4-aminopyridine (4-AP; 2.0 mM) prolonged the action potential, whereas charybdotoxin (100 nM), a blocker of calcium-activated potassium channels, had no effect. Whole cell currents were characterized in enzymatically isolated smooth muscle cells from the same preparation. 4-AP, a blocker of voltage-dependent K+ channels, suppressed 70% of the outward current at 0 mV. Charybdotoxin (100 nM) reduced an additional 15% of the current at 0 mV. Single calcium-activated potassium channels were identified. The potential for half-activation of these channels, at a cytosolic Ca2+ concentration of 100 nM, was 66.8 mV. A fivefold increase in cytosolic Ca2+ resulted in a shift of the activation curve by -53 mV. External tetraethylammonium chloride (200 microM) reduced the mean single channel current by 48% at 0 mV. The whole cell outward current was abolished by replacement of intracellular K+ for Cs+. Ca2+ currents were inhibited by nifedipine and were increased by BAY K 8644. We conclude that DHP-sensitive voltage-dependent Ca2+ channels are responsible for the depolarization of the action potentials and that the repolarization is due to primarily 4-AP-sensitive K+ current.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Properties of derived cochlear action potentials in forward tonal masking in guinea pigs.

Chronic experiments on guinea pigs were used to study the characteristics of cochlear nerve action potentials and the derived potential in conditions of forward masking. The auditory nerve action potential was recorded from the round window of the cochlea. The derived potential was obtained by subtracting the action potential recorded with masking from the response obtained in silence. These studies showed that the derived potential showed higher sensitivity to masking than the traditional measure of masking, i.e., the decrement in the amplitude of the auditory nerve action potential. The derived potential reflects not only changes in the action potential during masking, but also changes in its shape. Differences between the derived potential and the action potential decrement provide evidence that the amplitude and time changes in the derived potential provide more complete information on the nature of activity in the auditory fibers.

Action Potentials↗