scholarly journals Delays in inactivation development and activation kinetics in myxicola giant axons.

1982 ◽  
Vol 80 (1) ◽  
pp. 83-102 ◽  
Author(s):  
L Goldman ◽  
J L Kenyon
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Series Resistance ◽  
Activation Kinetics ◽  
Time To Peak ◽  
Exponential Decline ◽  
Na Inactivation ◽  
The Difference ◽  
True Property ◽  
Kinetics Of

Na inactivation was studied in Myxicola (two-pulse procedure, 6-ms gap between conditioning and test pulses). Inactivation developed with an initial delay (range 130-817 microseconds) followed by a simple exponential decline (time constant tau c). Delays (deviations from a simple exponential) are seen only for brief conditioning pulses were gNa is slightly activated. Hodgkin-Huxley kinetics with series resistance, Rs, predict deviations from a simple exponential only for conditioning pulses that substantially activate gNa. Reducing INa fivefold (Tris substitution) had no effect on either tau c or delay. Delay in not generated by Rs or by contamination from activation development. The slowest time constant in Na tails is approximately 1 ms (Goldman and Hahin, 1978) and the gap was 6 ms. Shortening the gap to 2 ms had no effect on either tau c or delay. Delay is a true property of the channel. Delay decreased with more positive conditioning potentials, and also decreased approximately proportionally with time to peak gNa during the conditioning pulse, as expected for sequentially coupled activation and inactivation. In a few cases the difference between Na current values for brief conditioning pulses and the tau c exponential could be measured. Difference values decayed exponentially with time constant tau m. The inactivation time course is described by a model that assumes a process with the kinetics of gNa activation as a precursor to inactivation.

scholarly journals Sodium and calcium currents in dispersed mammalian septal neurons.

1991 ◽  
Vol 97 (2) ◽  
pp. 303-320 ◽  
Author(s):  
A Castellano ◽  
J López-Barneo
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Calcium Currents ◽  
Closing Time ◽  
Patch Clamp Technique ◽  
Average Value ◽  
Time To Peak ◽  
Time Courses ◽  
Fast Activation ◽  
Septal Neurons

Voltage-gated Na+ and Ca2+ conductances of freshly dissociated septal neurons were studied in the whole-cell configuration of the patch-clamp technique. All cells exhibited a large Na+ current with characteristic fast activation and inactivation time courses. Half-time to peak current at -20 mV was 0.44 +/- 0.18 ms and maximal activation of Na+ conductance occurred at 0 mV or more positive membrane potentials. The average value was 91 +/- 32 nS (approximately 11 mS cm-2). At all membrane voltages inactivation was well fitted by a single exponential that had a time constant of 0.44 +/- 0.09 ms at 0 mV. Recovery from inactivation was complete in approximately 900 ms at -80 mV but in only 50 ms at -120 mV. The decay of Na+ tail currents had a single time constant that at -80 mV was faster than 100 microseconds. Depolarization of septal neurons also elicited a Ca2+ current that peaked in approximately 6-8 ms. Maximal peak Ca2+ current was obtained at 20 mV, and with 10 mM external Ca2+ the amplitude was 0.35 +/- 0.22 nA. During a maintained depolarization this current partially inactivated in the course of 200-300 ms. The Ca2+ current was due to the activity of two types of conductances with different deactivation kinetics. At -80 mV the closing time constants of slow (SD) and fast (FD) deactivating channels were, respectively, 1.99 +/- 0.2 and 0.11 +/- 0.03 ms (25 degrees C). The two kinds of channels also differed in their activation voltage, inactivation time course, slope of the conductance-voltage curve, and resistance to intracellular dialysis. The proportion of SD and FD channels varied from cell to cell, which may explain the differential electrophysiological responses of intracellularly recorded septal neurons.

Activity-Dependent [Ca2+]i Changes in Guinea Pig Vagal Motoneurons: Relationship to the Slow Afterhyperpolarization

1997 ◽  
Vol 78 (2) ◽  
pp. 825-834 ◽  
Author(s):  
Nechama Lasser-Ross ◽  
William N. Ross ◽  
Yosef Yarom
Keyword(s):  
Guinea Pig ◽  
Time Constant ◽  
Recovery Time ◽  
Time Course ◽  
Pyramidal Neurons ◽  
Cell Types ◽  
Time To Peak ◽  
Ca1 Region ◽  
Activity Dependent ◽  
Calcium Green

Lasser-Ross, Nechama, William N. Ross, and Yosef Yarom. Activity-dependent [Ca2+]i changes in guinea pig vagal motoneurons: relationship to the slow afterhyperpolarization. J. Neurophysiol. 78: 825–834, 1997. Vagal motoneurons in slices from the guinea-pig brain stem were injected with the fluorescent [Ca2+]i indicators fura-2, furaptra, or Calcium Green-1. Spike-induced fluorescence changes were measured in the soma and dendrites and simultaneously the long-lasting afterhyperpolarization was recorded with a sharp microelectrode in the soma. Na+ spikes or Ca2+ spikes increased [Ca2+]i (measured as a change in indicator fluorescence) in all locations in the soma and dendrites. Each spike in a train of action potentials caused a step increase in fluorescence of about equal amplitude when nonsaturating indicators were used. Peak changes at all locations occurred at the time of the last action potential. Transients measured with low concentrations of Calcium Green-1 or furaptra had a recovery time constant of ∼500–1,500 ms in the cell body. The recovery time course was faster in the dendrites than in the soma. The norepinephrine-sensitive, slow afterhyperpolarization (sAHP) had a time to peak of ∼800 ms and a recovery time constant of 2–5 s, much longer than the recovery time course of the fluorescence changes. Some of these experiments were repeated on pyramidal neurons from the CA1 region of the rat hippocampus with similar results. In both cell types, the data suggest that the time course of neither the rising phase nor the falling phase of the sAHP, nor the underlying conductance, directly reflects the time course of the [Ca2+]i change. The mechanism connecting the parameters remains unclear. One possibility is that an additional second messenger system is involved.

Kinetics of oxygen uptake at the onset of exercise near or above peak oxygen uptake

2000 ◽  
Vol 88 (5) ◽  
pp. 1812-1819 ◽  
Author(s):  
R. L. Hughson ◽  
D. D. O'Leary ◽  
A. C. Betik ◽  
H. Hebestreit
Keyword(s):  
Oxygen Uptake ◽  
Cardiovascular System ◽  
Time Constant ◽  
Exponential Model ◽  
Peak Oxygen Uptake ◽  
Phase 2 ◽  
Heavy Exercise ◽  
The Difference ◽  
Kinetics Of ◽  
Model Phase

We tested the hypothesis that kinetics of O2 uptake (V˙o 2) measured in the transition to exercise near or above peakV˙o 2(V˙o 2 peak) would be slower than those for subventilatory threshold exercise. Eight healthy young men exercised at ∼57, ∼96, and ∼125%V˙o 2 peak. Data were fit by a two- or three-component exponential model and with a semilogarithmic transformation that tested the difference between required V˙o 2 and measuredV˙o 2. With the exponential model, phase 2 kinetics appeared to be faster at 125% V˙o 2 peak[time constant (τ2) = 16.3 ± 8.8 (SE) s] than at 57%V˙o 2 peak(τ2 = 29.4 ± 4.0 s) but were not different from that at 96%V˙o 2 peakexercise (τ2 = 22.1 ± 2.1 s).V˙o 2 at the completion of phase 2 was 77 and 80%V˙o 2 peak in tests predicted to require 96 and 125%V˙o 2 peak. WhenV˙o 2 kinetics were calculated with the semilogarithmic model, the estimated τ2 at 96%V˙o 2 peak (49.7 ± 5.1 s) and 125%V˙o 2 peak (40.2 ± 5.1 s) were slower than with the exponential model. These results are consistent with our hypothesis and with a model in which the cardiovascular system is compromised during very heavy exercise.

scholarly journals Kinetics of Recovery of the Dark-adapted Salamander Rod Photoresponse

1998 ◽  
Vol 111 (1) ◽  
pp. 7-37 ◽  
Author(s):  
S. Nikonov ◽  
N. Engheta ◽  
E.N. Pugh
Keyword(s):  
Theoretical Analysis ◽  
Time Constant ◽  
Translation Invariance ◽  
Flash Intensity ◽  
Translation Invariant ◽  
Calcium Dependent ◽  
The Difference ◽  
Analytical Expressions ◽  
Kinetics Of ◽  
Flash Response

The kinetics of the dark-adapted salamander rod photocurrent response to flashes producing from 10 to 105 photoisomerizations (Φ) were investigated in normal Ringer's solution, and in a choline solution that clamps calcium near its resting level. For saturating intensities ranging from ∼102 to 104 Φ, the recovery phases of the responses in choline were nearly invariant in form. Responses in Ringer's were similarly invariant for saturating intensities from ∼103 to 104 Φ. In both solutions, recoveries to flashes in these intensity ranges translated on the time axis a constant amount (τc) per e-fold increment in flash intensity, and exhibited exponentially decaying “tail phases” with time constant τc. The difference in recovery half-times for responses in choline and Ringer's to the same saturating flash was 5–7 s. Above ∼104 Φ, recoveries in both solutions were systematically slower, and translation invariance broke down. Theoretical analysis of the translation-invariant responses established that τc must represent the time constant of inactivation of the disc-associated cascade intermediate (R*, G*, or PDE*) having the longest lifetime, and that the cGMP hydrolysis and cGMP-channel activation reactions are such as to conserve this time constant. Theoretical analysis also demonstrated that the 5–7-s shift in recovery half-times between responses in Ringer's and in choline is largely (4–6 s) accounted for by the calcium-dependent activation of guanylyl cyclase, with the residual (1–2 s) likely caused by an effect of calcium on an intermediate with a nondominant time constant. Analytical expressions for the dim-flash response in calcium clamp and Ringer's are derived, and it is shown that the difference in the responses under the two conditions can be accounted for quantitatively by cyclase activation. Application of these expressions yields an estimate of the calcium buffering capacity of the rod at rest of ∼20, much lower than previous estimates.

scholarly journals A photoisomerizable muscarinic antagonist. Studies of binding and of conductance relaxations in frog heart.

1982 ◽  
Vol 79 (4) ◽  
pp. 657-678 ◽  
Author(s):  
J Nargeot ◽  
H A Lester ◽  
N J Birdsall ◽  
J Stockton ◽  
N H Wassermann ◽  
...  
Keyword(s):  
Time Course ◽  
Potassium Conductance ◽  
Resting Potential ◽  
Frog Heart ◽  
Activation Kinetics ◽  
Frog Myocardium ◽  
Data Yield ◽  
Xenon Flashlamp ◽  
The Right ◽  
Kinetics Of

These experiments employ the photoisomerizable compound, 3,3'-bis-[alpha-(trimethylammonium)methyl]azobenzene (Bis-Q), to study the response to muscarinic agents in frog myocardium. In homogenates from the heart, trans-Bis-Q blocks the binding of [3H]-N-methylscopolamine to muscarinic receptors. In voltage-clamped atrial trabeculae, trans-Bis-Q blocks the agonist-induced potassium conductance. The equilibrium dose-response curve for carbachol is shifted to the right, suggesting competitive blockade. Both the biochemical and electrophysiological data yield a dissociation constant of 4-5 microM for trans-Bis-Q; the cis configuration is severalfold less potent as a muscarinic blocker. Voltage-clamped preparations were exposed simultaneously to carbachol and Bis-Q and were subjected to appropriately filtered flashes (less than 1 ms duration) from a xenon flashlamp. Trans leads to cis and cis leads to trans photoisomerizations cause small (less than 20%) increases and decreases, respectively, in the agonist-induced current. The relaxation follows an S-shaped time course, including an initial delay or period of zero slope. The entire waveform is described by [1 - exp(-kt)]n. At 23 degrees C, k is approximately 3 s-1 and n is 2. Neither k nor n is affected when: (a) [Bis-Q] is varied between 5 and 100 microM; (b) [carbachol] is varied between 1 and 50 microM; (c) carbachol is replaced by other agonists (muscarine, acetylcholine, or acetyl-beta-methylcholine); or (d) the voltage is varied between the normal resting potential and a depolarization of 80 mV. However, in the range of 13-30 degrees C, k increases with temperature; the Q10 is between 2 and 2.5. In the same range, n does not change significantly. Like other investigators, we conclude that the activation kinetics of the muscarinic K+ conductance are not determined by ligand-receptor binding, but rather by a subsequent sequence of two (or more) steps with a high activation energy.

scholarly journals Kinetics of oxygen consumption after a single flash of light in photoreceptors of the drone (Apis mellifera).

1982 ◽  
Vol 80 (1) ◽  
pp. 19-55 ◽  
Author(s):  
M Tsacopoulos ◽  
S Poitry
Keyword(s):  
Oxygen Consumption ◽  
Time Constant ◽  
Time Course ◽  
Sodium Pump ◽  
Fourier Transforms ◽  
Recovery Phase ◽  
Peak Amplitude ◽  
Single Flash ◽  
High Concentrations ◽  
Kinetics Of

The time course of the rate of oxygen consumption (QO2) after a single flash of light has been measured in 300-micrometers slices of drone retina at 22 degrees C. To measure delta QO2(t), the change in QO2 from its level in darkness, the transients of the partial pressure of O2 (PO2) were recorded with O2 microelectrodes simultaneously in two sites in the slice and delta QO2 was calculated by a computer using Fourier transforms. After a 40-ms flash of intense light, delta QO2, reached a peak of 40 microliters O2/g.min and then declined exponentially to the baseline with a time constant tau 1 = 4.96 +/- 0.49 s (SD, n = 10). The rising phase was characterized by a time constant tau 2 = 1.90 +/- 0.35 s (SD, n = 10). The peak amplitude of delta QO2 increased linearly with the log of the light intensity. Replacement of Na+ by choline, known to decrease greatly the light-induced transmembrane current, caused a 63% decrease of delta QO2. With these changes, however, the kinetics of delta QO2 (t) were unchanged. This suggest that the recovery phase is rate-limited by a single reaction with apparent first-order kinetics. Evidence is provided that suggests that this reaction may be the working of the sodium pump. Exposure of the retina to high concentrations of ouabain or strophanthidin (inhibitors of the sodium pump) reduced the peak amplitude of delta QO2 by approximately 80% and increased tau 1. The increase of tau 1 was an exponential function of the time of exposure to the cardioactive steroids. Hence, it seems likely that the greatest part of delta QO2 is used for the working of the pump, whose activity is the mechanism underlying the rate constant of the descending limb of delta QO2 (t).

Activation Kinetics of the Delayed Rectifier Potassium Current of Bullfrog Sympathetic Neurons

1998 ◽  
Vol 79 (5) ◽  
pp. 2345-2357 ◽  
Author(s):  
Kathryn G. Klemic ◽  
Dominique M. Durand ◽  
Stephen W. Jones
Keyword(s):  
Potassium Current ◽  
Time Course ◽  
Sympathetic Neurons ◽  
Delayed Rectifier ◽  
Activation Kinetics ◽  
Whole Cell ◽  
Delayed Rectifier Potassium Current ◽  
Kinetics Of ◽  
Cell Data ◽  
Allosteric Model

Klemic, Kathryn G., Dominique M. Durand, and Stephen W. Jones. Activation kinetics of the delayed rectifier potassium current of bullfrog sympathetic neurons. J. Neurophysiol. 79: 2345–2357, 1998. We examined the activation kinetics of the delayed rectifier K+ current of bullfrog sympathetic neurons, primarily using whole cell recording. On depolarization, currents activated with a sigmoid delay but did not show a Cole-Moore shift. The time course of activation differed systematically from an exponential raised to a power. At most voltages, a power of 2 gave the best overall fit but a power of 3 better described the initial delay. After the delay, the time course could be fitted by a single exponential. Time constants were 15–20 ms at 0 mV and decreased to a limiting τ = 7 ms at +50 to +100 mV. Tail currents were well fitted by single exponential functions and accelerated with hyperpolarization, from τ = 15–20 ms at 0 mV to τ = 2 ms at −110 mV ( e-fold for 40 mV). Eleven kinetic models were evaluated for their ability to describe the activation kinetics of the delayed rectifier. Hodgkin-Huxley–like models did not fit the data well. A linear model where voltage sensor movement is followed by a distinct channel opening step, allosteric models based on the Monod-Wyman–Changeux model, and an unconstrained C-C-C-O model could describe whole cell data from −100 to +40 mV. After including whole cell data at +60 and +80 mV, and a maximal p open of 0.8 from noise analysis of cell-attached patches, an allosteric model fit the data best, as the other models had difficulty describing qualitative features of the data. However, some more complex schemes (with additional free parameters) cannot be excluded. We propose the allosteric model as an empirical description of macroscopic ionic currents, and as a model worth considering in future studies on the molecular mechanism of potassium channel gating.

scholarly journals Kinetics of intramembrane charge movement and sodium current in frog node of Ranvier.

1982 ◽  
Vol 79 (4) ◽  
pp. 571-602 ◽  
Author(s):  
J M Dubois ◽  
M F Schneider
Keyword(s):  
Time Constant ◽  
Time Course ◽  
Sodium Current ◽  
Node Of Ranvier ◽  
Charge Movement ◽  
Intramembrane Charge Movement ◽  
Time Courses ◽  
Charge Movements ◽  
Kinetics Of ◽  
Microsecond Pulse

Intramembrane charge movement (Q) and sodium current (INa) were monitored in isolated voltage-clamped frog nodes of Ranvier, ON charge movements (QON) for pulses from the holding potential (-100 mV) to potentials V less than or equal to 0 mV followed single exponential time courses, whereas two exponentials were found for pulses to V greater than or equal to 20 mV. The voltage dependence of both QON and its time constant tauON indicated that the two ON components resolved at V greater than or equal to 20 mV were also present, though not resolvable, for pulses to V less than or equal to 0 mV. OFF charge movements (QOFF) monitored at various potentials were well described by single exponentials. When QOFF was monitored at -30 or -40 mV after a 200-microsecond pulse to +20 mV and QON was monitored at the same potential using pulses directly from -100 mV, tauON/tauOFF = 2.5 +/- 0.3. At a set OFF potential (-90 to -70 mV), tauOFF first increased with increasing duration tON of the preceding pulse to a given potential (0 to +30 mV) and then decreased with further increases in tON. The declining phase of tauOFF followed a time course similar to that of the decline in QOFF with tON. For the same pulse protocol, the OFF time constant tauNa for INA also first increased with tON but then remained constant over the tON interval during which tauOFF and QOFF were declining. After 200- or 300-microsecond pulses to +20, +20, or +50 mV, tauOFF/tauNa at -70 to -90 mV was 1.2 +/- 0.1. Similar tauOFF/tauNa ratios were predicted by channel models having three identical charged gating particles that can rapidly and reversibly form an immobile dimer or trimer after independently crossing the membrane from their OFF to their ON locations.

scholarly journals Rhodopsin kinetics in the cat retina.

1981 ◽  
Vol 77 (3) ◽  
pp. 317-334 ◽  
Author(s):  
H Ripps ◽  
L Mehaffey ◽  
I M Siegel
Keyword(s):  
Time Course ◽  
Continuous Light ◽  
Regenerative Process ◽  
Full Time ◽  
Difference Spectra ◽  
Cat Retina ◽  
Simple Exponential Function ◽  
Fundus Reflectometry ◽  
The Difference ◽  
Kinetics Of

The bleaching and regeneration of rhodopsin in the living cat retina was studied by means of fundus reflectometry. Bleaching was effected by continuous light exposures of 1 min or 20 min, and the changes in retinal absorbance were measured at 29 wavelengths. For all of the conditions studied (fractional bleaches of from 65 to 100%), the regeneration of rhodopsin to its prebleach levels required greater than 60 min in darkness. After the 1-min exposures, the difference spectra recorded during the first 10 min of dark adaptation were dominated by photoproduct absorption, and rhodopsin regeneration kinetics were obscured by these intermediate processes. Extending the bleaching duration to 20 min gave the products of photolysis an opportunity to dissipate, and it was possible to follow the regenerative process over its full time-course. It was not possible, however, to fit these data with the simple exponential function predicted by first-order reaction kinetics. Other possible mechanisms were considered and are presented in the text. Nevertheless, the kinetics of regeneration compared favorably with the temporal changes in log sensitivity determined electrophysiologically by other investigators. Based on the bleaching curve for cat rhodopsin, the photosensitivity was determined and found to approximate closely the value obtained for human rhodopsin; i.e., the energy Ec required to bleach 1-e-1 of the available rhodopsin was 7.09 log scotopic troland-seconds (corrected for the optics of the cat eye), as compared with approximately 7.0 in man.

scholarly journals Kinetics of light-dependent Ca fluxes across the plasma membrane of rod outer segments. A dynamic model of the regulation of the cytoplasmic Ca concentration.

1987 ◽  
Vol 90 (3) ◽  
pp. 397-425 ◽  
Author(s):  
D L Miller ◽  
J I Korenbrot
Keyword(s):  
Plasma Membrane ◽  
Outer Segment ◽  
Time Course ◽  
Small Volume ◽  
Dynamic Balance ◽  
Light Sensitivity ◽  
Ca Ions ◽  
Concentration Changes ◽  
The Difference ◽  
Kinetics Of

We measured simultaneously in single toad rods the membrane photocurrent and the Ca concentration in a small volume surrounding the outer segment. Illumination causes a rise in the extracellular Ca concentration. Photocurrents and Ca concentration changes occur over the same range of light intensities. Analysis of the time course of the Ca concentration changes suggests that these concentration changes arise from the difference in the transport rates of light-activated Ca influx and efflux across the outer segment plasma membrane. The Ca influx occurs through the light-sensitive channels of the outer segment membrane and the efflux through Na/Ca exchangers. In 0.1 mM external Ca, approximately 1-2% of the dark current is carried by Ca ions. The Ca efflux in the dark is identical to the influx, approximately 2 X 10(6) ions/s. Upon illumination, the Ca influx decreases with a time course and light sensitivity identical to those of the photocurrent. The Ca efflux, on the other hand, has very different kinetics from those of the photocurrent. Upon illumination, the Ca efflux decreases with a time course and light sensitivity determined by the change in membrane voltage and in the free cytoplasmic Ca concentration near the plasma membrane. In response to bright stimuli, which saturate the photocurrent for prolonged periods of time, the Ca efflux decays with an exponential time course from its value in darkness. The average time constant of this decay is 2.5 s. From the kinetics of the light-activated Ca fluxes, it is possible to predict that illumination causes a decrease in the cytoplasmic Ca concentration. We present a model of the regulation of the cytoplasmic Ca concentration by the dynamic balance of the Ca influx and efflux from the rod outer segment. The model accounts for our experimental observations and allows us to predict the time course and extent of the light-dependent decrease in the free cytoplasmic concentration.

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