Input Resistance, Time Constants, and Spike Initiation

1998 ◽  
Author(s):  
Christof Koch
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Action Potentials ◽  
Input Resistance ◽  
Current Injection ◽  
Membrane Conductances ◽  
Voltage Dependent ◽  
Dc Component ◽  
Definition Of ◽  
A Current

This chapter represents somewhat of a tephnical interlude. Having introduced the reader to both simplified and more complex compartmental single neuron models, we need to revisit terrain with which we are already somewhat familiar. In the following pages we reevaluate two important concepts we defined in the first few chapters: the somatic input resistance and the neuronal time constant. For passive systems, both are simple enough variables: Rin is the change in somatic membrane potential in response to a small sustained current injection divided by the amplitude of the current injection, while τm is the slowest time constant associated with the exponential charging or discharging of the neuronal membrane in response to a current pulse or step. However, because neurons express nonstationary and nonlinear membrane conductances, the measurement and interpretation of these two variables in active structures is not as straightforward as before. Having obtained a more sophisticated understanding of these issues, we will turn toward the question of the existence of a current, voltage, or charge threshold at which a biophysical faithful model of a cell triggers action potentials. We conclude with recent work that suggests how concepts from the subthreshold domain, like the input resistance or the average membrane potential, could be extended to the case in which the cell is discharging a stream of action potentials. This chapter is mainly for the cognoscendi or for those of us that need to make sense of experimental data by comparing therp to theoretical models that usually fail to reflect reality adequately. In Sec. 3.4, we defined Kii (f) for passive cable structures as the voltage change at location i in response to a sinusoidal current injection of frequency f at the same location. Its dc component is also referred to as input resistance or Rin. Three difficulties render this definition of input resistance problematic in real cells: (1) most membranes, in particular at the soma, show voltage-dependent nonlinearities, (2) the associated ionic membrane conductances are time dependent and (3) instrumental aspects, such as the effect of the impedance of the recording electrode on Rin, add uncertainty to the measuring process.

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.

Calcium-dependent potassium conductance in rat supraoptic nucleus neurosecretory neurons

1985 ◽  
Vol 54 (6) ◽  
pp. 1375-1382 ◽  
Author(s):  
C. W. Bourque ◽  
J. C. Randle ◽  
L. P. Renaud
Keyword(s):  
Time Constant ◽  
Action Potentials ◽  
Supraoptic Nucleus ◽  
Potassium Conductance ◽  
Reversal Potential ◽  
Input Resistance ◽  
Mean Amplitude ◽  
Progressive Increase ◽  
Calcium Dependent ◽  
Neurosecretory Neurons

Intracellular recordings of rat supraoptic nucleus neurons were obtained from perfused hypothalamic explants. Individual action potentials were followed by hyperpolarizing afterpotentials (HAPs) having a mean amplitude of -7.4 +/- 0.8 mV (SD). The decay of the HAP was approximated by a single exponential function having a mean time constant of 17.5 +/- 6.1 ms. This considerably exceeded the cell time constant of the same neurons (9.5 +/- 0.8 ms), thus indicating that the ionic conductance underlying the HAP persisted briefly after each spike. The HAP had a reversal potential of -85 mV and was unaffected by intracellular Cl- ionophoresis of during exposure to elevated extracellular concentrations of Mg2+. In contrast, the peak amplitude of the HAP was proportional to the extracellular Ca2+ concentration and could be reversibly eliminated by replacing Ca2+ with Co2+, Mn2+, or EGTA in the perfusion fluid. During depolarizing current pulses, evoked action potential trains demonstrated a progressive increase in interspike intervals associated with a potentiation of successive HAPs. This spike frequency adaptation was reversibly abolished by replacing Ca2+ with Co2+, Mn2+, or EGTA. Bursts of action potentials were followed by a more prolonged afterhyperpolarization (AHP) whose magnitude was proportional to the number of impulses elicited (greater than 20 Hz) during a burst. Current injection revealed that the AHP was associated with a 20-60% decrease in input resistance and showed little voltage dependence in the range of -70 to -120 mV. The reversal potential of the AHP shifted with the extracellular concentration of K+ [( K+]o) with a mean slope of -50 mV/log[K+]o.(ABSTRACT TRUNCATED AT 250 WORDS)

Epileptiform activity induced by low chloride medium in the CA1 subfield of the hippocampal slice

1990 ◽  
Vol 64 (6) ◽  
pp. 1747-1757 ◽  
Author(s):  
M. Avoli ◽  
C. Drapeau ◽  
P. Perreault ◽  
J. Louvel ◽  
R. Pumain
Keyword(s):  
Membrane Potential ◽  
Large Amplitude ◽  
Action Potentials ◽  
Hippocampal Slice ◽  
Epileptiform Activity ◽  
Field Potential ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Field Potentials ◽  
Maximal Amplitude

1. Extracellular and intracellular recordings and measurements of the extracellular concentration of free K+ ([K+]o) were performed in the CA1 subfield of the rat hippocampal slice during perfusion with artificial cerebrospinal fluid (ACSF) in which NaCl had been replaced with equimolar Na-isethionate or Na-methylsulfate (hereafter called low Cl- ACSF). 2. CAl pyramidal cells perfused with low Cl- ACSF generated intracellular epileptiform potentials in response to orthodromic, single-shock stimuli delivered in stratum (S.) radiatum. Low-intensity stimuli evoked a short-lasting epileptiform burst (SB) of action potentials that lasted 40–150 ms and was followed by a prolonged hyperpolarization. When the stimulus strength was increased, a long-lasting epileptiform burst (LB) appeared; it had a duration of 4–15 s and consisted of an early discharge of action potentials similar to the SB, followed by a prolonged, large-amplitude depolarizing plateau. The refractory period of the LB was longer than 20 s. SB and LB were also seen after stimulation of the alveus. 3. Variations of the membrane potential with injection of steady. DC current modified the shape of SB and LB. When microelectrodes filled with the lidocaine derivative QX-314 were used, the amplitudes of both SB and LB increased in a linear fashion during changes of the baseline membrane potential in the hyperpolarizing direction. The membrane input resistance, as measured by injecting brief square pulses of hyperpolarizing current, decreased by 65-80% during the long-lasting depolarizing plateau of LB. 4. A synchronous field potential and a transient increase in [K+]o accompanied the epileptiform responses. The extracellular counterpart of the SB was a burst of three to six population spikes and a small increase in [K+]o (less than or equal to 2 mM from a resting value of approximately 2.5 mM). The LB was associated with a large-amplitude, biphasic, negative field potential and a large increase in [K+]o (up to 12.4 mM above the resting value). Changes in [K+]o during the LB were largest at the border between S. oriens and S. pyramidale. This was also the site where the field potentials measured 2–5 s after the stimulus attained their maximal amplitude. Conversely, field potentials associated with the early component of the LB or with the SB displayed a maximal amplitude in the S. radiatum. 5. Spontaneous SBs and LBs were at times recorded in the CA1 and in the CA3 subfield.(ABSTRACT TRUNCATED AT 400 WORDS)

Ionic Currents Underlying Fast Action Potentials in the Obliquely Striated Muscle Cells of the Octopus Arm

2002 ◽  
Vol 88 (6) ◽  
pp. 3386-3397 ◽  
Author(s):  
Dan Rokni ◽  
Binyamin Hochner
Keyword(s):  
Time Constant ◽  
Action Potentials ◽  
Striated Muscle ◽  
Muscle Cells ◽  
Ionic Currents ◽  
Delayed Rectifier ◽  
Inactivation Kinetics ◽  
Activation Kinetics ◽  
Voltage Dependent ◽  
Neuromuscular Systems

The octopus arm provides a unique model for neuromuscular systems of flexible appendages. We previously reported the electrical compactness of the arm muscle cells and their rich excitable properties ranging from fast oscillations to overshooting action potentials. Here we characterize the voltage-activated ionic currents in the muscle cell membrane. We found three depolarization-activated ionic currents: 1) a high-voltage-activated L-type Ca2+ current, which began activating at approximately −35 mV, was eliminated when Ca2+ was substituted by Mg2+, was blocked by nifedipine, and showed Ca2+-dependent inactivation. This current had very rapid activation kinetics (peaked within milliseconds) and slow inactivation kinetics (τ in the order of 50 ms). 2) A delayed rectifier K+ current that was totally blocked by 10 mM TEA and partially blocked by 10 mM 4-aminopyridine (4AP). This current exhibited relatively slow activation kinetics (τ in the order of 15 ms) and inactivated only partially with a time constant of ∼150 ms. And 3) a transient A-type K+ current that was totally blocked by 10 mM 4AP and was partially blocked by 10 mM TEA. This current exhibited very fast activation kinetics (peaked within milliseconds) and inactivated with a time constant in the order of 60 ms. Inactivation of the A-type current was almost complete at −40 mV. No voltage-dependent Na+ current was found in these cells. The octopus arm muscle cells generate fast (∼3 ms) overshooting spikes in physiological conditions that are carried by a slowly inactivating L-type Ca2+ current.

Ratiometry of transmembrane voltage-sensitive fluorescent dye emission in hearts

2000 ◽  
Vol 279 (3) ◽  
pp. H1421-H1433 ◽  
Author(s):  
Stephen B. Knisley ◽  
Robert K. Justice ◽  
Wei Kong ◽  
Philip L. Johnson
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Signal To Noise Ratio ◽  
Green Emission ◽  
Motion Artifacts ◽  
Resting Membrane Potential ◽  
Baseline Drift ◽  
Fluorescence Measurements ◽  
Transmembrane Voltage ◽  
Voltage Dependent

Transmembrane voltage-sensitive fluorescence measurements are limited by baseline drift that can obscure changes in resting membrane potential and by motion artifacts that can obscure repolarization. Voltage-dependent shift of emission wavelengths may allow reduction of drift and motion artifacts by emission ratiometry. We have tested this for action potentials and potassium-induced changes in resting membrane potential in rabbit hearts stained with di-4-ANEPPS [Pyridinium, 4-(2-(6-(dibutylamino)-2-naphthalenyl) ethenyl)-1-(3-sulfopropyl)-, hydroxide, inner salt] using laser excitation (488 nm) and a two-photomultiplier tube system or spectrofluorometer (resolution of 500–1,000 Hz and <1 mm). Green and red emissions produced upright and inverted action potentials, respectively. Ratios of green emission to red emission followed action potential contours and exhibited larger fractional changes than either emission alone ( P < 0.001). The largest changes and signal-to-noise ratio (signal/noise) were obtained with numerator wavelengths of 525–550 nm and denominator wavelengths of 650–700 nm. Ratiometry lessened drift 56–66% ( P < 0.015) and indicated decreases in resting membrane potential. Ratiometry lessened motion artifacts and increased magnitudes of deflections representing phase-zero depolarizations relative to total deflections by 123–188% in intact hearts ( P < 0.02). Durations of action potentials at different pacing rates, temperatures, and potassium concentrations were independent of whether they were measured ratiometrically or with microelectrodes ( P ≥ 0.65). The ratiometric calibration slope was 0.017/100 mV and decreased with time. Thus emission ratiometry lessens the effects of motion and drift and indicates resting membrane potential changes and repolarization.

Sodium dependence of the thyrotrophin-induced depolarization in cultured porcine thyroid cells

1986 ◽  
Vol 108 (2) ◽  
pp. 225-230 ◽  
Author(s):  
T. A. Hambleton ◽  
J. R. Bourke ◽  
G. J. Huxham ◽  
S. W. Manley
Keyword(s):  
Membrane Potential ◽  
Action Potentials ◽  
Potassium Concentration ◽  
Sodium Current ◽  
Resting Membrane Potential ◽  
Thyroid Cell ◽  
Free Medium ◽  
Thyroid Cells ◽  
Voltage Dependent ◽  
Sodium And Potassium

ABSTRACT Cultured porcine thyroid cells exhibit a resting membrane potential of about − 73 mV and depolarize to about − 54 mV on exposure to TSH. The depolarizing response to TSH was preserved in a medium consisting only of inorganic salts and buffers, but was abolished in sodium-free medium, demonstrating dependence on an inward sodium current. Increasing the potassium concentration of the medium resulted in a reduction in the resting membrane potential of 60 mV per tenfold change in potassium concentration, and a diminished TSH response. A hyperpolarizing TSH response was observed in a sodium- and bicarbonate-free medium, indicating that a hyperpolarizing ion current (probably carried by potassium) was also enhanced in the presence of TSH. Tetrodotoxin blocked the TSH response. We conclude that the response of the thyroid cell membrane to TSH involves increases in permeability to sodium and potassium, and that the thyroid membrane ion channels bear some similarity to the voltage-dependent sodium channels of excitable tissues, despite the absence of action potentials in the thyroid. J. Endocr. (1986) 108, 225–230

An Intrinsic Oscillation in Interneurons of the Rat Lateral Geniculate Nucleus

1999 ◽  
Vol 81 (2) ◽  
pp. 702-711 ◽  
Author(s):  
J. Julius Zhu ◽  
William W. Lytton ◽  
Jin-Tang Xue ◽  
Daniel J. Uhlrich
Keyword(s):  
Membrane Potential ◽  
Lateral Geniculate Nucleus ◽  
Action Potentials ◽  
Optic Tract ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Lateral Geniculate ◽  
Bath Application ◽  
Voltage Dependent ◽  
Intrinsic Oscillation

Intrinsic oscillation in interneurons of the rat lateral geniculate nucleus. By using the whole cell patch recording technique in vitro, we examined the voltage-dependent firing patterns of 69 interneurons in the rat dorsal lateral geniculate nucleus (LGN). When held at a hyperpolarized membrane potential, all interneurons responded with a burst of action potentials. In 48 interneurons, larger current pulses produced a bursting oscillation. When relatively depolarized, some interneurons produced a tonic train of action potentials in response to a depolarizing current pulse. However, most interneurons produced only oscillations, regardless of polarization level. The oscillation was insensitive to the bath application of a combination of blockers to excitatory and inhibitory synaptic transmission, including 30 μM 6,7-dinitroquinoxaline-2,3-dione, 100 μM (±)-2-amino-5-phosphonopentanoic acid, 20 μM bicuculline, and 2 mM saclofen, suggesting an intrinsic event. The frequency of the oscillation in interneurons was dependent on the intensity of the injection current. Increasing current intensity increased the oscillation frequency. The maximal frequency of the oscillation was 5–15 Hz for most cells, with some ambiguity caused by the difficulty of precisely defining a transition from oscillatory to regular firing behavior. In contrast, the interneuron oscillation was little affected by preceding depolarizing and hyperpolarizing pulses. In addition to being elicited by depolarizing current injections, the oscillation could also be initiated by electrical stimulation of the optic tract when the interneurons were held at a depolarized membrane potential. This suggests that interneurons may be recruited into thalamic oscillations by synaptic inputs. These results indicate that interneurons may play a larger role in thalamic oscillations than was previously thought.

Electrical properties of neurons recorded from the rat supraoptic nucleus in vitro

1983 ◽  
Vol 217 (1207) ◽  
pp. 141-161 ◽  
Keyword(s):  
Membrane Potential ◽  
Electrical Properties ◽  
Time Constant ◽  
Synaptic Input ◽  
Action Potentials ◽  
Supraoptic Nucleus ◽  
Synaptic Activity ◽  
Intracellular Recordings ◽  
Average Cell ◽  
Spike Threshold

The electrical properties of neurons in the supraoptic nucleus (so.n.) have been studied in the hypothalamic slice preparation by intracellular and extracellular recording techniques, with Lucifer Yellow CH dye injection to mark the recording site as being the so. n. Intracellular recordings from so. n. neurons revealed them to have an average membrane potential of ─ 67±0.8 mV (mean±s. e. m.), membrane resistance of 145±9 MΩ with linear current–voltage relations from 40 mV in the hyperpolarizing direction to the level of spike threshold in the depolarizing direction. Average cell time constant was 14±2.2 ms. So. n. action potentials ranged in amplitude from 55 to 95 mV, with a mean of 76±2 mV, and a spike width of 2.6±0.5 ms at 30% of maximal spike height. Both single spikes and trains of spikes were followed by a strong, long-lasting hyperpolarization with a decay fitted by a single exponential having a time constant of 8.6±1.8 ms. Action potentials could be blocked by 10 -6 m tetrodotoxin. Spontaneously active so. n. neurons were characterized by synaptic input in the form of excitatory and inhibitory postsynaptic potentials, the latter being apparently blocked when 4 m KCI electrodes were used. Both forms of synaptic activity were blocked by application of divalent cations such as Mg 2+ , Mn 2+ or Co 2+ . 74% of so. n. neurons fired spontaneously at rates exceeding 0.1 spikes per second, with a mean for all cells of 2.9±0.2 s -1 . Of these cells, 21% fired slowly and continuously at 0.1─1.0 s -1 , 45 % fired continuously at greater than 1 Hz, and the remaining 34% fired phasically in bursts of activity followed by silence or low frequency firing. Spontaneously firing phasic cells showed a mean burst length of 16.7± 4.5 s and a silent period of 28.2±4.2 s. Intracellular recordings revealed the presence of slow variations in membrane potential which modified the neuron’s proximity to spike threshold, and controlled phasic firing. Variations in synaptic input were not observed to influence firing in phasic cells.

Triiodothyronine affects the electrical properties of GH3 cells

1990 ◽  
Vol 123 (1) ◽  
pp. 51-60 ◽  
Author(s):  
John S. du Pont
Keyword(s):  
Membrane Potential ◽  
Electrical Properties ◽  
Action Potentials ◽  
Channel Blocker ◽  
Membrane Resistance ◽  
Gh3 Cells ◽  
Current Clamp ◽  
Potential Capacity ◽  
Rat Pituitary ◽  
A Current

Abstract. Electrophysiological experiments show that T3 has a direct effect on the cell membrane of GH3 cells, a transformed line from the rat pituitary. Slope conductance versus membrane potential, resting membrane resistance, potential, capacity and action potentials were measured in this study. Using a current clamp technique, the effects of tetrodotoxin, tetraethylammonium, apamin, and nifedipine were measured and compared with those directly evoked by T3. T3 increased the slope conductance: 1. at around −60 mV, as did tetrodotoxin (Na+ channel blocker); 2. at about −40 mV, as did nifedipine (Ca2+ channel blocker), but decreased this conductance strongly between −20 and −30 mV, as did both nifedipine and apamin (Ca2+-sensitive K+ channel blocker). Action potentials were inhibited by T3 and by nifedipine. Action potentials in these cells are primarily related to Ca2+ ions. It seems that T3 inhibits the Ca2+ current and, as a consequence, the Ca2+-sensitive K+ current.

Electrically gated ionic channels in lipid bilayers

1977 ◽  
Vol 10 (1) ◽  
pp. 1-34 ◽  
Author(s):  
Gerald Ehrenstein ◽  
Harold Lecar
Keyword(s):  
Membrane Potential ◽  
Lipid Bilayers ◽  
Action Potentials ◽  
Cell Membranes ◽  
Electric Organ ◽  
Ionic Channels ◽  
Nerve Axon ◽  
Voltage Dependent

The generation of action potentials in nerve and muscle requires cell membranes with steeply voltage-dependent ionic permeabilities. The voltage-dependent, ion-selective pathways responsible for excitation have been characterized for numerous excitable tissues such as nerve axon, muscle, electric organ, algae and epithelia (Aidley, 1971; Hodgkin, 1964; Cole, 1968). The process of activating ionic pathways by some stimulus, such as a change in membrane potential, is called gating.

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