scholarly journals Dual effect of L-glutamate on excitatory postjunctional membranes of crayfish muscle.

1975 ◽  
Vol 65 (5) ◽  
pp. 677-691 ◽  
Author(s):  
P S Taraskevich
Keyword(s):  
Muscle Fibers ◽  
Reversal Potential ◽  
Dual Effect ◽  
Sodium Conductance ◽  
Crayfish Muscle ◽  
Permeability Changes ◽  
Extracellular Sodium ◽  
Sodium And Potassium

Iontophoretically applied glutamate produces different excitatory postjunctional permeability changes on separate muscle fibers in a single crayfish muslce. At junctions on some fibers glutamate appears to increase the conductance to both sodium and potassium whereas at others its effect is primarily on the sodium conductance. These results obtained by studying the reversal potential for the extracellularly recorded glutamate potential under conditions of varied extracellular sodium and potassium concentrations.

scholarly journals Role of sodium in ADP- and thrombin-induced megakaryocyte spreading.

1983 ◽  
Vol 96 (5) ◽  
pp. 1234-1240 ◽  
Author(s):  
R M Leven ◽  
W H Mullikin ◽  
V T Nachmias
Keyword(s):  
Membrane Potential ◽  
Intracellular Recording ◽  
Membrane Depolarization ◽  
Sodium Permeability ◽  
Sodium Conductance ◽  
Extracellular Sodium

We investigated the role of sodium in megakaryocyte spreading induced by thrombin and ADP. We found that if extracellular sodium was replaced by lithium, potassium, or choline, spreading was inhibited. When extracellular sodium was present, amiloride or tetrodotoxin inhibited spreading. Using intracellular recording we found spreading to be associated with a permanent membrane depolarization. The extent and rate of thrombin-induced depolarization was reduced when lithium replaced sodium. Unspread cells had an average membrane potential of -44.8 mV. Spread cells had an average membrane potential of -18.46 mV. When choline replaced sodium, or when in the presence of tetrodotoxin and amiloride, the spread cells repolarized, indicating that the depolarization is due to an increase in sodium permeability. Similar treatments did not change the membrane potential of unspread cells. Incubation of megakaryocytes with A23187 together with monensin or methylamine induced spreading. Methylamine occasionally caused spreading by itself, but neither ionophore alone caused spreading. These results indicate that megakaryocyte spreading induced by ADP and thrombin depends on an increase in sodium conductance.

Hodgkin–Huxley neurons with defective and blocked ion channels

2015 ◽  
Vol 26 (10) ◽  
pp. 1550112 ◽  
Author(s):  
James Christopher S. Pang ◽  
Johnrob Y. Bantang
Keyword(s):  
Ion Channels ◽  
Action Potentials ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Potassium Ions ◽  
Temporal Response ◽  
Constant Input ◽  
Control Drug ◽  
Channel Control ◽  
Sodium And Potassium

We utilize the original Hodgkin–Huxley (HH) model to consider the effects of defective ion channels to the temporal response of neurons. Statistics of firing rate and inter-spike interval (ISI) reveal that production of action potentials (APs) in neurons is not sensitive to changes in membrane conductance for sodium and potassium ions, as well as to the reversal potential for sodium ions, as long as the relevant parameters do not exceed 13% from their normal levels. We also found that blockage of a critical fraction of either sodium or potassium channels (dependent on constant input current) respectively limits the firing activity or increases spontaneous spiking activity of neurons. Our model may be used to guide experiment designs related to ion channel control drug development.

cAMP and calcium in generation of slow waves in cat colon

1982 ◽  
Vol 242 (2) ◽  
pp. G124-G127
Author(s):  
S. Anuras
Keyword(s):  
Calcium Concentration ◽  
Extracellular Fluid ◽  
Muscularis Propria ◽  
Slow Waves ◽  
Dibutyryl Camp ◽  
Longitudinal Strip ◽  
Extracellular Sodium ◽  
Camp Levels ◽  
Sodium And Potassium ◽  
Spike Bursts

Rhythmic oscillations in interactions between cAMP and calcium have been proposed to account for a variety of rhythmic phenomena in cells. This idea was investigated in relation to the rhythmic signals (electrical slow waves) found in the electromyogram of the cat colon. A longitudinal strip of muscularis propria from cat colon was studied in a superfusion bath that allowed recording of the electromyogram from eight sites that were 2 cm apart. The effect of increasing cAMP (by exposure of the tissue to cAMP, dibutyryl cAMP, isobutylmethylxanthine, theophylline, caffeine, and papaverine) was to reduce frequency and amplitude of slow waves and duration of migrating spike bursts. All these maneuvers raised tissue cAMP levels. Dibutyryl cGMP and cGMP had no effect. THe changes in slow waves, but not migrating spike bursts, seen with raised cAMP levels were partly reversed by raising the calcium concentration in the extracellular fluid. Raising the extracellular sodium and potassium concentrations had no effect. The results are consistent with the hypothesis that interactions between cAMP and calcium are involved in slow-wave generation in colon muscle.

Fast BK-Type Channel Mediates the Ca2+-Activated K+ Current in Crayfish Muscle

1999 ◽  
Vol 82 (4) ◽  
pp. 1655-1661 ◽  
Author(s):  
Alfonso Araque ◽  
Washington Buño
Keyword(s):  
Electrical Activity ◽  
Single Channel ◽  
Muscle Fibers ◽  
Ionic Channels ◽  
Bk Channels ◽  
Intrinsic Properties ◽  
Open Probability ◽  
Crayfish Muscle ◽  
Fast Activation ◽  
Inside Out

The role of the Ca2+-activated K+ current ( I K(Ca)) in crayfish opener muscle fibers is functionally important because it regulates the graded electrical activity that is characteristic of these fibers. Using the cell-attached and inside-out configurations of the patch-clamp technique, we found three different classes of channels with properties that matched those expected of the three different ionic channels mediating the depolarization-activated macroscopic currents previously described (Ca2+, K+, and Ca2+-dependent K+ currents). We investigated the properties of the ionic channels mediating the extremely fast activating and persistent I K(Ca). These voltage- and Ca2+-activated channels had a mean single-channel conductance of ∼ 70 pS and showed a very fast activation. Both the single-channel open probability and the speed of activation increased with depolarization. Both parameters also increased in inside-out patches, i.e., in high Ca2+concentration. Intracellular loading with the Ca2+ chelator bis(2-aminophenoxy) ethane- N, N,N′,N′-tetraacetic acid gradually reduced and eventually prevented channel openings. The channels opened at very brief delays after the pulse depolarization onset (<5 ms), and the time-dependent open probability was constant during sustained depolarization (≤560 ms), matching both the extremely fast activation kinetics and the persistent nature of the macroscopic I K(Ca). However, the intrinsic properties of these single channels do not account for the partial apparent inactivation of the macroscopic I K(Ca), which probably reflects temporal Ca2+ variations in the whole muscle fiber. We conclude that the channels mediating I K(Ca) in crayfish muscle are voltage- and Ca2+-gated BK channels with relatively small conductance. The intrinsic properties of these channels allow them to act as precise Ca2+ sensors that supply the exact feedback current needed to control the graded electrical activity and therefore the contraction of opener muscle fibers.

scholarly journals Sodium and Potassium Fluxes in Isolated Barnacle Muscle Fibers

1968 ◽  
Vol 51 (4) ◽  
pp. 445-477 ◽  
Author(s):  
F. J. Brinley
Keyword(s):  
Time Constant ◽  
Empirical Formula ◽  
Inhibitory Concentration ◽  
Muscle Fibers ◽  
Sodium Concentration ◽  
External Loading ◽  
Barnacle Muscle ◽  
Barnacle Muscle Fibers ◽  
Sodium And Potassium ◽  
Sodium Exchange

Sodium and potassium influxes and outfluxes have been studied in single isolated muscle fibers from the giant barnacle both by microinjection and by external loading. The sodium influxes and outfluxes were 49 and 39 pmoles /cm2-sec (temperature = 15–16°C) respectively. The potassium influxes and outfluxes were 28 and 60 pmoles/cm2-sec (temperature = 13–16°C) respectively. Replacement of external sodium by lithium reduced sodium outflux by 67% but had no effect on potassium outflux. Removal of external potassum reduced the sodium outflux by 51% but had no effect on potassium outflux. External strophanthidin (10–30 µM) reduced sodium outflux by 80–90% and increased potassium outflux by 40% in normal fibers. The time constant for sodium exchange increased linearly with internal sodium concentration, as did the fraction of sodium outflux insensitive to a maximally inhibitory concentration of external strophanthidin in the range of 10 tO 80 mM internal sodium. The strophanthidin-sensitive component of sodium outflux could be related to the internal sodium concentration by the following empirical formula: See PDF for Equation

scholarly journals Effects of Caffeine on Crayfish Muscle Fibers

1970 ◽  
Vol 55 (5) ◽  
pp. 665-687 ◽  
Author(s):  
Dante J. Chiarandini ◽  
John P. Reuben ◽  
Lucien Girardier ◽  
George M. Katz ◽  
Harry Grundfest
Keyword(s):  
Muscle Fibers ◽  
Bathing Medium ◽  
Contractile Responses ◽  
Crayfish Muscle ◽  
Contractile System ◽  
Mn Recovery

When caffeine evokes a contraction, and only then, crayfish muscle fibers become refractory to a second challenge with caffeine for up to 20 min in the standard saline (5 mM Ko). However, the fibers still respond with contraction to an increase in Ko, though with diminished tension. Addition of Mn slows recovery, but the latter is greatly accelerated during exposure of the fiber to high Ko, or after a brief challenge with high Ko. Neither the depolarization induced by the K, nor the repolarization after its removal accounts for the acceleration, which occurs only if the challenge with K had itself activated the contractile system; acceleration is blocked when contractile responses to K are blocked by reducing the Ca in the bath or by adding Mn. Recovery is accelerated by redistribution of intracellular Cl and by trains of intracellularly applied depolarizing pulses, but not by hyperpolarization. The findings indicate that two sources of Ca can be mobilized to activate the contractile system. Caffeine mobilizes principally the Ca store of the SR. Depolarizations that are induced by high Ko, by transient efflux of Cl, or by intracellularly applied currents mobilize another source of Ca which is strongly dependent upon the entry of Ca from the bathing medium. The sequestering mechanism of the SR apparently can utilize this second source of Ca to replenish its own store so as to accelerate recovery of responsiveness to a new challenge with caffeine.

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