scholarly journals Comparison of excitatory currents activated by different transmitters on crustacean muscle. II. Glutamate-activated currents and comparison with acetylcholine currents present on the same muscle.

1983 ◽  
Vol 81 (4) ◽  
pp. 571-588 ◽  
Author(s):  
C Lingle ◽  
A Auerbach
Keyword(s):  
Steady State ◽  
Time Constant ◽  
Voltage Dependence ◽  
Noise Analysis ◽  
Power Spectra ◽  
Synaptic Current ◽  
Cancer Borealis ◽  
Current Decay ◽  
Marine Crustacean ◽  
Conductance Increase

The properties of glutamate-activated excitatory currents on the gm6 muscle from the foregut of the spiny lobsters Panulirus argus and interruptus and the crab Cancer borealis were examined using either noise analysis, analysis of synaptic current decays, or slow iontophoretic currents. The properties of acetylcholine currents activated in nonjunctional regions of the gm6 muscle were also examined. At 12 degrees C and -80 mV, the predominant time constant of power spectra from glutamate-activated current noise was approximately 7 ms and the elementary conductance was approximately 34 pS. At 12 degrees C and -80 mV, the predominant time constant of acetylcholine-activated channels was approximately 11 ms with a conductance of approximately 12 pS. Focally recorded glutamatergic extracellular synaptic currents on the gm6 muscle decayed with time constants of approximately 7-8 ms at 12 degrees C and -80 mV. The decay time constant was prolonged e-fold about every 225-mV hyperpolarization in membrane potential. The Q10 of the time constant of the synaptic current decay was approximately 2.6. The voltage dependence of the steady-state conductance increase activated by iontophoretic application of glutamate has the opposite direction of the steady-state conductance activated by cholinergic agonists when compared on the gm6 muscles. The glutamate-activated conductance increase is diminished with hyperpolarization. The properties of the marine crustacean glutamate channels are discussed in relation to glutamate channels in other organisms and to the acetylcholine channels found on the gm6 muscle and the gm1 muscle of the decapod foregut (Lingle and Auerbach, 1983).

scholarly journals Comparison of excitatory currents activated by different transmitters on crustacean muscle. I. Acetylcholine-activated channels.

1983 ◽  
Vol 81 (4) ◽  
pp. 547-569 ◽  
Author(s):  
C Lingle ◽  
A Auerbach
Keyword(s):  
Membrane Potential ◽  
Time Course ◽  
Voltage Dependence ◽  
Single Channel ◽  
Noise Analysis ◽  
Synaptic Currents ◽  
Cancer Borealis ◽  
Open Time ◽  
Conductance Increase ◽  
Channel Open Time

The properties of acetylcholine-activated excitatory currents on the gm1 muscle of three marine decapod crustaceans, the spiny lobsters Panulirus argus and interruptus, and the crab Cancer borealis, were examined using either noise analysis, analysis of synaptic current decays, or analysis of the voltage dependence of ionophoretically activated cholinergic conductance increases. The apparent mean channel open time (tau n) obtained from noise analysis at -80 mV and 12 degrees C was approximately 13 ms; tau n was prolonged e-fold for about every 100-mV hyperpolarization in membrane potential; tau n was prolonged e-fold for every 10 degrees C decrease in temperature. Gamma, the single-channel conductance, at 12 degrees C was approximately 18 pS and was not affected by voltage; gamma was increased approximately 2.5-fold for every 10 degrees C increase in temperature. Synaptic currents decayed with a single exponential time course, and at -80 mV and 12 degrees C, the time constant of decay of synaptic currents, tau ejc, was approximately 14-15 ms and was prolonged e-fold about every 140-mV hyperpolarization; tau ejc was prolonged about e-fold for every 10 degrees C decrease in temperature. The voltage dependence of the amplitude of steady-state cholinergic currents suggests that the total conductance increase produced by cholinergic agonists is increased with hyperpolarization. Compared with glutamate channels found on similar decapod muscles (see the following article), the acetylcholine channels stay open longer, conduct ions more slowly, and are more sensitive to changes in the membrane potential.

Synaptic Current at the Rat Ganglionic Synapse and Its Interactions With the Neuronal Voltage-Dependent Currents

1998 ◽  
Vol 79 (2) ◽  
pp. 727-742 ◽  
Author(s):  
Oscar Sacchi ◽  
Maria Lisa Rossi ◽  
Rita Canella ◽  
Riccardo Fesce
Keyword(s):  
Steady State ◽  
Action Potential ◽  
Time Constant ◽  
Voltage Dependence ◽  
Sympathetic Neurons ◽  
Excitatory Postsynaptic Potential ◽  
Synaptic Current ◽  
Inactivation Curve ◽  
Voltage Dependent ◽  
Steady State Inactivation

Sacchi, Oscar, Maria Lisa Rossi, Rita Canella, and Riccardo Fesce. Synaptic current at the rat ganglionic synapse and its interactions with the neuronal voltage-dependent currents. J. Neurophysiol. 79: 727–742, 1998. The membrane current activated by fast nicotinic excitation of intact and mature rat sympathetic neurons was studied at 37°C, by using the two-microelectrode voltage-clamp technique. The excitatory postsynaptic current (EPSC) was modeled as the difference between two exponentials. A fast time constant (τ2; mean value 0.57 ms), which proves to be virtually voltage-independent, governs the current rise phase and a longer time constant (τ1; range 5.2–6.8 ms in 2 mM Ca2+) describes the current decay and shows a small negative voltage dependence. A mean peak synaptic conductance of 0.58 μS per neuron is measured after activation of the whole presynaptic input in 5 mM Ca2+ external solution (0.40 μS in 2 mM Ca2+). The miniature EPSCs also rise and decay with exponential time constants very similar to those of the compound EPSC recorded at the same voltage. A mean peak conductance of 4.04 nS is estimated for the unitary event. Deconvolution procedures were employed to decompose evoked macrocurrents. It is shown that under appropriate conditions the duration of the driving function describing quantal secretion can be reduced to <1 ms. The shape of the EPSC is accurately mimicked by a complete mathematical model of the sympathetic neuron incorporating the kinetic properties of five different voltage-dependent current types, which were characterized in a previous work. We show that I A channels are opened by depolarizing voltage steps or by synaptic potentials in the subthreshold voltage range, provided that the starting holding voltage is sufficiently negative to remove I A steady-state inactivation (less than −50 mV) and the voltage trajectories are sufficiently large to enter the I A activation range (greater than −65 mV). Under current-clamp conditions, this gives rise to an additional fast component in the early phase of membrane repolarization—in response to voltage pulses—and to a consistent distortion of the excitatory postsynaptic potential (EPSP) time course around its peak—in response to the synaptic signal. When the stimulation initiates an action potential, I A is shown to significantly increase the synaptic threshold conductance (up to a factor of 2 when I A is fully deinactivated), compared with that required when I A is omitted. The voltage dependence of this effect is consistent with the I A steady-state inactivation curve. It is concluded that I A, in addition to speeding up the spike repolarization process, also shunts the excitatory drive and delays or prevents the firing of the neuron action potential.

Developmental change in fast Na channel properties in embryonic chick ventricular heart cells

1995 ◽  
Vol 73 (10) ◽  
pp. 1475-1484 ◽  
Author(s):  
Hideaki Sada ◽  
Takashi Ban ◽  
Takeshi Fujita ◽  
Yoshio Ebina ◽  
Nicholas Sperelakis
Keyword(s):  
Steady State ◽  
Voltage Clamp ◽  
Time Constant ◽  
Voltage Dependence ◽  
Cell Voltage ◽  
Developmental Changes ◽  
Heart Cells ◽  
Embryonic Chick ◽  
Whole Cell ◽  
Whole Cell Voltage Clamp

To assess developmental changes in kinetic properties of the cardiac sodium current, whole-cell voltage-clamp experiments were conducted using 3-, 10-, and 17-day-old embryonic chick ventricular heart cells. Experimental data were quantified according to the Hodgkin–Huxley model. While the Na current density, as examined by the maximal conductance, drastically increased (six- to seven-fold) with development, other current–voltage parameters remained unchanged. Whereas the activation time constant and the steady-state activation characteristics were comparable among the three age groups, the voltage dependence of the inactivation time constant and the steady-state inactivation underwent a shift in the voltage dependence toward negative potentials during embryonic development. Consequently, the steady-state (window current) conductance, which was sufficient to induce automatic activity in the young embryos, was progressively reduced with age.Key words: cardiac electrophysiology, whole-cell voltage-clamp experiments, fast Na currents, heart, development, developmental changes.

scholarly journals Interaction of internal Ba2+ with a cloned Ca(2+)-dependent K+ (hslo) channel from smooth muscle.

1996 ◽  
Vol 107 (3) ◽  
pp. 399-407 ◽  
Author(s):  
F Diaz ◽  
M Wallner ◽  
E Stefani ◽  
L Toro ◽  
R Latorre
Keyword(s):  
Time Constant ◽  
Voltage Dependence ◽  
Membrane Surface ◽  
Potential Drop ◽  
Human Myometrium ◽  
K Channel ◽  
Xenopus Laevis Oocytes ◽  
Experimental Conditions ◽  
Internal Solution ◽  
Current Decay

We have studied potassium currents through a cloned Ca(2+)-dependent K+ channel (hslo) from human myometrium. Currents were recorded in inside-out macropatches from membranes of Xenopus laevis oocytes. In particular, the inactivation-like process that these channels show at high positive potentials was assessed in order to explore its molecular nature. This current inhibition conferred a bell shape to the current-voltage curves. The kinetic and voltage dependence of this process suggested the possibility of a Ba2+ block. There were the following similarities between the inactivation process observed at zero-added Ba2+ and the internal Ba2+ block of hslo channels: (a) in the steady state, the voltage dependence of the current inhibition observed at zero-added Ba2+ was the same as the voltage dependence of the Ba2+ block; (b) the time constant for recovery from current decay at zero-added Ba2+ was the same as the time constant for current recovery from Ba2+ blockade; and (c) current decay was largely suppressed in both cases by adding a Ba2+ chelator [(+)-18-crown-6-tetracarboxylic acid] to the internal solution. In our experimental conditions, we determined that the Kd for the complex chelator-Ba2+ is 1.6 x 10(-10) M. We conclude that the current decay observed at zero-added Ba2+ to the internal solution is due to contaminant Ba2+ present in our solutions (approximately 70 nM) and not to an intrinsic gating process. The Ba2+ blocking reaction in hslo channels is bimolecular. Ba2+ binds to a site (Kd = 0.36 +/- 0.05 mM at zero applied voltage) that senses 92 +/- 25% of the potential drop from the internal membrane surface.

scholarly journals Fast, Slow, and Steady-State Effects of Contralateral Acoustic Activation of the Medial Olivocochlear Efferent System in Awake Guinea Pigs: Action of Gentamicin

1997 ◽  
Vol 78 (4) ◽  
pp. 1826-1836 ◽  
Author(s):  
Deise Lima da Costa ◽  
Anne Chibois ◽  
Jean-Paul Erre ◽  
Christophe Blanchet ◽  
RENAUD CHARLET de Sauvage ◽  
...  
Keyword(s):  
Steady State ◽  
Time Constant ◽  
Decay Time ◽  
Guinea Pigs ◽  
Round Window ◽  
Broadband Noise ◽  
Decay Time Constant ◽  
Efferent System ◽  
Medial Olivocochlear ◽  
Medial Olivocochlear Efferent System

Lima da Costa, Deise, Anne Chibois, Jean-Paul Erre, Christophe Blanchet, Renaud Charlet de Sauvage, and Jean-Marie Aran. Fast, slow, and steady-state effects of contralateral acoustic activation of the medial olivocochlear efferent system in awake guinea pigs: action of gentamicin. J. Neurophysiol. 78: 1826–1836, 1997. The function of the medial olivocochlear efferent system was observed in awake guinea pigs by recording, in the absence of ipsilateral external acoustic stimulation, the ensemble background activity (EBA) of the VIIIth nerve from an electrode chronically implanted on the round window of one ear. The EBA was measured by calculating the power value of the round window signal in the 0.5- to 2.5-kHz band after digital or analog (active) filtering. This EBA was compared with and without the addition of a low-level broadband noise to the opposite ear. The contralateral broadband noise (CLBN, 55 dB SPL) induced, via the efferent system, a decrease (suppression) of this EBA. With the use of noise bursts of different durations, two components in this suppression could be observed. After the onset of a 1-s CLBN, the power value of the EBA decreased rapidly by 38.0 ± 4.2% (mean ± SD, n = 3), with a latency of <10 ms and a decay time constant of 13.1 ± 1.0 ms (fast effect). At the offset of the 1-s CLBN, EBA came back to prestimulation values with a similar latency and a time constant of 15.5 ± 2.9 ms. During longer CLBN stimulation (≥1 min), EBA presented, after the fast decrease, an additional, slower decrease of 15.6 ± 3.1%, with a delay of 9.8 ± 1.3 s and a decay time constant of 16.1 ± 5.0 s ( n = 12, slow effect), and then remained remarkably constant for as long as observed, i.e., >2 h (steady state). The average global suppression was thus up to 47.8 ± 5.8% of the basal, pre-CLBN-stimulation EBA value. At the offset of the CLBN, EBA returned to pre-CLBN level with fast and slow phases, with, for the slow phase, no delay and a time constant of 32.1 ± 8.1 s. Fast and slow changes in EBA power values were observed after a single injection of gentamicin (GM) at different doses (150, 200, and 250 mg/kg). At 150 and 200 mg/kg, GM progressively and reversibly blocked the rapid effect, but the slow component of the efferent medial suppression remained remarkably unchanged. However, at higher doses both the fast and slow suppressions were totally yet still reversibly blocked. These observations indicate that the medial olivocochlear efferent system exerts sustained influences on outer hair cells and that this effect develops in two different steps that may have different basic cellular mechanisms.

Voltage behavior along the irregular dendritic structure of morphologically and physiologically characterized vagal motoneurons in the guinea pig

1990 ◽  
Vol 63 (2) ◽  
pp. 333-346 ◽  
Author(s):  
R. Nitzan ◽  
I. Segev ◽  
Y. Yarom
Keyword(s):  
Steady State ◽  
Guinea Pig ◽  
Time Constant ◽  
Dendritic Structure ◽  
Input Resistance ◽  
Membrane Properties ◽  
Small Cells ◽  
Physiological Data ◽  
Motor Nucleus ◽  
Cable Length

1. Intracellular recordings from neurons in the dorsal motor nucleus of the vagus (vagal motoneurons, VMs) obtained in the guinea pig brain stem slice preparation were used for both horseradish peroxidase (HRP) labeling of the neurons and for measurements of their input resistance (RN) and time constant (tau 0). Based on the physiological data and on the morphological reconstruction of the labeled cells, detailed steady-state and compartmental models of VM were built and utilized to estimate the range of membrane resistivity, membrane capacitance, and cytoplasm resistivity values (Rm, Cm, and Ri, respectively) and to explore the integrative properties of these cells. 2. VMs are relatively small cells with a simple dendritic structure. Each cell has an average of 5.3 smooth (nonspiny), short (251 microns) dendrites with a low order (2) of branching. The average soma-dendritic surface area of VMs is 9,876 microns 2. 3. Electrically, VMs show remarkably linear membrane properties in the hyperpolarizing direction; they have an average RN of 67 +/- 23 (SD) M omega and a tau 0 of 9.4 +/- 4.1 ms. Several unfavorable experimental conditions precluded the possibility of faithfully recovering ("peeling") the first equalizing time constant (tau 1) and, thereby, of estimating the electrotonic length (Lpeel) of VMs. 4. Reconciling VM morphology with the measured RN and tau 0 through the models, assuming an Ri of 70 omega.cm and a spatially uniform Rm, yielded an Rm estimate of 5,250 omega.cm2 and a Cm of 1.8 microF/cm2. Peeling theoretical transients produced by these models result in an Lpeel of 1.35. Because of marked differences in the length of dendrites within a single cell, this value is larger than the maximal cable length of the dendrites and is twice as long as their average cable length. 5. The morphological and physiological data could be matched indistinguishably well if a possible soma shunt (i.e., Rm, soma less than Rm, dend) was included in the model. Although there is no unique solution for the exact model Rm, a general conclusion regarding the integrative capabilities of VM could be drawn. As long as the model is consistent with the experimental data, the average input resistance at the dendritic terminals (RT) and the steady-state central (AFT----S) and peripheral (AFS----T) attenuation factors are essentially the same in the different models. With Ri = 70 omega.cm, we calculated RT, AFS----T, and AFT----S to be, on the average, 580 M omega, 1.1, and 13, respectively.(ABSTRACT TRUNCATED AT 400 WORDS)

Voltage Dependence of the Glycine Receptor–Channel Kinetics in the Zebrafish Hindbrain

1999 ◽  
Vol 82 (5) ◽  
pp. 2120-2129 ◽  
Author(s):  
Pascal Legendre
Keyword(s):  
Time Constant ◽  
Rise Time ◽  
Time Course ◽  
Voltage Dependence ◽  
Good Description ◽  
Glycine Receptor ◽  
Relative Amplitude ◽  
Time Constants ◽  
Low Concentration ◽  
Voltage Dependent

Electrophysiological recordings of outside-out patches to fast-flow applications of glycine were made on patches derived from the Mauthner cells of the 50-h-old zebrafish larva. As for glycinergic miniature inhibitory postsynaptic currents (mIPSCs), depolarizing the patch produced a broadening of the transient outside-out current evoked by short applications (1 ms) of a saturating concentration of glycine (3 mM). When the outside-out patch was depolarized from −50 to +20 mV, the peak current varied linearly with voltage. A 1-ms application of 3 mM glycine evoked currents that activated rapidly and deactivated biexponentially with time constants of ≈5 and ≈30 ms (holding potential of −50 mV). These two decay time constants were increased by depolarization. The fast deactivation time constant increased e-fold per 95 mV. The relative amplitude of the two decay components did not significantly vary with voltage. The fast component represented 64.2 ± 2.8% of the total current at −50 mV and 54.1 ± 10% at +20 mV. The 20–80% rise time of these responses did not show any voltage dependence, suggesting that the opening rate constant is insensitive to voltage. The 20–80% rise time was 0.2 ms at −70 mV and 0.22 ms at +20 mV. Responses evoked by 100–200 ms application of a low concentration of glycine (0.1 mM) had a biphasic rising phase reflecting the complex gating behavior of the glycine receptor. The time constant of these two components and their relative amplitude did not change with voltage, suggesting that modal shifts in the glycine-activated channel gating mode are not sensitive to the membrane potential. Using a Markov model to simulate glycine receptor gating behavior, we were able to mimic the voltage-dependent change in the deactivation time course of the responses evoked by 1-ms application of 3 mM glycine. This kinetics model incorporates voltage-dependent closing rate constants. It provides a good description of the time course of the onset of responses evoked by the application of a low concentration of glycine at all membrane potentials tested.

scholarly journals Movement of Voltage Sensor S4 in Domain 4 Is Tightly Coupled to Sodium Channel Fast Inactivation and Gating Charge Immobilization

1999 ◽  
Vol 114 (2) ◽  
pp. 167-184 ◽  
Author(s):  
Frank J.P. Kühn ◽  
Nikolaus G. Greeff
Keyword(s):  
Steady State ◽  
Sodium Channel ◽  
Time Constant ◽  
Voltage Sensor ◽  
Functional Coupling ◽  
Fast Inactivation ◽  
Voltage Sensors ◽  
Steady State Inactivation ◽  
Arginine Residues ◽  
Domain 4

The highly charged transmembrane segments in each of the four homologous domains (S4D1–S4D4) represent the principal voltage sensors for sodium channel gating. Hitherto, the existence of a functional specialization of the four voltage sensors with regard to the control of the different gating modes, i.e., activation, deactivation, and inactivation, is problematic, most likely due to a functional coupling between the different domains. However, recent experimental data indicate that the voltage sensor in domain 4 (S4D4) plays a unique role in sodium channel fast inactivation. The correlation of fast inactivation and the movement of the S4D4 voltage sensor in rat brain IIA sodium channels was examined by site-directed mutagenesis of the central arginine residues to histidine and by analysis of both ionic and gating currents using a high expression system in Xenopus oocytes and an optimized two-electrode voltage clamp. Mutation R1635H shifts the steady state inactivation to more hyperpolarizing potentials and drastically increases the recovery time constant, thereby indicating a stabilized inactivated state. In contrast, R1638H shifts the steady state inactivation to more depolarizing potentials and strongly increases the inactivation time constant, thereby suggesting a preferred open state occupancy. The double mutant R1635/1638H shows intermediate effects on inactivation. In contrast, the activation kinetics are not significantly influenced by any of the mutations. Gating current immobilization is markedly decreased in R1635H and R1635/1638H but only moderately in R1638H. The time courses of recovery from inactivation and immobilization correlate well in wild-type and mutant channels, suggesting an intimate coupling of these two processes that is maintained in the mutations. These results demonstrate that S4D4 is one of the immobilized voltage sensors during the manifestation of the inactivated state. Moreover, the presented data strongly suggest that S4D4 is involved in the control of fast inactivation.

THERMAL ACCLIMATION, NEUROMUSCULAR SYNAPTIC DELAY AND MINIATURE END-PLATE CURRENT DECAY IN THE FROG RANA TEMPORARIA

1994 ◽  
Vol 187 (1) ◽  
pp. 131-142
Author(s):  
A Lagerspetz
Keyword(s):  
Time Constant ◽  
Rana Temporaria ◽  
Temperature Acclimation ◽  
Thermal Acclimation ◽  
Decay Phase ◽  
Synaptic Delay ◽  
Sartorius Muscle ◽  
Current Decay ◽  
End Plate ◽  
Frog Rana Temporaria

1. The effects of 1 or 2&shy;3 weeks of acclimation to 4 &deg;C and 24 &deg;C of overwintering grass frogs (Rana temporaria) on the synaptic delay and on the time constant of the decay phase (tau) of miniature end-plate currents (MEPCs) in the neuromuscular junction of sartorius muscle were studied. In order to equalize the possible effects of differential starvation, the animals were usually cross-acclimated to the two temperatures. 2. Synaptic delay was not affected by temperature acclimation but was slightly prolonged by the more profound starvation at the higher temperature when the cross-acclimation procedure was not used. The average Q10 of synaptic delay between 4 and 24 &deg;C was 2.60 and of minimum synaptic delays, 2.64. The corresponding values for apparent activation energy (Ea) were 65.79 and 66.48 kJ mol-1. 3. The time constant of the decay phase of MEPCs was not affected by temperature acclimation. The average Q10 between 4 and 24 &deg;C was 2.27. The corresponding Ea value was 56.02 kJ mol-1. 4. The function of peripheral neuromuscular synapses is well regulated and changes in its time relationships do not appear to be involved in the thermal acclimation of frogs.

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