scholarly journals Membrane Characteristics of the Canine Papillary Muscle Fiber

1969 ◽  
Vol 54 (6) ◽  
pp. 765-781 ◽  
Author(s):  
Yasuzi Sakamoto
Keyword(s):  
Action Potential ◽  
Conduction Velocity ◽  
Time Constant ◽  
Papillary Muscle ◽  
Time Course ◽  
Current Flow ◽  
Membrane Resistance ◽  
Muscle Membrane ◽  
Spatial Decay ◽  
Similar Time

Passive and active responses to intracellular and extracellular stimulation were studied in the canine papillary muscle. The electrotonic potential produced by extracellular polarization with the partition chamber method fitted the time course and the spatial decay expected from the cable theory (the time constant, 3.3 msec; the space constant, 1.2 mm). Contrariwise, spatial decay of the electrotonic potentials produced by intracellular polarization was very short and did not fit the decay curve expected for a simple cable, although only a small difference of time course in the electrotonic potentials produced by intracellular and extracellular polarizations was observed. A similar time course might result from the fact that when current flow results from intracellular polarization, the input resistance is less dependent on the membrane resistance. The foot of the propagated action potential rose exponentially with a time constant of 1.1 msec and a conduction velocity of 0.68 m/sec. The membrane capacity was calculated from the time constant of the foot potential and the conduction velocity to be 0.76 µF/cm2. The responses of the papillary muscle membrane to intracellular stimulation differed from those to extracellular stimulation applied with the partition method in the following ways: higher threshold potential, shorter latency for the active response, linearity of the current-voltage relationship, and no reduction in the membrane resistance at the crest of the action potential during current flow.

An electrically mediated inhibition in goldfish medulla

1975 ◽  
Vol 38 (2) ◽  
pp. 452-471 ◽  
Author(s):  
H. Korn ◽  
D. S. Faber
Keyword(s):  
Action Potential ◽  
Time Course ◽  
Current Flow ◽  
Input Resistance ◽  
Membrane Resistance ◽  
Neuronal Population ◽  
M Cell ◽  
Neuronal Membranes ◽  
Cathodal Current ◽  
Medullary Neurons

1. Passive hyperpolarizing potentials (PHPs) have been recorded intracellularly from goldfish medullary neurons in the vicinity of the Mauthner cell (M-cell). They are evoked when this cell is activated antidromically by stimulation of the spinal cord, and orthodromically via the ipsilateral eighth nerve; when appropriately timed they block or delay spikes induced both directly and transsynaptically. 2. Since the PHPs and the M-cell spike have the same latency, time course, and all-or-none character, they cannot be generated by chemically mediated synaptic transmission. This conclusion is further supported by the evidence that PHP amplitude and time course are independent of membrane potential. 3. The analysis of the mechanism underlying PHP generation has been based on the hypothesis that they are brought about by the extracellular currents flowing to the axon cap during an M-cell action potential. Specifically, it was postulated that some of this current is channeled back to the axon cap region intracellularly through processes of PHP-exhibiting neurons, and that these cells are passively hyperpolarized by the associated inward transmembrane current flow. This model would require that PHP-exhibiting neurons send processes into the axon cap. This hypothesis is confirmed by the following: a) When the PHP is timed to occur during the conductance increase associated with a spike after hyperpolarization, it is reduced, as would be expected for a passive current flow across a membrane resistance. b) PHPs are not found in all medullary neurons in the vicinity of the M-cell, but rather in a specific neuronal population. c) PHP-exhibiting neurons have been identified following Procion yellow injections; as predicted, they issue one process, presumably the axon, which projects toward the M-cell axon cap area. d) The PHP can be stimulated by passing a cathodal current from a microelectrode located in the axon cap; it is not mimicked when the cathodal electrode is moved outside this region. The currents necessary to mimic a PHP are comparable to the estimated current flowing back to the axon cap during an M-cell action potential. 4. The input resistance of PHP-exhibiting neurons is in the range of 4 M alpha, and their estimated specific membrane resistance is in the range of 900-2,000 alpha-cm-2, which is not an unusually low value for neuronal membranes. By contrast, the intracellular channeling of current during a PHP can rather be attributed to a high extracellular tissue resistance within the axon cap, which was found to be at least 2.5 times that of the surrounding medullary tissue..

Effects of octanol on canine subendocardial Purkinje-to-ventricular transmission

1985 ◽  
Vol 249 (6) ◽  
pp. H1228-H1231 ◽  
Author(s):  
R. W. Joyner ◽  
E. D. Overholt
Keyword(s):  
Action Potential ◽  
Conduction Velocity ◽  
Current Flow ◽  
Conduction Delay ◽  
Papillary Muscles ◽  
Maximal Rate ◽  
Gap Junctional ◽  
Junctional Resistance ◽  
P Cells

The effects of 0.2 mM octanol on action potential propagation were investigated using in vitro preparations of canine papillary muscles. In these preparations an action potential initiated in the superficial Purkinje (P) layer propagates across specific Purkinje-ventricular junction (PVJ) sites into the underlying ventricular (V) layer. The conduction delay at PVJ sites increased from 4.85 +/- 1.55 to 8.85 +/- 3.34 (mean +/- SD) ms (n = 10, P less than 0.005), an 82% increase. However, propagation within the V syncytium was much less affected, with a decrease of conduction velocity by only 10% and a decrease in the maximal rate of rise of the action potential of 23%. The results indicate that octanol, which has previously been shown to increase gap junctional resistance, has a preferential effect on PVJ sites, as predicted by the hypothesis that there is a restricted pathway for intracellular current flow from P cells to V cells at these sites.

Bullfrog dorsal root ganglion cells having tetrodotoxin-resistant spikes are endowed with nicotinic receptors

1989 ◽  
Vol 62 (3) ◽  
pp. 657-664 ◽  
Author(s):  
K. Morita ◽  
Y. Katayama
Keyword(s):  
Dorsal Root Ganglion ◽  
Conduction Velocity ◽  
Dorsal Root ◽  
Time Course ◽  
Ganglion Cells ◽  
Reversal Potential ◽  
Membrane Resistance ◽  
Fast Response ◽  
Dorsal Root Ganglion Cells

1. Intracellular recordings were made from bullfrog dorsal root ganglion (DRG) neurons in vitro. They were divided into three types, As, Ar, and C, according to their conduction velocity and their sensitivity to tetrodotoxin [TTX (less than or equal to 1 microM)]; an As neuron had a fast conduction velocity (13-50 m/s, mean = 31 m/s, n = 73) and TTX-sensitive sodium soma spikes: an Ar neuron showed a fast conduction velocity (4-28 m/s, mean = 14 m/s, n = 52) and TTX-resistant sodium soma spikes; and a C neuron had a slow conduction velocity (0.16-0.8 m/s, mean = 0.4 m/s, n = 49) and TTX-resistant sodium-calcium soma spikes. 2. Superfusion of acetylcholine [ACh (0.3 microM-1 mM)] produced a fast depolarization in 70% of Ar and in 50% of C neurons. No As neuron showed a fast depolarization in response to ACh. The ACh-induced fast response persisted in calcium-free or TTX-containing solutions. 3. The response in both Ar and C neurons was similar except in time course; the response was always more rapid in C than in Ar neurons. The response was always associated with a decreased membrane resistance and reversed in polarity at about -30 mV. The reversal potential varied with both sodium and potassium concentrations of the superfusing solutions. 4. Nicotine, (+)-tubocurarine [(+)-TC], and hexamethonium reversibly blocked the ACh fast response.(ABSTRACT TRUNCATED AT 250 WORDS)

Intracellular recording from pectoral fin motoneurons of the stingray Dasyatis sabina, an elasmobranch fish

1984 ◽  
Vol 51 (4) ◽  
pp. 666-679 ◽  
Author(s):  
B. J. Williams ◽  
M. H. Droge ◽  
R. B. Leonard
Keyword(s):  
Action Potential ◽  
Conduction Velocity ◽  
Initial Segment ◽  
Recurrent Events ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Pectoral Fin ◽  
Dasyatis Sabina ◽  
Axonal Conduction ◽  
Input Conductance

Intracellular recordings were made from antidromically identified pectoral fin motoneurons in unanesthetized, decerebrate stingrays (Dasyatis sabina). These recordings had the three all-or-none components seen in other vertebrate motoneuron recordings. About 25% of the impalements had resting membrane potentials that were greater than -80 mV, which is larger than those of motoneurons from other vertebrate species. A novel depolarizing afterpotential (DAP) is associated with the isolated action potential occurring at the first node of Ranvier of the axon (M-spike). Occlusion experiments exclude recurrent events as the source of this potential. A capacitive source for the DAP is postulated. Using morphological and passive electrical data on motoneurons from previous studies, calculations of the passive decay of the nodal spike indicate that the membrane resistance of the initial segment is low and nearly equal to that of nodal membrane. The soma-dendritic (SD) spike is followed by a prominent, humped delayed depolarization (DD). The DD is temporally associated with the onset of the action potential produced by the initial segment (IS spike). Sources of the long-lasting period of repolarization recorded with the IS spike, which may underlie the DD, are postulated. The afterhyperpolarization (AHP) of stingray motoneurons tends to be shorter and smaller in amplitude than that of other vertebrate motoneurons. A negligible conductance change was often found during the period following an SD spike. No significant correlation was found between AHP duration and axonal conduction velocity. The input conductance of stingray motoneurons ranged between 1.5 X 10(-7) and 13.3 X 10(-7) S. The relationship between input conductance and axonal conduction velocity was determined from 42 motoneurons. These data were fitted by a power function with an exponent of 1.7, indicating that, in terms of membrane conductance properties, large stingray motoneurons are simply scaled-up versions of the small motoneurons.

Changes in the electrophysiological properties of cat spinal motoneurons following the intramuscular injection of adriamycin compared with changes in the properties of motoneurons in aged cats

1995 ◽  
Vol 74 (5) ◽  
pp. 1972-1981 ◽  
Author(s):  
R. H. Liu ◽  
J. Yamuy ◽  
M. C. Xi ◽  
F. R. Morales ◽  
M. H. Chase
Keyword(s):  
Electrical Properties ◽  
Action Potential ◽  
Conduction Velocity ◽  
Time Constant ◽  
Correlation Coefficients ◽  
Input Resistance ◽  
Resting Membrane Potential ◽  
Electrophysiological Properties ◽  
Axonal Conduction ◽  
Adult Cat

1. This study was undertaken to investigate the effects of adriamycin (ADM, Doxorubicin) on the basic electrophysiological properties of spinal cord motoneurons in the adult cat. ADM was injected into the biceps, gastrocnemius, semitendinosus, and semimembranosus muscles of the left hindlimb (1.2 mg per muscle). Intracellular recordings from motoneurons innervating these muscles were carried out 12, 20, or 40 days after ADM administration and from corresponding motoneurons in untreated control cats. 2. Twelve days after ADM injection, motoneurons innervating ADM-treated muscles (ADM MNs) exhibited statistically significant increases in input resistance, membrane time constant, and amplitude of the action potential's afterhyperpolarization (AHP). In addition, there was a statistically significant decrease in rheobase and in the delay between the action potential of the initial segment (IS) and that of the somadendritic (SD) portion of the motoneuron (IS-SD delay). There were no significant changes in the resting membrane potential, threshold depolarization, action potential amplitude, or axonal conduction velocity. 3. The changes in electrical properties of motoneurons at 20 and 40 days after ADM injection were qualitatively similar to those observed at 12 days. However, at 40 days after ADM injection there was a statistically significant decrease in the axonal conduction velocity of the ADM MNs. 4. The normal correlations that are present between the AHP duration and electrical properties of the control motoneurons were observed in the ADM MNs, e.g., AHP duration was positively correlated with the input resistance and time constant and negatively correlated with the axonal conduction velocity. The correlation coefficients, however, were reduced in comparison with the control data. 5. This study demonstrates that ADM exerts significant effects on the electrical properties of motoneurons when injected into their target muscles. The majority of the changes in motoneuron electrical properties caused by ADM resemble those observed in motoneurons of aged cats. Additional research is required to determine whether the specific changes induced in motoneurons by ADM and those that occur in motoneurons in old age are due to similar degradative mechanisms.

Afterdepolarization mechanism in the in vitro, cesium-loaded, sympathetic preganglionic neuron of the cat

1987 ◽  
Vol 57 (5) ◽  
pp. 1325-1337 ◽  
Author(s):  
M. Yoshimura ◽  
C. Polosa ◽  
S. Nishi
Keyword(s):  
Action Potential ◽  
Action Potential Duration ◽  
Time Course ◽  
Choline Chloride ◽  
Membrane Potentials ◽  
Ca Channel ◽  
Krebs Solution ◽  
Similar Time ◽  
K Concentration

Intracellular recordings were performed in Cs-loaded sympathetic preganglionic neurons (SPNs) of the intermediolateral nucleus, identified by antidromic stimulation, in the slice of the T2 or T3 segment of the cat spinal cord. Loading the neurons with Cs resulted in broadening of the action potential, depression of the fast component of the afterhyperpolarization (AHP), and appearance of an afterdepolarization (ADP). A typical ADP in a Cs-loaded neuron had time to peak of 45-110 ms, half-decay time of 70-250 ms, and amplitude of 2-10 mV at membrane potentials between -60 and -70 mV and at a Ca and K concentration of 2.5 and 3.6 mM, respectively, in the superfusion medium. The ADP was associated with a decrease in neuron input resistance and increased in magnitude with hyperpolarization of the cell membrane. The relation between peak ADP amplitude and membrane potential was linear within the range of membrane potentials from -60 to -100 mV. The ADP was reversibly suppressed by the Ca-channel blocker cobalt (2 mM) or by low Ca Krebs solution (0.25 mM). Superfusion with BaCl2 (1.0 mM) or tetraethylammonium (TEA) (10-20 mM) caused an increase in amplitude of the ADP and an increase in action potential duration. Hyperpolarizing pulses, delivered during the course of the spike shoulder, resulted in a decrease of spike duration and ADP amplitude. The ADP was not affected by tetrodotoxin, at a dose blocking the Na-spike, and was enhanced, in association with an increase in action potential duration, when NaCl in the Krebs solution was replaced with choline chloride. Increasing intracellular Cl concentration or decreasing extracellular Cl concentration had no effect on the ADP. Changes in external K concentration from 3.6 to 10 or 0.36 mM increased and decreased, respectively, the amplitude of the ADP. In the absence of Cs, and ADP, with similar time course to that recorded in Cs-loaded SPNs, was recorded when CaCl2 was replaced by BaCl or NaCl was replaced by TEAC1. It is concluded that the SPN afterpotential includes a Ca-dependent inward current, in addition to the already described fast and slow outward K currents of the AHP.

scholarly journals The Role of the Putative Inactivation Lid in Sodium Channel Gating Current Immobilization

2000 ◽  
Vol 115 (5) ◽  
pp. 609-620 ◽  
Author(s):  
Michael F. Sheets ◽  
John W. Kyle ◽  
Dorothy A. Hanck
Keyword(s):  
Sodium Channel ◽  
Time Constant ◽  
Time Course ◽  
Gating Current ◽  
Similar Time ◽  
Charge Voltage ◽  
Voltage Gated Sodium Channels ◽  
Gating Charge ◽  
Domain Iii ◽  
A Site

We investigated the contribution of the putative inactivation lid in voltage-gated sodium channels to gating charge immobilization (i.e., the slow return of gating charge during repolarization) by studying a lid-modified mutant of the human heart sodium channel (hH1a) that had the phenylalanine at position 1485 in the isoleucine, phenylalanine, and methionine (IFM) region of the domain III–IV linker mutated to a cysteine (ICM-hH1a). Residual fast inactivation of ICM-hH1a in fused tsA201 cells was abolished by intracellular perfusion with 2.5 mM 2-(trimethylammonium)ethyl methanethiosulfonate (MTSET). The time constants of gating current relaxations in response to step depolarizations and gating charge–voltage relationships were not different between wild-type hH1a and ICM-hH1aMTSET. The time constant of the development of charge immobilization assayed at −180 mV after depolarization to 0 mV was similar to the time constant of inactivation of INa at 0 mV for hH1a. By 44 ms, 53% of the gating charge during repolarization returned slowly; i.e., became immobilized. In ICM-hH1aMTSET, immobilization occurred with a similar time course, although only 31% of gating charge upon repolarization (OFF charge) immobilized. After modification of hH1a and ICM-hH1aMTSET with Anthopleurin-A toxin, a site-3 peptide toxin that inhibits movement of the domain IV-S4, charge immobilization did not occur for conditioning durations up to 44 ms. OFF charge for both hH1a and ICM-hH1aMTSET modified with Anthopleurin-A toxin were similar in time course and in magnitude to the fast component of OFF charge in ICM-hH1aMTSET in control. We conclude that movement of domain IV-S4 is the rate-limiting step during repolarization, and it contributes to charge immobilization regardless of whether the inactivation lid is bound. Taken together with previous reports, these data also suggest that S4 in domain III contributes to charge immobilization only after binding of the inactivation lid.

Role of calcium influx and buffering in the kinetics of Ca(2+)-activated K+ current in rat vagal motoneurons

1992 ◽  
Vol 68 (6) ◽  
pp. 2237-2247 ◽  
Author(s):  
P. Sah
Keyword(s):  
Action Potential ◽  
Time Constant ◽  
Potassium Current ◽  
Time Course ◽  
Calcium Influx ◽  
Outward Current ◽  
Resting Potential ◽  
Motor Nucleus ◽  
Simple Diffusion ◽  
Single Action

1. Intracellular recordings were obtained from neurons of the dorsal motor nucleus of the vagus (DMV) in transverse slices of the rat medulla maintained in vitro. These neurons had a resting potential of -59.8 +/- 8.7 (SD) mV. Single action potentials elicited by brief depolarizing current pulses were followed by a prolonged afterhyperpolarization (AHP). Under voltage clamp, the current underlying the AHP was found to be a calcium-activated potassium current. 2. The outward current (GkCa,1) was voltage insensitive and was not blocked by tetraethylammonium (TEA) (10 mM). Unlike the slower time course calcium-activated potassium current recorded in some other neurons, GkCa,1 was blocked by apamin (25-100 nM), indicating that SK type calcium-activated potassium channels underlie this current. 3. GkCa,1 was maximal within 10 ms of the action potential and its decay was well described by a single exponential. After a single action potential the time constant of decay of GkCa,1 was 155 +/- 66 (+/- SD) ms. 4. Calcium influx was increased by adding TEA to the extracellular solution or by firing more than one action potential. As the calcium load was increased, both the peak amplitude and the time constant of decay of GkCa,1 increased. In cells impaled with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA)-filled electrodes, the time constant of decay of GkCa,1 after a single action current was 71 +/- 19 ms. 5. A simple diffusion-based model that incorporates two intrinsic calcium buffers is developed that accounts for many of the properties of GkCa,1. It is concluded that the decay of GkCa,1 reflects the time course of removal of calcium that has entered the cell during the action potential.

Activity-dependent changes in extracellular potassium and excitability in turtle olfactory nerve

1987 ◽  
Vol 57 (3) ◽  
pp. 740-754 ◽  
Author(s):  
D. L. Eng ◽  
J. D. Kocsis
Keyword(s):  
Conduction Velocity ◽  
Time Course ◽  
Compound Action Potential ◽  
Olfactory Nerve ◽  
Extracellular Potassium ◽  
Similar Time ◽  
Supernormal Period ◽  
Sucrose Gap ◽  
Activity Dependent

The excitability properties of turtle olfactory nerve (o.n.) were studied in vitro using potassium-sensitive microelectrodes (KSM), a modified sucrose gap chamber, and a standard nerve chamber to measure conduction velocity. A pronounced supernormal period (SNP), as indicated by increased conduction velocity of the o.n. fiber volley, lasting up to several seconds, was observed following a single stimulus. The compound action potential recorded in the sucrose gap chamber showed a prolonged depolarization with a similar time course to the SNP. When stimulation intensity was submaximal the response amplitude, and the extracellular potassium concentration [K+]o, continuously increased during repetitive stimulation. In contrast, when supramaximal stimuli were applied, the amplitude of the o.n. fiber volley was reduced during a high-frequency stimulus train for all responses after the initial one even though latency was maximally reduced, i.e., during supernormal conduction. Superfusion with various levels of K+ elicited changes in the excitability of the o.n. fibers. Small increases in [K+]o above the resting concentration of 2.6 mM led to an increase in resting excitability, whereas larger increases resulted in decreased excitability and conduction block. The SNP was eliminated when extracellular potassium was elevated between 3 and 4 mM above resting levels. Microstimulation of a small bundle of o.n. fibers led to an increase in [K+]o along the bundle but also around adjacent nonactivated fibers. The excitability of these neighboring nonactivated fibers was increased, further indicating the importance of activity-dependent changes in [K+]o in modulating axonal excitability. These results demonstrate the importance of activity-dependent increases in extracellular potassium in modulating nonmyelinated o.n. fiber excitability. They also indicate that increases in [K+]o and an associated membrane depolarization contribute to the increased excitability observed during fiber recruitment and the supernormal period.

scholarly journals ELECTRIC IMPEDANCE OF NITELLA DURING ACTIVITY

1938 ◽  
Vol 22 (1) ◽  
pp. 37-64 ◽  
Author(s):  
Kenneth S. Cole ◽  
Howard J. Curtis
Keyword(s):  
Action Potential ◽  
Current Flow ◽  
Short Circuit ◽  
Complex Impedance ◽  
Wheatstone Bridge ◽  
Membrane Resistance ◽  
Cell Axis ◽  
Excitation Wave ◽  
Water Plant ◽  
Membrane Changes

The changes in the alternating current impedance which occur during activity of cells of the fresh water plant Nitella have been measured with the current flow normal to the cell axis, at eight frequencies from 0.05 to 20 kilocycles per second, and with simultaneous records of the action potential under the impedance electrodes. At each frequency the resting cell was balanced in a Wheatstone bridge with a cathode ray oscillograph, and after electrical stimulation at one end of the cell, the changes in the complex impedance were determined from the bridge unbalance recorded by motion pictures of the oscillograph figure. An extension of the previous technique of interpretation of the transverse impedance shows that the normal membrane capacity of 0.9 µf./cm.2 decreases about 15 per cent without change of phase angle, while the membrane resistance decreases from 105 ohm cm.2 to about 500 ohm cm.2 during the passage of the excitation wave. This membrane change occurs during the latter part of the rising phase of the action potential, and it is shown that the membrane electromotive force remains unchanged until nearly the same time. The part of the action potential preceding these membrane changes is probably a passive fall of potential ahead of a partial short circuit.

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