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Results for “Action Potentials”

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PubMed1989

Changes in tetrodotoxin-resistant action potentials after passive transfer of myasthenia gravis patient sera.

Muscle electrical activity has been studied in mice after intraperitoneal injection of sera from myasthenia gravis (MG) patients. Myasthenic serum did not modify the electrical properties of innervated muscle fibres. The resting membrane potential and the action potential parameters remained unchanged. However, tetrodotoxin (TTX)-resistant action potentials of denervated muscles were reduced by myasthenic serum, possibly in association with receptor endocytosis induced by the immunoglobulin. However, a direct effect of MG serum on TTX-resistant sodium channels cannot be ruled out.

Action Potentials↗

PubMed1998

Determinants of action potential initiation in isolated rabbit atrial and ventricular myocytes.

Action potential conduction through the atrium and the ventricle of the heart depends on the membrane properties of the atrial and ventricular cells, particularly with respect to the determinants of the initiation of action potentials in each cell type. We have utilized both current- and voltage-clamp techniques on isolated cells to examine biophysical properties of the two cell types at physiological temperature. The resting membrane potential, action potential amplitude, current threshold, voltage threshold, and maximum rate of rise measured from atrial cells (-80 +/- 1 mV, 109 +/- 3 mV, 0.69 +/- 0.05 nA, -59 +/- 1 mV, and 206 +/- 17 V/s, respectively; means +/- SE) differed significantly (P < 0.05) from those values measured from ventricular cells (-82.7 +/- 0.4 mV, 127 +/- 1 mV, 2.45 +/- 0.13 nA, -46 +/- 2 mV, and 395 +/- 21 V/s, respectively). Input impedance, capacitance, time constant, and critical depolarization for activation also were significantly different between atrial (341 +/- 41 M omega, 70 +/- 4 pF, 23.8 +/- 2. 3 ms, and 19 +/- 1 mV, respectively) and ventricular (16.5 +/- 5.4 M omega, 99 +/- 4.3 pF, 1.56 +/- 0.32 ms, and 36 +/- 1 mV, respectively) cells. The major mechanism of these differences is the much greater magnitude of the inward rectifying potassium current in ventricular cells compared with that in atrial cells, with an additional difference of an apparently lower availability of inward Na current in atrial cells. These differences in the two cell types may be important in allowing the atrial cells to be driven successfully by normal regions of automaticity (e.g., the sinoatrial node), whereas ventricular cells would suppress action potential initiation from a region of automaticity (e.g., an ectopic focus).

Action Potentials↗

PubMed1985

Stimulation rate modulates effects of the dihydropyridine CGP 28 392 on cardiac calcium-dependent action potentials.

Calcium (Ca2+)-dependent action potentials were recorded from 22 mM potassium (K+)-depolarized guinea-pig papillary muscle at several different pacing frequencies in the absence and presence of CGP 28 392 (10 microM), a Ca2+ channel agonist. The maximum upstroke velocity (Vmax) of the slow response action potential was measured to determine relative changes in Ca2+ current as a function of pacing frequency. CGP 28 392 increased Vmax more than two fold at low rates of stimulation (1 or 12 pulses min-1), but had no significant effect on Vmax during rapid pulsing (200 pulses min-1). The enhancement of Vmax was dependent upon extracellular [K+]. Increasing extracellular [K+] from 22 mM to 27 mM suppressed the frequency-dependent agonist effects and increased the antagonist effects on Vmax. These results indicate that CGP 28 392 is a partial Ca2+-channel agonist and suggest that its effects on Ca2+ current are voltage-dependent.

Action Potentials↗

PubMed1979

Detection of tobramycin- and netilmicin-induced ototoxicity in guinea pigs with evoked action potentials.

To evaluate the action potentials evoked in the cochlea in aminoglycoside-induced ototoxicity, 80 guinea pigs were given 25, 50, 75, or 100 mg of tobramycin or netilmicin/kg per day for 14 or 28 days. Ten other guinea pigs (controls) were given 200 mg of ampicillin/kg per day for 14 or 28 days. Cochlear evoked action potentials (CEAP) before and after treatment were measured, and the cochlea was examined microscopically after treatment. Comparison of initial and final values showed that the threshold of the main negative (N1) wave rose (p less than 0.00001 for dose and duration factors), the amplitude decreased (P less than 0.00001 for dose factors at sound intensities of 120 and 90 dB, P less than 0.001 at 70 dB), and the latency lengthened (P less than 0.0001 for dose factors at 120 and 90 dB). The CEAP method appeared to be more sensitive than microscopic examination of the cochlea for detection of ototoxicity induced by the lower dosages of the aminoglycosides. No significant differences were observed between the effects of tobramycin and netilmicin. In conclusion, the CEAP method appears to be a promising tool for detection of aminoglycoside-induced ototoxicity.

Acoustic Stimulation↗

PubMed1978

[Relationship between the frequencies of pacemaker and action potentials in the duodenal smooth muscle of dogs].

In dogs with electrodes indwelled into the duodenum, four phases of the change of duodenum pacesetter potentials were revealed at rest in hunger whereas no such changes were observed during digestion. The frequency ranges of both the pacesetter potentials and the bursts of action potentials were wider in hunger than during digestion. Without the digestive activity, the periodicity of the frequency oscillations of the pacemaker potentials corresponded with the periodicity of action potentials, whereas during the process of digestion the constancy of the pacesetter potential frequency corresponded with the action potential constancy. The regularities of optimal conditions for action potentials of the duodenum smooth muscles are discussed as well as the methodological conditions for revealing the authentic character of changes in the pacesetter potential frequency.

Action Potentials↗

PubMed1999

Potentiation of Ca2+ influx through NMDA channels by action potentials: a computer model.

In pyramidal cells, somatic action potentials can propagate actively back into the apical dendrites and potentiate calcium influx at simultaneously activated glutamatergic synapses, presumably by relieving the voltage-dependent block of NMDA channels. We have used computer simulations to investigate the conditions under which this potentiation will be optimal. We find that a spike with a long duration and limited amplitude (peak of approximately -10 mV) will be most effective. A back-propagating action potential will achieve this form if the dendritic membrane has a low K+ channel density and a modest Na+ channel density (30-70 pS/microm2, similar to experimentally observed densities). The relative increase in calcium due to the backpropagating spike will be small, however, unless the accumulated calcium is rapidly removed.

Action Potentials↗

PubMed1997

Action potential initiation and propagation in rat neocortical pyramidal neurons.

1. Initiation and propagation of action potentials evoked by extracellular synaptic stimulation was studied using simultaneous dual and triple patch pipette recordings from different locations on neocortical layer 5 pyramidal neurons in brain slices from 4-week-old rats (P26-30) at physiological temperatures. 2. Simultaneous cell-attached and whole-cell voltage recordings from the apical trunk (up to 700 microns distal to the soma) and the soma indicated that proximal synaptic stimulation (layer 4) initiated action potentials first at the soma, whereas distal stimulation (upper layer 2/3) could initiate dendritic regenerative potentials prior to somatic action potentials following stimulation at higher intensity. 3. Somatic action potentials, once initiated, propagated back into the apical dendrites in a decremented manner which was frequency dependent. The half-width of back propagating action potentials increased and their maximum rate of rise decreased with distance from the soma, with the peak of these action potentials propagating with a conduction velocity of approximately 0.5 m s-1. 4. Back-propagation of action potentials into the dendritic tree was associated with dendritic calcium electrogenesis, which was particularly prominent during bursts of somatic action potentials. 5. When dendritic regenerative potentials were evoked prior to somatic action potentials, the more distal the dendritic recording was made from the soma the longer the time between the onset of the dendritic regenerative potential relative to somatic action potential. This suggested that dendritic regenerative potentials were initiated in the distal apical dendrites, possibly in the apical tuft. 6. At any one stimulus intensity, the initiation of dendritic regenerative potentials prior to somatic action potentials could fluctuate, and was modulated by depolarizing somatic or hyperpolarizing dendritic current injection. 7. Dendritic regenerative potentials could be initiated prior to somatic action potentials by dendritic current injections used to simulate the membrane voltage change that occurs during an EPSP. Initiation of these dendritic potentials was not affected by cadmium (200 microM), but was blocked by TTX (1 microM). 8. Dendritic regenerative potentials in some experiments were initiated in isolated from somatic action potentials. The voltage change at the soma in response to these dendritic regenerative events was small and subthreshold, showing that dendritic regenerative events are strongly attenuated as they spread to the soma. 9. Simultaneous whole-cell recordings from the axon initial segment and the soma indicated that synaptic stimulation always initiated action potentials first in the axon. The further the axonal recording was made from the soma the greater the time delay between axonal and somatic action potentials, indicating a site of action potential initiation in the axon at least 30 microns distal to the soma. 10. Simultaneous whole-cell recordings from the apical dendrite, soma and axon initial segment showed that action potentials were always initiated in the axon prior to the soma, and with the same latency difference, independent of whether dendritic regenerative potentials were initiated or not. 11. It is concluded that both the apical dendrites and the axon of neocortical layer 5 pyramidal neurons in P26-30 animals are capable of initiating regenerative potentials. Regenerative potentials initiated in dendrites, however, are significantly attenuated as they spread to the soma and axon. As a consequence, action potentials are always initiated in the axon before the soma, even when synaptic activation is intense enough to initiate dendritic regenerative potentials. Once initiated, the axonal action potentials are conducted orthogradely into the axonal arbor and retrogradely into the dendritic tree.

Action Potentials↗

PubMed1982

Desensitization of the muscarinic receptor controlling action potential of bullfrog atrial muscles.

Action potentials of the bullfrog atrial muscle, being depressed by carbachol in concentrations of (1-5) X 10(-7) M, were found to show a slow recovery when application of the drug was sustained. The rate of onset of recovery largely varied depending on individual preparations. The recovery of action potentials was neither due to changes in the ionic distribution across the membrane nor to a secondary action of catecholamine which was released by the nicotinic action of carbachol on sympathetic nerve terminals. These results suggested that the muscarinic ACh receptor responsible for the depression of action potentials showed desensitization to the action of its agonist. The slow inward current recorded by the voltage-clamp experiment showed a decrease and subsequent slow recovery in the presence of carbachol. This suggested that the muscarinic ACh receptor associating with the ionic channel of the slow inward current showed desensitization. It may be suggested on the basis of these experimental results that 1) the muscarinic ACh receptor of bullfrog atrial muscle may compose a receptor-ionic channel complex (RICC) with voltage-dependent CA2+ channel and 2) the molecular reaction between this RICC and agonist may be comparable to that occurring in the nicotinic RICC of the frog end-plate.

Acetylcholine↗

PubMed1986

Fatigue from high- and low-frequency muscle stimulation: role of sarcolemma action potentials.

This study compared the effect of high- (75 Hz, 1 min) and low- (5 Hz, 1.5 min) frequency stimulation on sarcolemmal action potentials of rat phrenic nerve-diaphragm preparations, measured in vitro at 25 degrees C. High-frequency stimulation reduced peak tetanic tension to 21 +/- 1% (means +/- SE) of initial, whereas 5 Hz stimulation produced less of a decline (71 +/- 2% of initial). Despite an initial faster rate of force recovery after 75-Hz stimulation, tetanic tension was still significantly depressed at 0.25 and 1 min relative to the values after 5-Hz stimulation (P less than 0.05). Resting membrane potential, and action potential overshoot and area were not significantly altered by fatigue. Action potential amplitude (AMP) was initially depressed by repetitive stimulation but increased significantly during recovery (P less than 0.05). No significant difference occurred in AMP recovery between the high- vs. low-frequency stimulation groups. The rate of rise and fall of the action potential was reduced after fatiguing stimulation but increased significantly with time (P less than 0.05). Moreover, the time to peak height of the action potential was prolonged by fatigue but significantly declined to resting values with time (P less than 0.05). During recovery, fatigue from high-frequency stimulation was associated with a greater prolongation in duration and time to baseline of the action potential relative to low-frequency stimulation (P less than 0.05). Action potential variables altered by stimulation generally recovered within 1 to 3 min, whereas peak tetanic tension did not completely return to resting values until 10 to 15 min of recovery. We conclude that high- and low-frequency stimulation elicits virtually identical perturbations in sarcolemmal action potentials, and thus changes in surface membrane properties cannot explain the decreased tetanic tension that follows 75-Hz stimulation. It appears that events distal to the sarcolemma are responsible for fatigue from both high- and low-frequency stimulation.

Action Potentials↗

PubMed1996

Different mechanisms underlying the repolarization of narrow and wide action potentials in pyramidal cells and interneurons of cat motor cortex.

Two different types of action potentials were observed among the pyramidal cells and interneurons in cat motor cortex: the narrow action potentials and the wide action potentials. These two types of action potentials had similar rising phases (528.8 +/- 77.0 vs 553.1 +/- 71.8 mV/ms for the maximal rising rate), but differed in spike duration (0.44 +/- 0.09 vs 1.40 +/- 0.39 ms) and amplitude (57.31 +/- 8.22 vs 72.52 +/- 8.31 mV), implying that the ionic currents contributing to repolarization of these action potentials are different. Here we address this issue by pharmacological manipulation and using voltage-clamp technique in slices of cat motor cortex. Raising extracellular K+ concentration (from 3 mM to 10 mM), applying a low dose of 4-aminopyridine (2-200 microM) or administering a low concentration of tetraethylammonium (0.2-1.0 mM) each not only broadened the narrow action potentials, but also increased their amplitudes. In contrast, high K+ medium or low dose of tetraethylammonium only broadened the wide action potentials, leaving their amplitudes unaffected, and 4-aminopyridine had only a slight broadening effect on the wide spikes. These results implied that K+ currents were involved in the repolarization of both types of action potentials, and that the K+ currents in the narrow action potentials seemed to activate much earlier than those in the wide spikes. This early activated K+ current may counteract the rapid sodium current, yielding the extremely brief duration and small amplitude of the narrow spikes. The sensitivity of the narrow spikes to 4-aminopyridine may not be mainly attributed to blockade of the classical A current (IA), because depolarizing the membrane potential to inactivate IA did not reproduce the effects of 4-aminopyridine. Blockade of Ca2+ influx slowed the last two-thirds repolarization of the wide action potentials. On the contrary, the narrow action potentials were not affected by Ca(2+)-current blockers, but if they were first broadened by 4-aminopyridine or tetraethylammonium, subsequent application of Ca(2+)-free medium caused further broadening, suggesting that the narrow action potentials were too brief to activate the Ca(2+)-activated potassium currents for their repolarization. Therefore, the effects of low concentrations of tetraethylammonium on the narrow spikes appeared to be mainly due to blockade of an outward current that was different from the tetraethylammonium-sensitive Ca(2+)-activated potassium current (IC). In the neurons with the narrow spikes, voltage-clamp experiments revealed two voltage-gated outward currents that were sensitive to tetraethylammonium and 4-aminopyridine, respectively. Both currents were activated rapidly following the onset of depolarizing steps. Interestingly, the tetraethylammonium-sensitive current was a transient outward current that inactivated rapidly (tau < or = 5 ms), while the 4-aminopyridine-sensitive current was relatively persistent during maintained depolarization. The 4-aminopyridine-sensitive current did not show obvious inactivation even at membrane potential of -40 mV, which completely inactivated the transient tetraethylammonium-sensitive, current. The results indicate that different potassium currents are involved in the repolarization of the narrow and wide action potentials in cat motor cortex. A novel tetraethylammonium-sensitive transient outward current and a 4-aminopyridine-sensitive outward current are responsible for the short duration and small amplitude of the narrow action potentials in the interneurons and some of the layer V pyramidal cells. These two currents are voltage-gated and Ca(2+)-independent. For the wide action potentials that characterize most pyramidal neurons, a Ca(2+)-independent tetraethylammonium-sensitive outward current and a Ca(2+)-activated potassium current are the main contributors to their repolarization.

4-Aminopyridine↗

PubMed1999

Influence of CO2 laser application to the guinea-pig cochlea on compound action potentials.

HYPOTHESIS: Experiments in guinea pigs were performed to clarify which, if any, of the CO2 lasers in different modes (continuous wave [cw] and superpulse) can damage the inner ear on application of the laser parameters required for stapedotomy and to determine their application safety. METHODS: The laser effect connected with perforating the basal convolution of the guinea-pig cochlea (cochleostomy) was examined. Acoustic evoked potentials (compound action potentials [CAPs]) yielded information on inner-ear function. RESULTS: In cw mode, even single applications of an approximately four times higher power density (60,000 W/cm2) than necessary for stapedotomy at a pulse duration of 50 msec (energies up to 1 J) and 20-fold applications of effective parameters for a footplate perforation (power density 16,000 W/cm2; energy 0.2 J) did not cause CAP changes. Experimental studies with the CO2 superpulse laser used (peak pulse powers: ca. 300 W) have demonstrated that irreversible CAP alterations already occur in the effective laser range in > 40% of the animals. CONCLUSIONS: Because damage is expected only at much higher energies (> 2 J) than those used clinically, the CO2 laser in cw mode has a high application safety for laser stapedotomy. The application of the CO2 laser in superpulse mode with peak pulse powers of approximately 300 W in stapedotomy appears to be more unreliable and dangerous for the inner ear.

Animals↗

PubMed1981

Action potential synchrony in embryonic precontractile chick heart: optical monitoring with potentiometric dyes.

1. Using an optical method for monitoring membrane potential, we recorded spontaneous action potentials simultaneously in several different areas of the 7-9 somite embryonic chick hearts. 2. Absorption signals resembling spontaneous action potentials were well synchronized among the different areas in the prebeating embryonic heart during the 7-9 somite stages of development, and the synchronization spread over the entire area of the heart. From these experimental results, it is evident that there is electrical coupling among embryonic chick heart cells even in the early stages of cardiogenesis. 3. When an embryonic heart was separated into right and left or anterior and posterior parts, the action potential synchrony between the two halves was completely blocked; however, the synchrony and the intrinsic rhythmicity in action potential recurrence remained in each part.

Action Potentials↗

PubMed1997

Slow recovery from inactivation of Na+ channels underlies the activity-dependent attenuation of dendritic action potentials in hippocampal CA1 pyramidal neurons.

Na+ action potentials propagate into the dendrites of pyramidal neurons driving an influx of Ca2+ that seems to be important for associative synaptic plasticity. During repetitive (10-50 Hz) firing, dendritic action potentials display a marked and prolonged voltage-dependent decrease in amplitude. Such a decrease is not apparent in somatic action potentials. We investigated the mechanisms of the different activity dependence of somatic and dendritic action potentials in CA1 pyramidal neurons of adult rats using whole-cell and cell-attached patch-clamp methods. There were three main findings. First, dendritic Na+ currents decreased in amplitude when repeatedly activated by brief (2 msec) depolarizations. Recovery was slow and voltage-dependent. Second, Na+ currents decreased much less in somatic than in dendritic patches. Third, although K+ currents remained constant during trains, K+ currents were necessary for dendritic action potential amplitude to decrease in whole-cell experiments. These results suggest that regional differences in Na+ and K+ channels determine the differences in the activity dependence of somatic and dendritic action potential amplitudes.

Action Potentials↗

PubMed2006

Modeling fibrillation potentials--a new analytical description for the muscle intracellular action potential.

The single-fiber action potential (SFAP) can be modeled as a convolution of a biolectrical source (the excitation) and a transfer function, representing the electrical volume conduction. In the Dimitrov-Dimitrova (D-D) convolutional model, the first temporal derivative of the intracellular action potential (IAP) is used as the source. In this model, the ratio between the amplitudes of the second and first phases of the SFAP (which we call the PPR, after peak-to-peak ratio) increases invariably with radial distance. This is not the case of real recorded fibrillation potentials (FPs). Moreover, FPs show a wider PPR range than that which the D-D model can provide. These discrepancies suggest that the D-D model should be revised. Since the volume conduction parameters seem to have no apparent effects on the PPR, we assume that the origin of this difference lies in the excitation source. This paper presents a new analytical description of the IAP based on that expressed in the D-D model. The new approximation is shown to model FPs with a range of PPRs comparable to that observed in a set of real FPs which we used as our test signals.

Action Potentials↗

PubMed1985

The slow repolarization phase of the action potential in rat heart.

Intracellular action potentials and isometric force were measured from thin trabeculae of the right ventricle of rat heart. Characteristic for the action potential of rat myocardium is a short plateau and a slow final repolarization phase. We have studied the influence of ionic composition of the medium and of stimulation frequency on the slow phase of repolarization and its relation to peak force. The results confirmed a positive correlation between peak force and the duration of the slow phase of repolarization, as has been reported for other species. An increase of [Ca2+]o caused a shortening of the slow phase of repolarization when peak force was kept constant. In low [Na+]o peak force was increased and the slow phase of repolarization was shortened. Reperfusion with normal medium after a period in low [Na+]o induced a transient prolongation of the slow phase of repolarization and reduction of peak force. The transient lasted about 20 min. In the presence of the Ca2+ entry blocker nifedipine the action potential duration and peak force were reduced. Low [Na+]o caused less shortening of the slow phase of repolarization and a greater increase of peak force. The slow phase of repolarization was prolonged transiently following reperfusion at normal [Na+]o, but only during a few beats. These results are in agreement with the hypothesis that the slow phase of repolarization is due to an inward current generated by Na+-Ca2+ exchange, as latter mechanism is known to be sensitive to the intracellular and extracellular concentrations of both Na+ and Ca2+.

Action Potentials↗

PubMed1996

Characteristics of action potentials and their underlying outward currents in rat taste receptor cells.

1. Taste receptor cells produce action potentials as a result of transduction mechanisms that occur when these cells are stimulated with tastants. These action potentials are thought to be key signaling events in relaying information to the central nervous system. We explored the ionic basis of action potentials from dissociated posterior rat taste cells using the patch-clamp recording technique in both voltage-clamp and current-clamp modes. 2. Action potentials were evoked by intracellular injection of depolarizing current pulses from a holding potential of -80 mV. The threshold potential for firing of action potentials was approximately -35 mV; the input resistance of these cells averaged 6.9 G omega. With long depolarizing pulses, two or three action potentials could be elicited with successive attenuation of the spike height. Afterhyperpolarizations were observed often. 3. Both sodium and calcium currents contribute to depolarizing phases of the action potential. Action potentials were blocked completely in the presence of the sodium channel blocker tetrodotoxin. Calcium contributions could be visualized as prolonged calcium plateaus when repolarizing potassium currents were blocked and barium was used as a charge carrier. 4. Outward currents were composed of sustained delayed rectifier current, transient potassium current, and calcium-activated potassium current. Transient and sustained potassium currents activated close to -30 mV and increased monotonically with further depolarization. Up to half the outward current inactivated with decay constants on the order of seconds. Sustained and transient currents displayed steep voltage dependence in conductance and inactivation curves. Half inactivation occurred at -20 +/- 3.1 mV (mean +/- SE) with a decrease of 11.2 +/- 0.5 mV per e-fold. Half maximal conductance occurred at 3.6 +/- 1.8 mV and increased 12.2 +/- 0.6 mV per e-fold. Calcium-activated potassium current was evidenced by application of apamin and the use of calcium-free bathing solution. It was most obvious at more depolarized holding potentials that inactivated much of the transient and sustained outward currents. 5. Potassium currents contribute to both the repolarization and afterhyperpolarization phases of the action potential. These currents were blocked by bath application of tetraethylammonium, which also substantially broadened the action potential. Application of 4-aminopyridine was able to selectively block transient potassium currents without affecting sustained currents. This also broadened the action potential as well as eliminated the afterhyperpolarization. 6. A second type of action potential was observed that differed in duration. These slow action potentials had t1/2 durations of 9.6 ms compared with 1.4 ms for fast action potentials. Input resistances of the two groups were indistinguishable. Approximately one-fourth of the cells eliciting action potentials were of the slow type. 7. Cells eliciting fast action potentials had large outward currents capable of producing a quick repolarization, whereas cells with slow action potentials had small outward currents by comparison. The average values of fast cells were 2,563 pA and 1.4 ms compared with 373 pA and 9.6 ms for slow cells. Current and duration values were related exponentially. No significant difference was noted for inward currents. 8. These results suggest that many taste receptor cells conduct action potentials, which may be classified broadly into two groups on the basis of action potential duration and potassium current magnitude. These groups may be related to cell turnover. The physiological role of action potentials remains to be elucidated but may be important for communication within the taste bud as well as to the afferent nerve.

Action Potentials↗

PubMed1992

Design and use of an "optrode" for optical recordings of cardiac action potentials.

An optical method was used to measure action potentials from frog ventricle, in vitro, under normal physiological conditions with 0.5-1 mM Ca2+ Ringer's solution. The approach presented in this paper involves a portable fluorimeter coupled to a multimode optical fiber running into a glass pipette ("optrode") to carry both excitation light to and fluorescence from the ventricle stained with the voltage sensitive dye di-4-ANEPPS. A suction technique was used to stabilize the optrode-tissue interface, significantly reducing motion artifacts from the beating ventricle. The typical fractional change in fluorescence intensity for an action potential was -9%. The optical recordings faithfully reproduced membrane action potentials as measured with microelectrode recordings. To confirm further the validity of our method we studied the effect of an increasing stimulation rate on the optical action potential. The amplitude of the action potential did not increase, and the change in action potential duration was similar to published results obtained with microelectrode recordings, suggesting that our optical action potentials are relatively free of motion artifacts. Finally, our optical recordings suggest that during anodal and cathodal point stimulation, the time course of membrane potential differs from that predicted simply by a passive cable model.

Action Potentials↗

PubMed1958

Prolonged action potentials from single nodes of Ranvier.

The duration of action potentials from single nodes of Ranvier can be increased by several methods. Extraction of water from the node (e.g. by 2 to 3 M glycerin) causes increased durations up to 1000 msec. 1 to 5 min. after application of the glycerin the duration of the action potential again decreases to the normal value. Another type of prolonged action potential can be observed in solutions which contain K or Rb ions at concentrations between 50 mM and 2 M. The nodes respond only if the resting potential is restored by anodal current. The kinetics of these action potentials is slightly different. Their maximal durations are longer (up to 10 sec.). Like the normal action potential, they are initiated by cathodal make or anodal break. They also occur in external solutions which contain no sodium. The same type of action potentials as in KCl is found when the node is depolarized for some time (15 to 90 sec., 100 to 200 mv.) and is then stimulated by cathodal current. These action potentials require no K or Na ions in the external medium. Their maximal duration increases with the strength and duration of the preceding depolarization. The possible origin of the action potentials in KCl and after depolarization, and their relation to the normal action potentials and the negative after-potential are discussed.

Action Potentials↗