Electrical properties of frog motoneurons in the in situ spinal cord

1976 ◽  
Vol 39 (3) ◽  
pp. 459-473 ◽  
Author(s):  
P. C. Magherini ◽  
W. Precht
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Rana Temporaria ◽  
Reversal Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Spike Initiation

Electrical properties of the spinal motoneurons of Rana temporaria and R. esculenta were investigated in the in situ spinal cord at 20-22 degrees C by means of intracellular recording and current injection. Input resistance values depended on the method of measurement in a given cell but were generally inversely related to axon conduction velocity. The membrane-potential response to a subthreshold current pulse was composed of at least two exponentials with mean time constants of 2.5 and 20 ms. The membrance potential reached by the peak of a spike depended on the mode of spike initiation and membrane potential. Preceding a suprathreshold depolarization by a hyperpolarizing pulse could delay and eliminate spike initiation, similar to effects reported in certain invertebrate neurons. Antidromic invasion frequently failed in motoneurons of normal resting potential. Antidromic spike components (m,IS, SD) were similar to those of cat motoneurons. The delayed depolarization and the long afterhyperpolarization following an antidromic spike had many properties in common with the analogous afterpotentials of cat motoneurons. The reversal potential of the short afterhyperpolarization occurring immediately after the spike varied with resting potential and could not be used to determine potassium equilibrium potential. Sustained rhythmic firing could be evoked by continuous synaptic drive or long pulses of injected current. The plot of firing rate versus current strength had a substantial linear region. Both steady firing and adaptation properties varied markedly with motoneuron input resistance.

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

Sustained depolarizing potentials in reticulospinal axons during evoked seizure activity in lamprey spinal cord

1978 ◽  
Vol 41 (2) ◽  
pp. 384-393 ◽  
Author(s):  
G. Matthews ◽  
W. O. Wickelgren
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Input Resistance ◽  
Response Amplitude ◽  
Resting Potential ◽  
Mammalian Brain ◽  
Extracellular Potassium ◽  
Synaptic Potential ◽  
Axonal Membrane ◽  
Passive Current

1. Intracellular recordings were made from lamprey reticulospinal axons (Muller axons) during seizures evoked by electrical stimulation of the isolated spinal cord in saline containing either 0 Cl or 1 mM picrotoxin. The seizures had tonic and clonic-phases similar to ictal seizures in mammalian brain. 2. During seizures Muller axons were depolarized by 10-15 mV. These seizure-depolarizations were not due to any direct effect of the evoking stimulus on the Muller axons themselves nor were they initiated by an accumulation or extracellular potassium. 3. A decrease in axonal input resistance occurred during a seizure-depolarization. Also, the amplitude of a seizure-depolarization was decreased by depolarizing the axon 5-15 mV with injected current. Further, hyperpolarizing the axon increased the amplitude of the seizure-depolarization, but the growth flattened out beyond 30-40 mV of hyperpolarization. The decrease in input resistance during the seizure-depolarization and the dependence of the response amplitude on axonal membrane potential suggested that the seizure-depolarization was an excitatory synaptic potential. However, the failure of the seizure-depolarization amplitude to continue to grow at membrane potentials greater than 30 mV negative to the resting potential was not consistent with this interpretation. 4. A synaptic conductance change as the cause of the seizure-depolarization was ruled out by setting the axonal membrane potential at different levels with injected current and monitoring the input resistance of the axon before and during seizure-depolarizations. It was found that no change in input resistance occurred during the seizure-depolarization when the axon was hyperpolarized more than approximately 30 mV, the same potential at which the growth in the response amplitude ceased. From analysis of these data and the passive current-voltage properties of Muller axons it is concluded that the seizure-depolarization is not a chemical synaptic potential, but rather the result of the passive injection of depolarizing current into the axons. 5. The source of the depolarizing current which flows into Muller axons during seizures is probably paroxysmal action-potential activity in spinal motoneurons and interneurons, many of which are electrically coupled to Muller axons.

Control of intracellular calcium by membrane potential in human melanoma cells

1993 ◽  
Vol 265 (6) ◽  
pp. C1501-C1510 ◽  
Author(s):  
B. Nilius ◽  
G. Schwarz ◽  
G. Droogmans
Keyword(s):  
Cell Proliferation ◽  
Membrane Potential ◽  
Intracellular Calcium ◽  
Reversal Potential ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Human Melanoma Cells

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

Effect of procaine on electrical properties of squid axon membrane

1959 ◽  
Vol 196 (5) ◽  
pp. 1071-1078 ◽  
Author(s):  
Robert E. Taylor
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Squid Axon ◽  
Voltage Step ◽  
Axon Membrane ◽  
Rate Of Development

Procaine (0.025–0.1%; pH 7.9) caused a reduction in the amount and rate of development of the early transient (sodium) and late steady state (potassium) currents which occur during a depolarizing voltage step applied to the excised, voltage clamped squid axon. Consistent results were obtained by holding the membrane potential at a hyperpolarized value prior to the applied step. No effect was seen on the resting potential, on the sodium equilibrium potential, or on the proportion of the sodium carrying system which was ‘inactive’ at any membrane potential. The blocking action of procaine is a result of the inhibition by the drug of the sodium carrying system. The effect of procaine on the potassium conductance is such as to oppose the blocking action.

scholarly journals Current Separations in Myxicola Giant Axons

1969 ◽  
Vol 54 (6) ◽  
pp. 741-754 ◽  
Author(s):  
L. Goldman ◽  
L. Binstock
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Reversal Potential ◽  
Transient Current ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Resting Membrane Potential ◽  
Concentration Data ◽  
Giant Axons ◽  
Current Reversal

The effect of reducing the external sodium concentration, [Na]o, on resting potential, action potential, membrane current, and transient current reversal potential in Myxicola giant axons was studied. Tris chloride was used as a substitute for NaCl. Preliminary experiments were carried out to insure that the effect of Tris substitution could be attributed entirely to the reduction in [Na]o. Both choline and tetramethylammonium chloride were found to have additional effects on the membrane. The transient current is carried largely by Na, while the delayed current seems to be independent of [Na]o. Transient current reversal potential behaves much like a pure Nernst equilibrium potential for sodium. Small deviations from this behavior are consistent with the possibility of some small nonsodium component in the transient current. An exact PNa/PK for the transient current channels could not be computed from these data, but is certainly well greater than unity and possibly quite large. The peak of the action potential varied with [Na]o as expected for a sodium action potential with some substantial potassium permeability at the time of peak. Resting membrane potential is independent of [Na]o. This finding is inconsistent with the view that the resting membrane potential is determined only by the distribution of K and Na, and PNa/PK. It is suggested that PNa/PK's obtained from resting membrane potential-potassium concentration data do not always have the physical meaning generally attributed to them.

Mechanisms of Afterhyperpolarization in Lobster Olfactory Receptor Neurons

1998 ◽  
Vol 80 (3) ◽  
pp. 1268-1276 ◽  
Author(s):  
Frank S. Corotto ◽  
William C. Michel
Keyword(s):  
Voltage Clamp ◽  
Olfactory Receptor ◽  
Reversal Potential ◽  
Input Resistance ◽  
Olfactory Receptor Neurons ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Pipette Solution ◽  
Cation Current ◽  
Receptor Neurons

Corotto, Frank S. and William C. Michel. Mechanisms of afterhyperpolarization in lobster olfactory receptor neurons. J. Neurophysiol. 80: 1268–1276, 1998. In lobster olfactory receptor neurons (ORNs), depolarizing responses to odorants and current injection are accompanied by the development of an afterhyperpolarization (AHP) that likely contributes to spike-frequency adaptation and that persists for several seconds after termination of the response. A portion of the AHP can be blocked by extracellular application of 5 mM CsCl. At this concentration, CsCl specifically blocks the hyperpolarization-activated cation current ( I h) in lobster ORNs. This current is likely to be active at rest, where it provides a constant, depolarizing influence. Further depolarization deactivates I h, thus allowing the cell to be briefly hyperpolarized when that depolarizing influence is removed, thus generating an AHP. Reactivation of I h would terminate the AHP. The component of the AHP that could not be blocked by Cs+ (the Cs+-insensitive AHP) was accompanied by decreased input resistance, suggesting that this component is generated by increased conductance to an ion with an equilibrium potential more negative than the resting potential. The Cs+-insensitive AHP in current clamp and the underlying current in voltage clamp displayed a reversal potential of approximately –75 mV. Both E K and E Cl are predicted to be in this range. Similar results were obtained with the use of a high Cl– pipette solution, although that shifted E Cl from –72 mV to –13 mV. However, when E K was shifted to more positive or negative values, the reversal potential also shifted accordingly. A role for the Ca2+-mediated K+ current in generating the Cs+-independent AHP was explored by testing cells in current and voltage clamp while blocking I K(Ca) with Cs+/Co2+-saline. In some cells, the Cs+-independent AHP and its underlying current could be completely and reversibly blocked by Cs+/Co2+ saline, whereas in other cells some fraction of it remained. This indicates that the Cs+-independent AHP results from two K+ currents, one that requires an influx of extracellular Ca2+ and one that does not. Collectively, these findings indicate that AHPs result from three phenomena that occur when lobster ORNs are depolarized: 1) inactivation of the hyperpolarization-activated cation current, 2) activation of a Ca2+-mediated K+ current, and 3) activation of a K+ current that does not require influx of extracellular Ca2+. Roles of these processes in modulating the output of lobster ORNs are discussed.

Mechanism of action of galanin on myenteric neurons

1988 ◽  
Vol 60 (3) ◽  
pp. 966-979 ◽  
Author(s):  
K. Tamura ◽  
J. M. Palmer ◽  
C. K. Winkelmann ◽  
J. D. Wood
Keyword(s):  
Mechanism Of Action ◽  
Reversal Potential ◽  
Input Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Simultaneous Application ◽  
Membrane Hyperpolarization ◽  
K Channels ◽  
Myenteric Neurons ◽  
Spike Initiation

1. Conventional intracellular recording methods were used to investigate the mechanism of action of galanin on electrical behavior of AH/type 2 myenteric neurons in the guinea pig small intestine. 2. The overall action of galanin was inhibitory and consisted of membrane hyperpolarization, decreased input resistance, and suppression of excitability. 3. The action of galanin was on the somatic membrane. There were no effects on spike initiation or propagation velocity in the processes. 4. The reversal potential for the hyperpolarizing action of galanin was near the estimated K+ equilibrium potential and was dependent on the concentration of K+ in the bathing medium. 5. Treatment with tetraethylammonium (TEA) broadened the action-potential and enhanced long-lasting hyperpolarizing after-potentials (AH). Application of galanin or depletion of Ca2+ in the bathing medium offset the effects of TEA on the spike and the AH. Galanin or reduced Ca2+ had the same effect when both TEA and tetrodotoxin (TTX) were present. 6. Simultaneous application of TEA and 4-aminopyridine (4-AP) evoked spontaneous spike discharge with broadened spikes and enhanced AH. This activity was suppressed by galanin. 7. Intrasomatic injection of Cs+ in the presence of TTX appeared to abolish all K+ conductances leaving pure Ca2+ spikes in response to depolarizing current pulse. Galanin abolished these Ca2+ spikes. 8. The results suggest two major mechanisms of action for galanin. One is to open K+ channels, decrease input resistance, and hyperpolarize the membrane toward EK+. The second is blockade of voltage gated Ca2+ channels and suppression of the AH by indirect prevention of opening of Ca2+-dependent K+ channels.

Effects of ouabain on background and voltage-dependent currents in canine colonic myocytes

1990 ◽  
Vol 259 (3) ◽  
pp. C402-C408 ◽  
Author(s):  
E. P. Burke ◽  
K. M. Sanders
Keyword(s):  
Membrane Potential ◽  
Potential Gradient ◽  
Circular Muscle ◽  
Input Resistance ◽  
Pump Current ◽  
Muscle Layer ◽  
Membrane Properties ◽  
Resting Potential ◽  
Voltage Dependent ◽  
In Cells

Previous studies have suggested that the membrane potential gradient across the circular muscle layer of the canine proximal colon is due to a gradient in the contribution of the Na(+)-K(+)-ATPase. Cells at the submucosal border generate approximately 35 mV of pump potential, whereas at the myenteric border the pump contributes very little to resting potential. Results from experiments in intact muscles in which the pump is blocked are somewhat difficult to interpret because of possible effects of pump inhibitors on membrane conductances. Therefore, we studied isolated colonic myocytes to test the effects of ouabain on passive membrane properties and voltage-dependent currents. Ouabain (10(-5) M) depolarized cells and decreased input resistance from 0.487 +/- 0.060 to 0.292 +/- 0.040 G omega. The decrease in resistance was attributed to an increase in K+ conductance. Studies were also performed to measure the ouabain-dependent current. At 37 degrees C, in cells dialyzed with 19 mM intracellular Na+ concentration [( Na+]i), ouabain caused an inward current averaging 71.06 +/- 7.49 pA, which was attributed to blockade of pump current. At 24 degrees C or in cells dialyzed with low [Na+]i (11 mM), ouabain caused little change in holding current. With the input resistance of colonic cells, pump current appears capable of generating at least 35 mV. Thus an electrogenic Na+ pump could contribute significantly to membrane potential.

Cholecystokinin-gated currents in neurons of the rat solitary complex in vitro

1993 ◽  
Vol 70 (6) ◽  
pp. 2584-2595 ◽  
Author(s):  
P. Branchereau ◽  
J. Champagnat ◽  
M. Denavit-Saubie
Keyword(s):  
Voltage Clamp ◽  
Potassium Current ◽  
Reversal Potential ◽  
Input Resistance ◽  
Calcium Currents ◽  
Equilibrium Potential ◽  
Potassium Ions ◽  
Nernst Equation ◽  
Membrane Hyperpolarization ◽  
Cckb Receptor

1. Ionic conductances controlled by type A and type B cholecystokinin (CCK) receptors were studied in neurons of the rat nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMNV), using intracellular and whole-cell patch clamp recordings in current or voltage clamp configuration during bath application of agonists (CCK8, CCK4, BC 264) and antagonists. 2. CCKA receptor-related inhibition was associated with a membrane hyperpolarization and a decrease in input resistance that developed 2-6 min after the arrival of drug into the extracellular medium. These effects were induced by 5 nM CCK8 but not BC 264 and they were blocked by the CCKA antagonist, L-364,718, but not by the CCKB antagonist, L-365,260. 3. CCKA receptor-related inhibition was generated by a potassium current that reversed at a reversal potential E(rev) of -73 +/- 1 (mean +/- SE) mV with bathing potassium concentration [K+]o = 6 mM and at -88 +/- 1 with [K+]o = 3 mM, in agreement with the Nernst equation for potassium ions. 4. CCKB receptor-related excitation was associated with a membrane depolarization and an increase of the input resistance induced by the following agonists at threshold concentrations: CCK8 (0.2 nM) > or = BC 264 (0.4 nM) > CCK4 (10.9 nM). The increase of input resistance was abolished by L-365,260 and was maintained after blockade of the CCKA current by L-364,718. 5. CCKB receptor-related excitation, in the neurons (30% of cases) in which clear response reversal was observed, appeared to be generated by a decrease of a potassium conductance. Responses showed a reversal potential E(rev) of -68 +/- 4 mV with [K+]o = 6 mM and -89 +/- 1 mV with [K+]o = 3 mM, verifying predictions from the Nernst equation applied to potassium ions. However, in 70% of cases, clear reversal was not observed at membrane potentials negative to the theoretical potassium equilibrium potential EK. 6. In voltage clamp studies, CCK8 induced a 181 +/- 17 pA inward current associated with a 26 +/- 4% decrease in the instantaneous current (I(ins)) generated by hyperpolarizing voltage steps. This effect on I(ins) was demonstrated in the absence of effects on the outward noninactivating potassium current (IM) and on the inward noninactivating cationic current (IQ). 7. CCKB receptor-mediated excitation was not suppressed by cobalt, a blocker of calcium currents, and was not associated with a change of the calcium-dependent potassium current (IK(Ca)).(ABSTRACT TRUNCATED AT 400 WORDS)

Hyperpolarization-Activated Inward Current in Neurons of the Rat's Dorsal Nucleus of the Lateral Lemniscus In Vitro

1997 ◽  
Vol 78 (5) ◽  
pp. 2235-2245 ◽  
Author(s):  
Xiao Wen Fu ◽  
Borys L. Brezden ◽  
Shu Hui Wu
Keyword(s):  
Membrane Potential ◽  
Input Resistance ◽  
Resting Potential ◽  
Extracellular Potassium ◽  
Current Clamp ◽  
Lateral Lemniscus ◽  
Inward Current ◽  
Dorsal Nucleus ◽  
Maximal Activation

Fu, Xiao Wen, Borys L. Brezden, and Shu Hui Wu. Hyperpolarization-activated inward current in neurons of the rat's dorsal nucleus of the lateral lemniscus in vitro. J. Neurophysiol. 78: 2235–2245, 1997. The hyperpolarization-activated current ( I h) underlying inward rectification in neurons of the rat's dorsal nucleus of the lateral lemniscus (DNLL) was investigated using whole cell patch-clamp techniques. Patch recordings were made from DNLL neurons of young rats (21–30 days old) in 400 μm tissue slices. Under current clamp, injection of negative current produced a graded hyperpolarization of the cell membrane, often with a gradual sag in the membrane potential toward the resting value. The rate and magnitude of the sag depended on the amount of hyperpolarizing current. Larger current resulted in a larger and faster decay of the voltage. Under voltage clamp, hyperpolarizing voltage steps elicited a slowly activating inward current that was presumably responsible for the sag observed in the voltage response to a steady hyperpolarizing current recorded under current clamp. Activation of the inward current ( I h) was voltage and time dependent. The current just was seen at a membrane potential of −70 mV and was activated fully at −140 mV. The voltage value of half-maximal activation of I h was −78.0 ± 6.0 (SE) mV. The rate of I h activation was best approximated by a single exponential function with a time constant that was voltage dependent, ranging from 276 ± 27 ms at −100 mV to 186 ± 11 ms at −140 mV. Reversal potential ( E h) of I h current was more positive than the resting potential. Raising the extracellular potassium concentration shifted E h to a more depolarized value, whereas lowering the extracellular sodium concentration shifted E h in a more negative direction. I h was sensitive to extracellular cesium but relatively insensitive to extracellular barium. The current amplitude near maximal-activation (about −140 mV) was reduced to 40% of control by 1 mM cesium but was reduced to only 71% of control by 2 mM barium. When the membrane potential was near the resting potential (about −60 mV), cesium had no effect on the membrane potential, current-evoked firing rate and input resistance but reduced the spontaneous firing. When the membrane potential was more negative than −70 mV, cesium hyperpolarized the cell, decreased current-evoked firing and increased the input resistance. I h in DNLL neurons does not contribute to the normal resting potential but may enhance the extent of excitation, thereby making the DNLL a consistently powerful inhibitory source to upper levels of the auditory system.

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