scholarly journals Quantitative Analysis of Electrotonic Structure and Membrane Properties of NMDA-Activated Lamprey Spinal Neurons

1995 ◽  
Vol 7 (3) ◽  
pp. 486-506 ◽  
Author(s):  
C. R. Murphey ◽  
L. E. Moore ◽  
J. T. Buchanan
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Membrane Properties ◽  
Neuronal System ◽  
Cable Model ◽  
Spinal Neurons ◽  
Time Constants ◽  
Cable Properties ◽  
Wide Range ◽  
Voltage Dependent

Parameter optimization methods were used to quantitatively analyze frequency-domain-voltage-clamp data of NMDA-activated lamprey spinal neurons simultaneously over a wide range of membrane potentials. A neuronal cable model was used to explicitly take into account receptors located on the dendritic trees. The driving point membrane admittance was measured from the cell soma in response to a Fourier synthesized point voltage clamp stimulus. The data were fitted to an equivalent cable model consisting of a single lumped soma compartment coupled resistively to a series of equal dendritic compartments. The model contains voltage-dependent NMDA sensitive (INMDA), slow potassium (IK), and leakage (IL) currents. Both the passive cable properties and the voltage dependence of ion channel kinetics were estimated, including the electrotonic structure of the cell, the steady-state gating characteristics, and the time constants for particular voltage- and time-dependent ionic conductances. An alternate kinetic formulation was developed that consisted of steady-state values for the gating parameters and their time constants at half-activation values as well as slopes of these parameters at half-activation. This procedure allowed independent restrictions on the magnitude and slope of both the steady-state gating variable and its associated time constant. Quantitative estimates of the voltage-dependent membrane ion conductances and their kinetic parameters were used to solve the nonlinear equations describing dynamic responses. The model accurately predicts current clamp responses and is consistent with experimentally measured TTX-resistant NMDA-induced patterned activity. In summary, an analysis method is developed that provides a pragmatic approach to quantitatively describe a nonlinear neuronal system.

scholarly journals Voltage-gated transient currents in bovine adrenal fasciculata cells. I. T-type Ca2+ current.

1993 ◽  
Vol 102 (2) ◽  
pp. 217-237 ◽  
Author(s):  
B Mlinar ◽  
B A Biagi ◽  
J J Enyeart
Keyword(s):  
Time Constant ◽  
Low Voltage ◽  
Zona Fasciculata ◽  
Patch Clamp Technique ◽  
Time Constants ◽  
Voltage Gated ◽  
Wide Range ◽  
Boltzmann Function ◽  
Voltage Dependent ◽  
Ca2 Channels

The whole cell version of the patch clamp technique was used to identify and characterize voltage-gated Ca2+ channels in enzymatically dissociated bovine adrenal zona fasciculata (AZF) cells. The great majority of cells (84 of 86) expressed only low voltage-activated, rapidly inactivating Ca2+ current with properties of T-type Ca2+ current described in other cells. Voltage-dependent activation of this current was fit by a Boltzmann function raised to an integer power of 4 with a midpoint at -17 mV. Independent estimates of the single channel gating charge obtained from the activation curve and using the "limiting logarithmic potential sensitivity" were 8.1 and 6.8 elementary charges, respectively. Inactivation was a steep function of voltage with a v1/2 of -49.9 mV and a slope factor K of 3.73 mV. The expression of a single Ca2+ channel subtype by AZF cells allowed the voltage-dependent gating and kinetic properties of T current to be studied over a wide range of potentials. Analysis of the gating kinetics of this Ca2+ current indicate that T channel activation, inactivation, deactivation (closing), and reactivation (recovery from inactivation) each include voltage-independent transitions that become rate limiting at extreme voltages. Ca2+ current activated with voltage-dependent sigmoidal kinetics that were described by an m4 model. The activation time constant varied exponentially at test potentials between -30 and +10 mV, approaching a voltage-independent minimum of 1.6 ms. The inactivation time constant (tau i) also decreased exponentially to a minimum of 18.3 ms at potentials positive to 0 mV. T channel closing (deactivation) was faster at more negative voltages; the deactivation time constant (tau d) decreased from 8.14 +/- 0.7 to 0.48 +/- 0.1 ms at potentials between -40 and -150 mV. T channels inactivated by depolarization returned to the closed state along pathways that included two voltage-dependent time constants. tau rec-s ranged from 8.11 to 4.80 s when the recovery potential was varied from -50 to -90 mV, while tau rec-f decreased from 1.01 to 0.372 s. At potentials negative to -70 mV, both time constants approached minimum values. The low voltage-activated Ca2+ current in AZF cells was blocked by the T channel selective antagonist Ni2+ with an IC50 of 20 microM. At similar concentrations, Ni2+ also blocked cortisol secretion stimulated by adrenocorticotropic hormone. Our results indicate that bovine AZF cells are distinctive among secretory cells in expressing primarily or exclusively T-type Ca2+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

Ca-Induced K+-Outward Current in Paramecium Tetraurelia

1980 ◽  
Vol 88 (1) ◽  
pp. 293-304 ◽  
Author(s):  
YOUKO SATOW ◽  
CHING KUNG
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Outward Current ◽  
Paramecium Tetraurelia ◽  
Ca Channels ◽  
Outward Currents ◽  
Ciliary Reversal ◽  
Voltage Dependent ◽  
K Current ◽  
K Outward Current

Late K-outward currents upon membrane depolarization were recorded in Paramecium tetraurelia under a voltage clamp. A Ca-induced K-outward component is demonstrated by subtracting the value of the outward current in a pawn A mutant lacking functional Ca-channels (pwA500). The Ca-induced K-outward current activates slowly, reaching a peak after 100 to 1000 ms. The current then remains steady or reaches the steady state after a decline of several seconds. EGTA2- injection experiments show that the Ca-induced K-outward current is dependent on the internal Ca2+ concentration. The current is shown to depend on the voltage-dependent Ca conductance, by study of the leaky pawn A mutant (pwA132), which has a lowered Ca conductance as well as a lowered Ca-induced K-current. The Ca-induced GK is thus indirectly dependent on the voltage. The maximal GK is about 40 nmho/cell at + 7 mV in 4 mM-K+. The Ca-induced K current is sustained throughout the prolonged depolarization and the prolonged ciliary reversal.

Voltage-clamp analysis of the ionic conductances in a leech neuron with a purely calcium-dependent action potential

1987 ◽  
Vol 58 (6) ◽  
pp. 1468-1484 ◽  
Author(s):  
J. Johansen ◽  
J. Yang ◽  
A. L. Kleinhaus
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Time Course ◽  
Outward Current ◽  
Time Constants ◽  
Exponential Time ◽  
Calcium Dependent ◽  
Voltage Dependent ◽  
Ca Currents ◽  
Single Exponential

1. The purely calcium-dependent action potential of the anterior lateral giant (ALG) cell in the leech Haementeria was examined under voltage clamp. 2. Analysis with ion substitutions showed that the ALG cell action potential is generated by only two time- and voltage-dependent conductance systems, an inward Ca-dependent current (ICa) and an outward Ca-dependent K current IK(Ca). 3. The kinetic properties of the inward current were examined both in Cs-loaded neurons with Ca as the current carrier as well as in Ba-containing Ringer solutions with Ba as the current carrier, since Ba effectively blocked all time- and voltage-dependent outward current. 4. During a maintained depolarization, Ba and Ca currents activated with a time constant tau m, they then inactivated with the decay following a single exponential time course with a time constant tau h. The time constants for decay of both Ba and Ca currents were comparable, suggesting that the mechanism of inactivation of ICa in the ALG cell is largely voltage dependent. In the range of potentials from 5 to 45 mV, tau m varied from 8 to 2 ms and tau h varied from 250 to 125 ms. 5. The activation of currents carried by Ba, after correction for inactivation, could be described reasonably well by the expression I'Ba = I'Ba(infinity) [1--exp(-t/tau m)]. 6. The steady-state activation of the Ba-conductance mBa(infinity) increased sigmoidally with voltage and was approximated by the equation mBa(infinity) = (1 + exp[(Vh-6)/3])-1. The steady-state inactivation hBa(infinity) varied with holding potential and could be described by the equation hBa(infinity) = [1 + exp(Vh + 10/7)]-1. Recovery from inactivation of IBa was best described by the sum of two exponential time courses with time constants of 300 ms and 1.75 s, respectively. 7. The outward current IK(Ca) developed very slowly (0.5–1 s to half-maximal amplitude) and did not inactivate during a 20-s depolarizing command pulse. Tail current decay of IK(Ca) followed a single exponential time course with voltage-dependent time constants of between 360 and 960 ms. The steady-state activation n infinity of IK(Ca) increased sigmoidally with depolarization as described by the equation n infinity = [1 + exp(Vh-13.5)/-8)]-1. 8. The reversal potentials of IK(Ca) tail currents were close to the expected equilibrium potential for potassium and they varied linearly with log [K]o with a slope of 51 mV. These results suggest a high selectivity of the conductance for K ions.(ABSTRACT TRUNCATED AT 400 WORDS)

Voltage-clamp analysis of a Ca2+- and voltage-dependent chloride conductance in cultured mouse spinal neurons

1986 ◽  
Vol 55 (6) ◽  
pp. 1115-1135 ◽  
Author(s):  
D. G. Owen ◽  
M. Segal ◽  
J. L. Barker
Keyword(s):  
Voltage Clamp ◽  
Reversal Potential ◽  
Gamma Aminobutyric Acid ◽  
Spinal Neurons ◽  
Exponential Process ◽  
Voltage Clamp Analysis ◽  
Voltage Dependent ◽  
Inward Currents ◽  
Ca 50 ◽  
O 10

Current and voltage-clamp recordings were made at room temperature from cultured mouse spinal neurons using conventional two-electrode voltage-clamp techniques and electrodes filled with either 3 M KCl, 3 M CsCl, or 3 M Cs2SO4. In the presence of tetraethylammonium and tetrodotoxin, “fast” (rapidly rising and falling) action potentials (FAP) of variable duration were recorded in most neurons. “Slow” (slowly rising and falling) depolarizing potentials (SDP) occurred in 23% of the cells, when using KCl-filled electrodes, and in 82% of the cells with CsCl-filled electrodes. The SDP was frequently preceded by an FAP, although in some cells activation of the SDP occurred before the FAP threshold was reached and in a graded fashion. Both the FAP and SDP were abolished by Cd2+ and other Ca2+ antagonists. In cells exhibiting SDPs, voltage-clamp analysis revealed a sustained (noninactivating) inward current (Isin) during depolarizing steps to potentials more positive than -45 mV. Repolarizing steps resulted in slowly decaying inward tail currents (Itail). Both Isin and Itail were abolished in solutions nominally free of Cao2+, or containing Ca2+-channel antagonists. Bao2+ did not support Isin. The data indicated a U-shaped activation curve for Isin, peaking at about -10 mV. Activation of Isin occurred exponentially with a time constant of approximately 140 ms at -23 mV, becoming faster at more depolarized potentials (ca. 50 ms at -2 mV). Deactivation was slow, giving rise to tail currents lasting seconds. In some cases deactivation could be described by a single exponential process, although frequently the kinetics were more complex. Deactivation was faster at hyperpolarized potentials and sensitive to extracellular ([Ca2+]o), duration of activating voltage steps, and the degree of activation of Isin. Using CsCl-filled electrodes, the reversal potential (Erev) for Isin was -1.7 mV (SEM 3.5 mV, n = 20). Erev always corresponded to the reversal potential for gamma-aminobutyric acid-evoked currents in the same cell. In experiments in which Cs2SO4-filled electrodes were used, Erev was estimated to be -44 mV (SEM 2.3 mV, n = 9). Neither complete substitution of Nao+ with choline ions nor elevation of [K+]o 10-fold significantly affected the estimated Erev. However, substitution of Cl0- with isethionate or methanesulphonate increased the amplitude of inward currents (recorded with CsCl-filled electrodes) and shifted Erev to more depolarized potentials. The results indicate that Cl- are the primary charge carriers for this current and that Cai2+ is required for its activation, leading us to identify it as ICl(Ca).(ABSTRACT TRUNCATED AT 400 WORDS)

Passive and active membrane properties of canine gastric antral circular muscles

1986 ◽  
Vol 251 (2) ◽  
pp. C268-C273 ◽  
Author(s):  
A. J. Bauer ◽  
K. M. Sanders
Keyword(s):  
Electrical Activity ◽  
Time Constant ◽  
Myenteric Plexus ◽  
Circular Muscle ◽  
Membrane Properties ◽  
Time Constants ◽  
Active Membrane ◽  
Cable Properties ◽  
Length Constant ◽  
Chamber Technique

Experiments were performed to determine the mechanisms responsible for the gradient of electrical activity within circular muscle of the canine gastric antrum. Cable properties of canine gastric antral circular muscles were determined using the partitioned chamber technique of Abe and Tomita (J. Physiol. Lond. 196: 87-100, 1968). The length constant of the circular muscle near the myenteric plexus was 2.4 mm. This was significantly greater than the length constant of the circular muscle near the submucosa (1.7 mm). Membrane time constants were determined by two techniques. Although the time constant of the circular muscle near the myenteric plexus tended to be greater than that of the circular muscle near the submucosa, this difference was not statistically significant. The two regions of circular muscle also differed in their relative levels of excitability. Submucosal circular muscles demonstrated considerably more outward rectification on depolarization and were difficult to bring to threshold for slow waves. This study demonstrates that significant differences exist in the passive and active membrane properties of myenteric and submucosal circular muscle cells. The data help explain the gradient of electrical activity through the thickness of antral circular muscle.

scholarly journals The calcium-independent transient outward potassium current in isolated ferret right ventricular myocytes. I. Basic characterization and kinetic analysis.

1993 ◽  
Vol 101 (4) ◽  
pp. 571-601 ◽  
Author(s):  
D L Campbell ◽  
R L Rasmusson ◽  
Y Qu ◽  
H C Strauss
Keyword(s):  
Steady State ◽  
Ventricular Myocytes ◽  
Nonlinear Least Squares ◽  
Patch Clamp Technique ◽  
Time Constants ◽  
Whole Cell Patch Clamp ◽  
Voltage Dependent ◽  
Steady State Inactivation ◽  
K Current ◽  
Necessary And Sufficient

Enzymatically isolated myocytes from ferret right ventricles (12-16 wk, male) were studied using the whole cell patch clamp technique. The macroscopic properties of a transient outward K+ current I(to) were quantified. I(to) is selective for K+, with a PNa/PK of 0.082. Activation of I(to) is a voltage-dependent process, with both activation and inactivation being independent of Na+ or Ca2+ influx. Steady-state inactivation is well described by a single Boltzmann relationship (V1/2 = -13.5 mV; k = 5.6 mV). Substantial inactivation can occur during a subthreshold depolarization without any measurable macroscopic current. Both development of and recovery from inactivation are well described by single exponential processes. Ensemble averages of single I(to) channel currents recorded in cell-attached patches reproduce macroscopic I(to) and indicate that inactivation is complete at depolarized potentials. The overall inactivation/recovery time constant curve has a bell-shaped potential dependence that peaks between -10 and -20 mV, with time constants (22 degrees C) ranging from 23 ms (-90 mV) to 304 ms (-10 mV). Steady-state activation displays a sigmoidal dependence on membrane potential, with a net aggregate half-activation potential of +22.5 mV. Activation kinetics (0 to +70 mV, 22 degrees C) are rapid, with I(to) peaking in approximately 5-15 ms at +50 mV. Experiments conducted at reduced temperatures (12 degrees C) demonstrate that activation occurs with a time delay. A nonlinear least-squares analysis indicates that three closed kinetic states are necessary and sufficient to model activation. Derived time constants of activation (22 degrees C) ranged from 10 ms (+10 mV) to 2 ms (+70 mV). Within the framework of Hodgkin-Huxley formalism, Ito gating can be described using an a3i formulation.

Active Dendritic Membrane Properties of XenopusLarval Spinal Neurons Analyzed With a Whole Cell Soma Voltage Clamp

2000 ◽  
Vol 83 (3) ◽  
pp. 1381-1393 ◽  
Author(s):  
Benoit Saint Mleux ◽  
L. E. Moore
Keyword(s):  
Action Potential ◽  
Frequency Domain ◽  
Voltage Clamp ◽  
Membrane Potentials ◽  
Calcium Currents ◽  
Membrane Properties ◽  
Constant Current ◽  
Negative Slope ◽  
Spinal Neurons ◽  
Current Clamp

Voltage- and current-clamp measurements of inwardly directed currents were made from the somatic regions of Xenopus laevisspinal neurons. Current-voltage ( I-V) curves determined under voltage clamp, but not current clamp, were able to indicate a negative slope conductance in neurons that showed strong accommodating action potential responses to a constant current stimulation. Voltage-clamp I-V curves from repetitive firing neurons did not have a net negative slope conductance and had identical I-V plots under current clamp. Frequency domain responses indicate negative slope conductances with different properties with or without tetrodotoxin, suggesting that both sodium and calcium currents are present in these spinal neurons. The currents obtained from a voltage clamp of the somatic region were analyzed in terms of spatially controlled soma membrane currents and additional currents from dendritic potential responses. Linearized frequency domain analysis in combination with both voltage- and current-clamp responses over a range of membrane potentials was essential for an accurate determination of consistent neuronal model behavior. In essence, the data obtained at resting or hyperpolarized membrane potentials in the frequency domain were used to determine the electrotonic structure, while both the frequency and time domain data at depolarized potentials were required to characterize the voltage-dependent channels. Finally, the dendritic and somatic membrane properties were used to reconstruct the action potential behavior and quantitatively predict the dependence of neuronal firing properties on electrotonic structure. The reconstructed action potentials reproduced the behavior of two broad distributions of interneurons characterized by their degree of accommodation. These studies suggest that in addition to the ionic conductances, electrotonic structure is correlated with the action potential behavior of larval neurons.

Whole-cell voltage-clamp study of the fading of GABA-activated currents in acutely dissociated hippocampal neurons

1986 ◽  
Vol 56 (1) ◽  
pp. 1-18 ◽  
Author(s):  
J. R. Huguenard ◽  
B. E. Alger
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Time Course ◽  
Reversal Potential ◽  
Cell Voltage ◽  
Membrane Properties ◽  
Equilibrium Potential ◽  
Spinal Cord Neurons ◽  
Whole Cell ◽  
Whole Cell Voltage Clamp

The lability of the responses of mammalian central neurons to gamma-aminobutyric acid (GABA) was studied using neurons acutely dissociated from the CA1 region of the adult guinea pig hippocampus as a model system. GABA was applied to the neuronal somata by pressure ejection and the resulting current (IGABA) recorded under whole-cell voltage clamp. In initial experiments we examined several basic properties of cells in this preparation. Our data confirm that passive and active membrane properties are similar to those which characterize cells in other preparations. In addition, GABA-dependent conductance (gGABA), reversal potential (EGABA), and the interaction of GABA with pentobarbital and bicuculline all appeared to be normal. Dendritic GABA application could cause depolarizing GABA responses, and somatic GABA application caused hyperpolarizations due to chloride (Cl-) movements. Repetitive brief applications (5-15 ms) of GABA (10(-5) to 10(-3) M) at a frequency of 0.5 Hz led to fading of successive peaks of IGABA until, at a given holding potential, a steady state was reached in which IGABA no longer changed. Imposing voltage steps lasting seconds during a train of steady-state GABA responses led initially to increased IGABA that then diminished with maintenance of the step voltage. The rate of decrease of IGABA at each new holding potential was independent of the polarity of the step in holding potential but was highly dependent on the rate of GABA application. Application rates as low as 0.05 Hz led to fading of IGABA, even with activation of relatively small conductances (5-15 nS). Since IGABA evoked by somatic GABA application in these cells is carried by Cl-, the Cl- equilibrium potential (ECl) is equal to the reversal potential for IGABA, i.e., to EGABA. The fading of IGABA with changes in holding potential can be almost entirely accounted for by a shift in ECl resulting from transmembrane flux of Cl- through the GABA-activated conductance. Maneuvers that prevent changes in the intracellular concentration of Cl-ions, [Cl-]i, including holding the membrane potential at EGABA during repetitive GABA application or buffering [Cl-]i with high pipette [Cl-], prevent changes in EGABA. Desensitization of the GABA response (an actual decrease in gGABA) occurs in these neurons during prolonged application of GABA (greater than 1 s) but with a slower time course than changes in EGABA. Whole-cell voltage-clamp techniques applied to tissue-cultured spinal cord neurons indicated that rapid shifts in EGABA result from repetitive GABA application in these cells as well.(ABSTRACT TRUNCATED AT 250 WORDS)

Voltage and beat dependence of Ca2+ transient in feline ventricular myocytes

1989 ◽  
Vol 257 (3) ◽  
pp. H746-H759 ◽  
Author(s):  
W. H. duBell ◽  
S. R. Houser
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Sarcoplasmic Reticulum ◽  
Voltage Clamp ◽  
Ventricular Myocytes ◽  
Rest Period ◽  
Voltage Dependent ◽  
Early Peak ◽  
Comparable Magnitude ◽  
Voltage Relationship

The positive contractile staircase after a period of rest is attributable to a positive staircase in the magnitude of the Ca2+ transient. The present study used voltage-clamp techniques and the fluorescent Ca2+ indicator, indo-1, to examine the effects of membrane potential, the duration of depolarization, and the slow inward Ca2+ current (Isi) in the regulation of the magnitude of the steady-state Ca2+ transient and the development of the steady state during the positive staircase. In the steady state, the Ca2+ transient was greatest at +10 mV, the potential at which Isi was also the greatest. However, the Isi-voltage relationship was much more bell-shaped than the Ca2+ transient-voltage relationship. The magnitude and duration of the steady-state Ca2+ transient was not affected by pulse durations as short as 25 ms. However, prolonged voltage pulses were essential to maintain the steady state. The development of the positive staircase was very voltage dependent. After a rest period, a positive staircase was seen when voltage-clamp drives were done to +30 mV but not when done to -10 mV, potentials that elicit Isi of comparable magnitude. These results support the idea that the early peak of Isi can act as a trigger for release of Ca2+ from the sarcoplasmic reticulum. However, sarcoplasmic reticulum Ca2+ loading is dependent on prolonged depolarization and may be mediated through Na+-Ca2+ exchange.

Membrane Properties of Principal Neurons of the Lateral Superior Olive

2001 ◽  
Vol 86 (2) ◽  
pp. 922-934 ◽  
Author(s):  
T. J. Adam ◽  
P. G. Finlayson ◽  
D.W.F. Schwarz
Keyword(s):  
Sound Intensity ◽  
Membrane Properties ◽  
Intensity Difference ◽  
Lateral Superior Olive ◽  
Voltage Range ◽  
Superior Olive ◽  
Temporal Properties ◽  
Cable Properties ◽  
Voltage Dependent ◽  
Cochlear Hearing Loss

In the lateral superior olive (LSO) the firing rate of principal neurons is a linear function of inter-aural sound intensity difference (IID). The linearity and regularity of the “chopper response” of these neurons have been interpreted as a result of an integration of excitatory ipsilateral and inhibitory contralateral inputs by passive soma-dendritic cable properties. To account for temporal properties of this output, we searched for active time- and voltage-dependent nonlinearities in whole cell recordings from a slice preparation of the rat LSO. We found nonlinear current-voltage relations that varied with the membrane holding potential. Repetitive regular firing, supported by voltage oscillations, was evoked by current pulses injected from holding potentials near rest, but the response was reduced to an onset spike of fixed short latency when the pulse was injected from de- or hyperpolarized holding potentials. The onset spike was triggered by a depolarizing transient potential that was supported by T-type Ca2+-, subthreshold Na+-, and hyperpolarization-activated ( I H) conductances sensitive, respectively, to blockade with Ni2+, tetrodotoxin (TTX), and Cs+. In the hyperpolarized voltage range, the I H, was largely masked by an inwardly rectifying K+ conductance ( I KIR) sensitive to blockade with 200 μM Ba2+. In the depolarized range, a variety of K+ conductances, including A-currents sensitive to blockade with 4-aminopyridine (4-AP) and additional tetraethylammonium (TEA)-sensitive currents, terminated the transient potential and firing of action potentials, supporting a strong spike-rate adaptation. The “chopper response,” a hallmark of LSO principal neuron firing, may depend on the voltage- and time-dependent nonlinearities. These active membrane properties endow the LSO principal neurons with an adaptability that may maintain a stable code for sound direction under changing conditions, for example after partial cochlear hearing loss.

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