scholarly journals The Effect of Glycerol Treatment of Voltage-Clamped Snake Muscle Fibers

1973 ◽  
Vol 61 (2) ◽  
pp. 176-184 ◽  
Author(s):  
Hiroshi Washio
Keyword(s):  
Normal Saline ◽  
Surface Membrane ◽  
Muscle Fibers ◽  
Outward Current ◽  
Tension Development ◽  
Normal Medium ◽  
Outward Currents ◽  
Delayed Rectification ◽  
Glycerol Treatment ◽  
Contractile Activation

The effect of glycerol treatment on the membrane currents and tension development was studied in voltage clamped snake muscle fibers. In muscle fibers which were exposed for 1 h to a normal saline containing 400 mM glycerol and then returned to a normal medium, graded depolarizations did not accompany contractile responses. However, when the fiber was depolarized to a certain level, an increment of outward current appeared which partially inactivated with time. The threshold for delayed rectification in glycerol-treated fibers was almost the same as that of intact fibers in spite of the absence of contractile tension. The results suggest that the delayed rectification may be attributed at least in part to the surface membrane and that the contractile activation probably does not depend simply on the inactivating outward currents through the delayed rectification channel.

scholarly journals Voltage Clamp Experiments on Single Muscle Fibers of Rana pipiens

1972 ◽  
Vol 60 (1) ◽  
pp. 1-19 ◽  
Author(s):  
L. E. Moore
Keyword(s):  
Voltage Clamp ◽  
Rana Pipiens ◽  
Muscle Fibers ◽  
Petroleum Jelly ◽  
Single Muscle ◽  
Transverse Tubular System ◽  
Anomalous Rectification ◽  
Outward Currents ◽  
Delayed Rectification ◽  
Tubular System

A voltage clamp for single muscle fibers has been developed. Stability of the system was achieved when an artificial node was created by enclosing a single muscle fiber in a petroleum jelly seal which served as an analogue of the myelin sheath. Typical voltage clamp records were obtained with large inward transient currents followed by a delayed rectification of the outward currents. These currents looked qualitatively similar when the transverse tubular system was destroyed. Errors in current measurement, especially those due to anomalous rectification, are discussed.

A Regenerative Calcium Response in Paramecium

1972 ◽  
Vol 56 (3) ◽  
pp. 667-681
Author(s):  
YUTAKA NAITOH ◽  
ROGER ECKERT ◽  
KENNETH FRIEDMAN
Keyword(s):  
Surface Membrane ◽  
Maximum Amplitude ◽  
Outward Current ◽  
Fold Increase ◽  
Ion Concentration ◽  
Regenerative Response ◽  
Stimulus Current ◽  
Delayed Rectification ◽  
Graded Response ◽  
Maximum Rate Of Rise

1. Standard intracellular current-passing and recording techniques were used to investigate the electrical properties of the membrane of Paramecium caudatum. 2. The surface membrane produces regenerative depolarizations graded in amplitude and rate of rise with the intensity of applied outward current pulses. In a solution of 1 mM-CaCl2, 1 mM-KCl and 1 mM Tris-HCl at pH 7.2 and 18 °C the overshoot reaches a maximum amplitude of + 5 to + 15 mV, and shows a maximum rate of rise of about 7 V/sec. 3. The overshoot is insensitive to Li,+, Na+, Cl-, TTX and procaine, but increases slightly (up to 10 mV/10-fold rise in ion concentration) in the presence of K+, Rb+, Cs+, NH+4, Mg2+ and tetraethylammonium. 4. The overshoot increases 22-25 mV for each 10-fold increase in external [Ca]. Ba2+ and Sr2+ convert the graded response to one that is all-or-none. 5. Repolarization following the peak of the response is more rapid than expected from the time constant of the resting membrane, suggesting delayed rectification. 6. A conditioning depolarization causes inactivation of the regenerative response, and hyperpolarization depresses the response to a given stimulus current. Refractoriness persists for up to 200 msec after each response. 7. The regenerative response of the membrane is consistent with a transient increase in conductance to Ca2+ (Ba2+, Sr2+) with a consequent inwardly directed calcium current. This agrees with recent evidence that ciliary reversal (which accompanies depolarization) is produced by an influx of Ca2+.

scholarly journals Effect of External Calcium and of Temperature on Contraction in Snake Muscle Fibers

1974 ◽  
Vol 63 (4) ◽  
pp. 415-431 ◽  
Author(s):  
Hiroshi Washio
Keyword(s):  
Time Course ◽  
Contractile Response ◽  
Muscle Fibers ◽  
Outward Current ◽  
Bathing Solution ◽  
Minimum Duration ◽  
Delayed Rectification ◽  
Rate Of Recovery ◽  
Lower Temperature ◽  
External Calcium

The effect of external calcium and of temperature on the contractile responses has been studied in voltage clamped snake twitch muscle fibers. Increasing [Ca++]o from 0.2 to 7.0 mM raised contractile threshold by 15–20 mV, the latter coinciding with the appearance of delayed rectification. The duration of contracture, the rates of rise and decay of tension depended on the level of depolarization and [Ca++]o. The minimum duration of repolarization necessary to restore the contractile response was much shorter in high [Ca++]o. When the bathing solution was cooled to 10 from 20°C the time-course of contracture was markedly prolonged and the outward current was reduced without significant change in maximum tension. The threshold for contraction tended to be somewhat lower at the lower temperature. The contractile repriming was much slower at low temperature. However, reduction in temperature slowed the rate of recovery much less at low [Ca++]o than at normal [Ca++]o.

scholarly journals Choline and NMDG directly reduce outward currents: reduced outward current when these substances replace Na+ is alone not evidence of Na+-activated K+ currents

2018 ◽  
Vol 120 (6) ◽  
pp. 3217-3233 ◽  
Author(s):  
Jeffrey B. Thuma ◽  
Scott L. Hooper
Keyword(s):  
Sodium Chloride ◽  
Potassium Channels ◽  
Normal Saline ◽  
Choline Chloride ◽  
Outward Current ◽  
Sodium Concentration ◽  
Outward Currents ◽  
High Concentrations ◽  
Retzius Cells ◽  
Extracellular Sodium

Choline chloride is often, and N-methyl-d-glucamine (NMDG) sometimes, used to replace sodium chloride in studies of sodium-activated potassium channels. Given the high concentrations used in sodium replacement protocols, it is essential to test that it is not the replacement substances themselves, as opposed to the lack of sodium, that cause any observed effects. We therefore compared, in lobster stomatogastric neurons and leech Retzius cells, the effects of applying salines in which choline chloride replaced sodium chloride, and in which choline hydroxide or sucrose was added to normal saline. We also tested, in stomatogastric neurons, the effect of adding NMDG to normal saline. These protocols allowed us to measure the direct effects (i.e., effects not due to changes in sodium concentration or saline osmolarity or ionic strength) of choline on stomatogastric and leech currents, and of NMDG on stomatogastric currents. Choline directly reduced transient and sustained depolarization-activated outward currents in both species, and NMDG directly reduced transient depolarization-activated outward currents in stomatogastric neurons. Experiments with lower choline concentrations showed that adding as little as 150 mM (stomatogastric) or 5 mM (leech) choline reduced at least some depolarization-activated outward currents. Reductions in outward current with choline chloride or NMDG replacement alone are thus not evidence of sodium-activated potassium currents. NEW & NOTEWORTHY We show that choline or N-methyl-d-glucamine (NMDG) directly (i.e., not due to changes in extracellular sodium) decrease outward currents. Prior work studying sodium-activated potassium channels in which sodium was replaced with choline or NMDG without an addition control may therefore be artifactual.

The Effects of Pentobarbital on the Electrical and Mechanical Properties of Frog and Snake Twitch Muscle Fibers

1973 ◽  
Vol 51 (2) ◽  
pp. 68-78 ◽  
Author(s):  
J. G. Foulks ◽  
Florence A. Perry ◽  
H. D. Sanders ◽  
H. Washio
Keyword(s):  
Surface Membrane ◽  
Muscle Fibers ◽  
Membrane Resistance ◽  
Frog Skeletal Muscle ◽  
Depressant Effect ◽  
Tension Development ◽  
High Calcium ◽  
Marked Enhancement ◽  
High Concentrations ◽  
Permeant Anion

Pentobarbital (0.4–1.2 mM) produces marked enhancement of twitch tension in frog skeletal muscle. Latency is reduced and the rate of tension development is increased. In ordinary media, the agent impairs K contractures but this depressant effect can be eliminated by using a high calcium medium containing acetate in place of chloride. In such solutions, pentobarbital reduces the [K]0 necessary for K contractures. In snake twitch fibers depolarized by means of a voltage clamp, pentobarbital shifted the relation between membrane potential and contracture tension to a more negative level of potential. High concentrations of pentobarbital have a depolarizing effect which is greatly accentuated in a medium containing no permeant anion. The drug reduces the rate and extent of the depolarization produced by elevation of [K]0, and increases membrane resistance. These observations indicate that pentobarbital reduces the potassium permeability of the surface membrane of twitch muscle fibers.

Nitric oxide mediates outward potassium currents in opossum esophageal circular smooth muscle

1996 ◽  
Vol 270 (6) ◽  
pp. G932-G938 ◽  
Author(s):  
J. Jury ◽  
K. R. Boev ◽  
E. E. Daniel
Keyword(s):  
Nitric Oxide ◽  
Smooth Muscle ◽  
Circular Muscle ◽  
Outward Current ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Pipette Solution ◽  
Whole Cell ◽  
Circular Smooth Muscle ◽  
Outward Currents

Single smooth muscle cells from the opossum body circular muscle were isolated and whole cell currents were characterized by the whole cell patch-clamp technique. When the cells were held at -50 mV and depolarized to 70 mV in 20-mV increments, initial small inactivating inward currents were evoked (-30 to 30 mV) followed by larger sustained outward currents. Depolarization from a holding potential of -90 mV evoked an initial fast inactivating outward current sensitive to 4-aminopyridine but not to high levels of ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA). The outward currents reversed near K+ equilibrium potential and were abolished when KCl was replaced by CsCl in the pipette solution. The sustained outward current was inhibited by quinine and cesium. High EGTA in the pipette solution reduced but did not abolish the sustained outward currents, suggesting that both Ca(2+)-dependent and -independent currents were evoked. The nitric oxide (NO)-releasing agents Sin-1 and sodium nitroprusside increased outward K+ currents. High levels of EGTA in the pipette solution abolished the increase in outward current induced by Sin-1. The presence of cyclopiazonic acid, an inhibitor of the sarcoplasmic reticulum (SR) Ca2+ pump, blocked the effects of NO-releasing agents. We conclude that NO release activates K+ outward currents in opossum esophagus circular muscle, which may depend on Ca2+ release from the SR stores.

Metabotropic glutamate receptor agonist-induced hyperpolarizations in rat basolateral amygdala neurons: receptor characterization and ion channels

1996 ◽  
Vol 76 (5) ◽  
pp. 3059-3069 ◽  
Author(s):  
K. H. Holmes ◽  
N. B. Keele ◽  
V. L. Arvanov ◽  
P. Shinnick-Gallagher
Keyword(s):  
Dicarboxylic Acid ◽  
Glutamate Receptor ◽  
Basolateral Amygdala ◽  
Metabotropic Glutamate Receptor ◽  
Outward Current ◽  
Channel Blockers ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Metabotropic Glutamate ◽  
Outward Currents

1. Metabotropic glutamate receptor (mGluR)-agonist-induced hyperpolarizations and corresponding outward currents were analyzed in basolateral amygdala (BLA) neurons in rat brain slice preparations with current-clamp and single-electrode voltage-clamp recording to characterize the mGluR subtype(s) and the ion channel(s) mediating this response. 2. The mGluR agonist (1S,3R)-1-amino-cyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD) induced a membrane hyperpolarization or outward current in BLA neurons in a concentration-dependent manner (median effective concentration = 34 microM; range = 10-200 microM); the 1S,3R-ACPD hyperpolarizations are recorded in 89% of neurons that accommodate or cease firing in response to a 400-ms depolarizing current injection (0.5 nA). 3. mGluR agonists elicited hyperpolarizations or outward currents in a concentration-dependent manner in the following rank order of potency: (2S,3S,4S)-alpha-(carboxycyclopropyl)glycine (L-CCG-I) > 1S,3R-ACPD > (s)-4-carboxyphenylglycine = (RS)-4-carboxy-3-hydroxyphenylglycine (4C3HPG) > L-aminophosphonobutyric acid > (1S,3S)-1-amino-cyclopentane-1,3-dicarboxylic acid. In contrast, the mGluR agonists quisqualate and ibotenate induced only depolarizations in the presence of D-2-amino-5-phosphonovalerate and 6-cyano-7-nitroquinoxaline-2,3-dione in BLA neurons. 4. The 1S,3R-ACPD-induced outward current is mediated through a large-conductance calcium-dependent potassium (BK) conductance. The BK channel blockers iberiotoxin and charybdotoxin blocked the response, as did the potassium channel blockers tetraethylammonium and 4-aminopyridine; the small-conductance calcium-activated potassium channel blocker apamin did not affect the response. 5. The mGluR-agonist-induced hyperpolarization is blocked in amygdala slices from animals pretreated with pertussis toxin (PTX). 1S,3R-ACPD hyperpolarizations were recorded in neurons contralateral but not ipsilateral to the site of PTX injection. 6. The antagonist (+/-)-alpha-methyl-4-carboxyphenylglycine (MCPG, 500 microM) reduced significantly the 1S,3R-ACPD-induced hyperpolarization. 7. In conclusion, the relative potency of L-CCG-I and 4C3HPG in evoking only hyperpolarizations (outward currents) in accommodating neurons, and the observation that MCPG (500 microM) reduces the hyperpolarization, suggest that a group-II-like mGluR underlies the hyperpolarizing response. The mGluR-induced response is sensitive to iberiotoxin and to pretreatment with PTX, suggesting activation of BK channels through a group II mGluR linked to a PTX-sensitive G protein in BLA neurons.

X-linked vacuolated myopathy: Complement membrane attack complex on surface membrane of injured muscle fibers

1995 ◽  
Vol 37 (5) ◽  
pp. 637-645 ◽  
Author(s):  
Marcello Villanova ◽  
Jean Pierre Louboutin ◽  
Danielle Chateau ◽  
Bruno Eymard ◽  
Marguerite Sagniez ◽  
...  
Keyword(s):  
Surface Membrane ◽  
Muscle Fibers ◽  
Membrane Attack Complex
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