Internal cesium ions block various K conductances in spinal motoneurons

1981 ◽  
Vol 59 (12) ◽  
pp. 1280-1284 ◽  
Author(s):  
E. Puil ◽  
R. Werman
Keyword(s):  
Action Potentials ◽  
Considerable Increase ◽  
Membrane Conductance ◽  
Membrane Properties ◽  
Resting Potential ◽  
Large Reduction ◽  
Spinal Motoneurons ◽  
Spike Generation ◽  
Cesium Ions ◽  
Voltage Dependent

Conventional intracellular recording with low resistance electrodes was used to examine the effects of iontophoretic injections of Cs+ ions (30–200 nA for 30–500 s) into spinal motoneurons of cats anesthetized with pentobarbital and paralyzed with gallamine. The most striking effects of internal Cs+ were a great prolongation of the falling phase of action potentials, a large reduction in the amplitude of their afterhyperpolarizations, and a considerable increase in the size of delayed depolarizations. A reduction of resting membrane conductance (up to half of control values) and a small increase in membrane potential usually were evident. Although the rate of rise and amplitude of spikes sometimes were increased, the above effects on membrane properties usually were accompanied by block of antidromic invasion or synaptic spike generation, and inactivation of directly evoked spikes. Recovery of spike genesis was very rapid but the prolongation of spikes and other effects of Cs+ lasted 4–35 min, depending on the amount of Cs+ application. Larger injections of Cs+ resulted in greater depolarizations of up to 13 mV. It is concluded that internal Cs+ ions block voltage-dependent K+ conductance of spike repolarization, the Ca2+-activated K+ conductance responsible for the afterhyperpolarization, and some of the K+ conductance responsible for the resting potential. It is suggested that the enhanced delayed depolarization may result from a Cs+-blockade of an early outward K+ current which would unmask an inward current of Ca2+ ions.

Properties of visceral primary afferent neurons in the nodose ganglion of the rabbit

1985 ◽  
Vol 54 (2) ◽  
pp. 245-260 ◽  
Author(s):  
C. E. Stansfeld ◽  
D. I. Wallis
Keyword(s):  
Action Potentials ◽  
Input Resistance ◽  
Nodose Ganglion ◽  
Time Dependent ◽  
Membrane Properties ◽  
Resting Potential ◽  
Inward Rectification ◽  
C Cells ◽  
Axonal Conduction ◽  
A Cells

The active and passive membrane properties of rabbit nodose ganglion cells and their responsiveness to depolarizing agents have been examined in vitro. Neurons with an axonal conduction velocity of less than 3 m/s were classified as C-cells and the remainder as A-cells. Mean axonal conduction velocities of A- and C-cells were 16.4 m/s and 0.99 m/s, respectively. A-cells had action potentials of brief duration (1.16 ms), high rate of rise (385 V/s), an overshoot of 23 mV, and relatively high spike following frequency (SFF). C-cells typically had action potentials with a "humped" configuration (duration 2.51 ms), lower rate of rise (255 V/s), an overshoot of 28.6 mV, an after potential of longer duration than A-cells, and relatively low SFF. Eight of 15 A-cells whose axons conducted at less than 10 m/s had action potentials of longer duration with a humped configuration; these were termed Ah-cells. They formed about 10% of cells whose axons conducted above 2.5 m/s. The soma action potential of A-cells was blocked by tetrodotoxin (TTX), but that of 6/11 C-cells was unaffected by TTX. Typically, A-cells showed strong delayed (outward) rectification on passage of depolarizing current through the soma membrane and time-dependent (inward) rectification on inward current passage. Input resistance was thus highly sensitive to membrane potential close to rest. In C-cells, delayed rectification was not marked, and slight time-dependent rectification occurred in only 3 of 25 cells; I/V curves were normally linear over the range: resting potential to 40 mV more negative. Data on Ah-cells were incomplete, but in our sample of eight cells time-dependent rectification was absent or mild. C-cells had a higher input resistance and a higher neuronal capacitance than A-cells. In a proportion of A-cells, RN was low at resting potential (5 M omega) but increased as the membrane was hyperpolarized by a few millivolts. A-cells were depolarized by GABA but were normally unaffected by 5-HT or DMPP. C-cells were depolarized by GABA in a similar manner to A-cells but also responded strongly to 5-HT; 53/66 gave a depolarizing response, and 3/66, a hyperpolarizing response. Of C-cells, 75% gave a depolarizing response to DMPP.(ABSTRACT TRUNCATED AT 400 WORDS)

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.

Is cyclic guanosine monophosphate the internal 'second messenger' for cholinergic actions on central neurons?

1976 ◽  
Vol 54 (2) ◽  
pp. 172-176 ◽  
Author(s):  
K. Krnjević ◽  
E. Puil ◽  
R. Werman
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Cyclic Guanosine Monophosphate ◽  
Guanosine Monophosphate ◽  
Resting Potential ◽  
Electrical Excitability ◽  
Spinal Motoneurons ◽  
Central Neurons ◽  
Intracellular Cgmp ◽  
Post Synaptic Potential

The most consistent effects produced by intracellular injections of guanosine 3′,5′-cyclic monophosphate (cGMP) (but not 5′-guanosine 5′-monophosphate in spinal motoneurons of cats are a rise in membrane conductance, acceleration in time course of spike potentials, and accentuation of the post-spike hyperpolarization. Associated changes in resting potential are smaller, less constant, and more often in the depolarizing than hyperpolarizing direction. cGMP tends to increase electrical excitability but reduces excitatory post-synaptic potential amplitudes. Most of the effects of intracellular cGMP are quite different from, or indeed opposite to, those of either extra- or intracellular applications of acetylcholine and therefore not consistent with the proposal that cGMP is the internal mediator of muscarinic actions.

Membrane Properties Related to the Firing Behavior of Zebrafish Motoneurons

2003 ◽  
Vol 89 (2) ◽  
pp. 657-664 ◽  
Author(s):  
Robert R. Buss ◽  
Charles W. Bourque ◽  
Pierre Drapeau
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Membrane Conductance ◽  
Membrane Properties ◽  
High Threshold ◽  
Calcium Dependent ◽  
Larval Zebrafish ◽  
Plateau Potential ◽  
Potassium Conductances ◽  
Action Potential Burst

The physiological and pharmacological properties of the motoneuron membrane and action potential were investigated in larval zebrafish using whole cell patch current-clamp recording techniques. Action potentials were eliminated in tetrodotoxin, repolarized by tetraethylammonium (TEA) and 3,4-diaminopyridine (3,4-AP)-sensitive potassium conductances, and had a cobalt-sensitive, high-threshold calcium component. Depolarizing current injection evoked a brief (approximately 10–30 ms) burst of action potentials that was terminated by strong, outwardly rectifying voltage-activated potassium and calcium-dependent conductances. In the presence of intracellular cesium ions, a prolonged plateau potential often followed brief depolarizations. During larval development (hatching to free-swimming), the resting membrane conductance increased in a population of motoneurons, which tended to reduce the apparent outward rectification of the membrane. The conductances contributing to action potential burst termination are hypothesized to play a role in patterning the synaptically driven motoneuron output in these rapidly swimming fish.

Effects of Octopamine on Calcium Action Potentials in Insect Oocytes

1989 ◽  
Vol 142 (1) ◽  
pp. 115-124
Author(s):  
M. J. O'DONNELL ◽  
B. SINGH
Keyword(s):  
Action Potentials ◽  
Rank Order ◽  
Potassium Conductance ◽  
Membrane Resistance ◽  
Threshold Concentration ◽  
Resting Potential ◽  
Calcium Dependent ◽  
Octopamine Receptors ◽  
Voltage Dependent ◽  
Maximum Rate Of Rise

Our experiments show that octopamine receptors are present on the developing follicles of an insect, Rhodnius prolixus. Application of D,L-octopamine decreased the duration and overshoot of calcium-dependent action potentials (APs), and increased the intrafollicular concentration of cyclic AMP. The threshold concentration of D,L-octopamine for the reduction in electrical excitability was between 1 and 5×10−7moll−1, and maximal effects of a 40–50% reduction in AP overshoot and duration were apparent at 10−4moll−1. At concentrations above 10−5moll−1, a small (<10%) hyperpolarization of the resting potential was also apparent. Effects of D,L-octopamine on oocyte excitability were independent of these small shifts in resting potential. Current injection experiments, in which calcium entry was blocked by cobalt, demonstrated that D,L-octopamine reduced membrane resistance at both hyperpolarizing and depolarizing potentials. Octopamine did not affect the maximum rate of rise of the AP, dV/dtmax, which is an indicator of inward calcium current. It is suggested that octopamine may mediate its effects on excitability through an increase in a voltage-dependent potassium conductance. Application of other phenolamines indicated a rank order of potency of D, Loctopamine > D,L-synephrine > tyramine. The α-adrenergic agonists clonidine, naphazoline and tolazoline were without significant effect at 10−5-10−3moll−1. Reduction of excitability by D,L-octopamine was effectively blocked by phentolamine and metoclopramide. Yohimbine and gramine were less effective as antagonists. Possible functions of octopamine receptors in insect follicles are discussed.

Nonequivalent cylinder models of neurons: interpretation of voltage transients generated by somatic current injection

1988 ◽  
Vol 60 (1) ◽  
pp. 125-148 ◽  
Author(s):  
P. K. Rose ◽  
A. Dagum
Keyword(s):  
Regional Differences ◽  
Dendritic Tree ◽  
Membrane Properties ◽  
Reliable Estimate ◽  
Voltage Response ◽  
Spinal Motoneurons ◽  
Membrane Resistivity ◽  
Voltage Dependent ◽  
Voltage Transients ◽  
Specific Membrane

1. Numerical methods were used to simulate the voltage responses to an intrasomatic current step of neuronal models that incorporated tapering dendrites, dendrites of unequal electrotonic length, nonlinear membrane properties, and regional differences in specific membrane resistivity (Rm). A "peeling" technique was used to estimate the time constants (tau 0 and tau 1) and coefficients (a0 and a1) of the first two exponential terms of the series of exponential terms whose sum represented the slope of the voltage response. 2. The electrotonic structure of models with a uniform Rm was calculated using equations derived by Rall or Johnston or Brown et al. The adequacy of these methods were tested using a wide variety of models that conformed to the equivalent cylinder approximation of Rall. Johnston's method provided the most reliable estimate of electrotonic length (L) and the ratio of the dendritic conductance to the somatic conductance (rho). However, if L exceeded 2 and rho was eight or larger, the equations derived by Johnston could frequently not be solved due to small errors in the peeled values of tau 0, tau 1, a0, and a1. Although the method suggested by Brown et al. could be applied to all models, this method invariably underestimated L and rho. These errors were particularly large for model neurons with L values of 1.5 or larger and rho values of four or larger. Estimates of L using Rall's method were only reliable if rho was large and L was two or less. 3. Changing the geometry of the dendritic tree (dendritic tapering or dendrites of unequal L) or the addition of a time- and voltage-dependent conductance designed to mimic a sag process commonly seen in spinal motoneurons caused systematic changes in tau 0, tau 1, a0, and a1. The sag process always led to an underestimate of tau 0 even after applying a correction procedure. On the other hand, the ratio, tau 0/tau 1, was not affected by the sag process or dendritic tapering.(ABSTRACT TRUNCATED AT 400 WORDS)

Segment-specific effects of FMRFamide on membrane properties of heart interneurons in the leech

1995 ◽  
Vol 74 (4) ◽  
pp. 1485-1497 ◽  
Author(s):  
J. Schmidt ◽  
S. Gramoll ◽  
R. L. Calabrese
Keyword(s):  
Outward Current ◽  
Membrane Conductance ◽  
Membrane Properties ◽  
Inward Current ◽  
Specific Effects ◽  
Outward Currents ◽  
Voltage Dependent ◽  
Inward Currents ◽  
K Current ◽  
Conductance Increase

1. The effects of Phe-Met-Arg-Phe (FMRF)amide (10(-6) M) on membrane properties of heart interneurons in the third, fourth, and fifth segmental ganglia [HN(3), HN(4), and HN(5) cells, respectively] of the leech were studied using discontinuous current-clamp and single-electrode voltage-clamp techniques. FMRFamide was focally applied onto the soma of the cell under investigation. 2. Application of FMRFamide depolarized HN(3) and HN(4) cells by evoking an inward current. These responses were subject to pronounced desensitization. The inward currents evoked by application of FMRFamide were associated with an increase in membrane conductance and appeared to be voltage dependent. Currents were enhanced at more depolarized potentials. 3. The responsiveness of the HN(3) and HN(4) cells was not affected when the Ca2+ concentration in the bath saline was reduced from normal (1.8 mM) to 0.1 mM. The depolarizing response on application of FMRFamide was blocked when Co2+ was substituted for Ca2+. 4. HN(3) and HN(4) cells did not respond to FMRFamide application in Na(+)-free solution. Inward currents were largely reduced when bath saline with 30% of the normal Na+ concentration was used. When Li+ was substituted for Na+ in the saline, application of FMRFamide still evoked depolarizing responses in HN(3) and HN(4) cells. 5. We conclude that focal application of FMRFamide onto the somata of HN(3) and HN(4) cells evokes a voltage-dependent inward current, carried largely by Na+. 6. Focal application of FMRFamide onto somata of HN(5) cells hyperpolarized these cells by activating a voltage-dependent outward current. 7. HN(5) cells were loaded with Cl- until inhibitory postsynaptic potentials carried by Cl- reversed. Cl(-)-loaded cells still responded with a hyperpolarization when FMRFamide was applied onto their somata. Therefore the outward current evoked by FMRFamide appears to be mediated by a K+ conductance increase. 8. Application of FMRFamide onto the somata of HN(5) cells enhanced outward currents that were evoked by depolarizing voltage steps from a holding potential of -45 mV. 9. We conclude that the hyperpolarizing response of HN(5) cells to focal application of FMRFamide onto their somata is the result of an up-regulation of a voltage-dependent K+ current.

Effects of bromocriptine on prolactin release, electrical membrane properties and transmembrane Ca2+ fluxes in cultured rat pituitary adenoma cells

1986 ◽  
Vol 111 (2) ◽  
pp. 185-192 ◽  
Author(s):  
P. W. Johansen ◽  
O. Sand ◽  
J. G. Iversen ◽  
E. Haug ◽  
K. M. Gautvik
Keyword(s):  
Pituitary Adenoma ◽  
Action Potentials ◽  
Inhibitory Effect ◽  
Membrane Properties ◽  
Free Solution ◽  
Prolactin Release ◽  
Clonal Strain ◽  
Rat Pituitary ◽  
Basal Release ◽  
Voltage Dependent

Abstract. The effects of the dopamine (DA) agonist bromocriptine on prolactin (Prl) release, electrical membrane properties and transmembrane Ca2 + fluxes have been studied in a clonal strain of rat pituitary adenoma cells (GH3). These cells generate Ca2+ dependent action potentials, and produce and secrete spontaneously both Prl and growth hormone. Prl release stimulated by thyroliberin (TRH) and elevated extracellular K+ concentration was completely blocked by bromocriptine, whereas the basal release was only moderately affected. The TRH and K+ evoked Prl release were half maximally inhibited by bromocriptine at 5–10 and 10–50 μm, respectively. The normal biphasic membrane response to TRH and the depolarizing effect of elevated K+ concentration were not altered by bromocriptine, whereas the Ca2+-spikes in Na+-free solution were suppressed by the drug. We therefore suggest that bromocriptine blocks the voltage sensitive Ca2+-channels of GH3 cells. In agreement with this notion, bromocriptine also suppressed the basal and TRH induced 45Ca2+ efflux from preloaded cells. We conclude that the inhibitory effect of bromocriptine on the voltage dependent Ca2+-channels is an important mechanism responsible for suppression of Prl release.

Excitation–contraction coupling in crab muscle fibers with swollen T tubules

1985 ◽  
Vol 63 (7) ◽  
pp. 879-885 ◽  
Author(s):  
J. H. Leal-Cardoso ◽  
G. Suarez-Kurtz
Keyword(s):  
Time Course ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Membrane Properties ◽  
Membrane Excitability ◽  
High Potassium ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Voltage Dependent ◽  
T Tubules

Single crab (Callinectes danae) fibers were equilibrated with isotonic, high KC1 solutions and were subsequently returned to the control saline. This caused marked swelling of the T tubules. Fibers treated with 100 mM KCl had a 2.5-mV residual depolarization, a 50% decrease in effective membrane resistance (Reff) and a 75% reduction in membrane time constant (τm). These fibers exhibited large increases in membrane conductance upon depolarization and were inexcitable; membrane depolarization with current pulses elicited no contraction. The effects of the KCl treatment on membrane properties were not reproduced by treatment with high potassium gluconate solutions, which did not cause tubular swelling. Tetrabutylammonium (10 mM) or Ba ions (10–20 mM), but not tetraethylammonium (40–100 mM), Sr ions (15–70 mM), or procaine (1–8 mM) reversed the effects of the KCl treatment on Reff, τm, membrane excitability, and excitation–contraction coupling. The time course of the Ba effects was consistent with the suggestion that the KCl treatment increases the K conductance of the tubular membranes, which in turn prevents the activation of voltage-dependent Ca channels located in the membranes of the T system. This results in inhibition of the Ca-dependent electrogenesis and consequently, the absence of contraction upon depolarization of the plasma membrane.

Intracellular Mg2+ increases neuronal excitability

1976 ◽  
Vol 54 (1) ◽  
pp. 73-77 ◽  
Author(s):  
K. Krnjević ◽  
E. Puil ◽  
R. Werman
Keyword(s):  
Neuronal Excitability ◽  
Membrane Conductance ◽  
Resting Potential ◽  
Spinal Motoneurons ◽  
Intracellular Ca

Injection of Mg2+into spinal motoneurons of cats leads to a depolarization, associated with a fall in membrane conductance, diminution in post-spike hyperpolarization, and increased excitability. This action has an apparent reversal level substantially more negative than the resting potential, and can be ascribed to a fall in K+ membrane conductance. Since these effects are opposite to those produced by intracellular Ca2+, it is suggested that Mg2+ probably competes with Ca2+ the Ca2+ -activated K+ ionophores. Neuronal excitability can be regulated by the ratio of internal free Ca2+/Mg2+.

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