Transient potassium currents in slow muscle fibers

1978 ◽  
Vol 56 (5) ◽  
pp. 882-885
Author(s):  
James G. McLarnon
Keyword(s):  
Voltage Clamp ◽  
Potassium Current ◽  
Muscle Fibers ◽  
Potassium Conductance ◽  
Transient Behavior ◽  
Slow Muscle ◽  
Membrane Bound ◽  
Test Current ◽  
Charged Group ◽  
Voltage Clamp Method

Transient changes in potassium conductance in chronically depolarized slow muscle fibers have been studied using a voltage clamp method. The transient behavior included current decays from initial to steady state for hyperpolarizing and depolarizing voltage clamp steps. A two-pulse voltage clamp sequence (conditioning step followed by test step) showed the initial potassium test current to depend sigmoidally on conditioning potential implicating the involvement of a membrane-bound charged group in regulating potassium current.

Cholecystokinin-gated currents in neurons of the rat solitary complex in vitro

1993 ◽  
Vol 70 (6) ◽  
pp. 2584-2595 ◽  
Author(s):  
P. Branchereau ◽  
J. Champagnat ◽  
M. Denavit-Saubie
Keyword(s):  
Voltage Clamp ◽  
Potassium Current ◽  
Reversal Potential ◽  
Input Resistance ◽  
Calcium Currents ◽  
Equilibrium Potential ◽  
Potassium Ions ◽  
Nernst Equation ◽  
Membrane Hyperpolarization ◽  
Cckb Receptor

1. Ionic conductances controlled by type A and type B cholecystokinin (CCK) receptors were studied in neurons of the rat nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMNV), using intracellular and whole-cell patch clamp recordings in current or voltage clamp configuration during bath application of agonists (CCK8, CCK4, BC 264) and antagonists. 2. CCKA receptor-related inhibition was associated with a membrane hyperpolarization and a decrease in input resistance that developed 2-6 min after the arrival of drug into the extracellular medium. These effects were induced by 5 nM CCK8 but not BC 264 and they were blocked by the CCKA antagonist, L-364,718, but not by the CCKB antagonist, L-365,260. 3. CCKA receptor-related inhibition was generated by a potassium current that reversed at a reversal potential E(rev) of -73 +/- 1 (mean +/- SE) mV with bathing potassium concentration [K+]o = 6 mM and at -88 +/- 1 with [K+]o = 3 mM, in agreement with the Nernst equation for potassium ions. 4. CCKB receptor-related excitation was associated with a membrane depolarization and an increase of the input resistance induced by the following agonists at threshold concentrations: CCK8 (0.2 nM) > or = BC 264 (0.4 nM) > CCK4 (10.9 nM). The increase of input resistance was abolished by L-365,260 and was maintained after blockade of the CCKA current by L-364,718. 5. CCKB receptor-related excitation, in the neurons (30% of cases) in which clear response reversal was observed, appeared to be generated by a decrease of a potassium conductance. Responses showed a reversal potential E(rev) of -68 +/- 4 mV with [K+]o = 6 mM and -89 +/- 1 mV with [K+]o = 3 mM, verifying predictions from the Nernst equation applied to potassium ions. However, in 70% of cases, clear reversal was not observed at membrane potentials negative to the theoretical potassium equilibrium potential EK. 6. In voltage clamp studies, CCK8 induced a 181 +/- 17 pA inward current associated with a 26 +/- 4% decrease in the instantaneous current (I(ins)) generated by hyperpolarizing voltage steps. This effect on I(ins) was demonstrated in the absence of effects on the outward noninactivating potassium current (IM) and on the inward noninactivating cationic current (IQ). 7. CCKB receptor-mediated excitation was not suppressed by cobalt, a blocker of calcium currents, and was not associated with a change of the calcium-dependent potassium current (IK(Ca)).(ABSTRACT TRUNCATED AT 400 WORDS)

Extracellular divalent cations in excitation–contraction coupling: hypertonic solution effects

1982 ◽  
Vol 60 (4) ◽  
pp. 440-445
Author(s):  
Isao Oota ◽  
Isao Kosaka ◽  
Torao Nagai ◽  
Hideyo Yabu
Keyword(s):  
Skeletal Muscle ◽  
Divalent Cations ◽  
Muscle Fibers ◽  
Hypertonic Solution ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Skeletal Muscle Fibers ◽  
Membrane Bound

It is the purpose of this article to point out that the membrane-bound Ca plays an important role in excitation–contraction (E–C) coupling of skeletal muscle fibers and that other divalent cations are unable to substitute for this role of membrane-bound Ca.

Vertebrate slow muscle fibers.

1970 ◽  
Vol 50 (1) ◽  
pp. 40-62 ◽  
Author(s):  
A Hess
Keyword(s):  
Muscle Fibers ◽  
Slow Muscle

Isoproterenol enhances a calcium-independent potassium current in mouse anterior pituitary tumor cells

1992 ◽  
Vol 68 (1) ◽  
pp. 117-123
Author(s):  
R. Weik ◽  
J. Spiess
Keyword(s):  
Tumor Cells ◽  
Pituitary Tumor ◽  
Anterior Pituitary ◽  
Potassium Current ◽  
Calcium Influx ◽  
Potassium Conductance ◽  
Patch Clamp Technique ◽  
Calcium Dependent ◽  
Gs Protein ◽  
Current Reduction

1. The patch-clamp technique was used to study the action of the beta-adrenergic agonist (-)-isoproterenol in anterior pituitary tumor cells of the mouse. 2. (-)-Isoproterenol induced an inward-rectifying potassium conductance with half-maximal stimulation at a concentration of approximately 67 nM. The isomer (+)-isoproterenol was less effective in stimulating the current. 3. The effect of (-)-isoproterenol was abolished by cholera toxin treatment, indicating the involvement of a Gs protein, whereas pertussis toxin treatment did not exhibit a current reduction. 4. We blocked or stimulated phosphorylation pathways in cells to test the involvement of adenosine 3',5'-cyclic monophosphate (cAMP). It was concluded that the current stimulation probably was not exclusively mediated by cAMP. 5. Activation of calcium-dependent potassium channels by an isoproterenol-induced calcium influx into the cell could be excluded. 6. Therefore it is suggested that the observed activation of a potassium current by isoproterenol could be directly mediated by a Gs protein

Serotonin and forskolin increase an inwardly rectifying potassium conductance in cultured identified Aplysia neurons

1987 ◽  
Vol 58 (5) ◽  
pp. 909-921 ◽  
Author(s):  
D. P. Lotshaw ◽  
I. B. Levitan
Keyword(s):  
Voltage Clamp ◽  
Potassium Conductance ◽  
Phosphodiesterase Inhibitor ◽  
Identified Neurons ◽  
Inward Rectification ◽  
Current Response ◽  
Aplysia Neurons ◽  
Voltage Dependent ◽  
K Concentration ◽  
Inwardly Rectifying

1. The effect of serotonin (5-HT) and forskolin on an inwardly rectifying K+ conductance (IKR) was studied using voltage-clamp techniques in several identified Aplysia neurons isolated and maintained in primary cell culture. 2. Inward rectification was observed in the current-voltage relationship of the identified neurons R15, R2, B1, and B2 and was predominately due to IKR, as demonstrated by the dependence of inward rectification on the extracellular K+ concentration, instantaneous kinetics of the membrane current response to hyperpolarizing voltage clamp pulses, and voltage-dependent Ba2+ block of the inwardly rectifying current. 3. 5-HT increased IKR conductance between 100 and 400% in the identified neuron R15 in culture and increased IKR conductance approximately 50% in the identified neurons B1, B2, and R2 in culture. The adenylate cyclase activator, forskolin, plus a phosphodiesterase inhibitor, Ro 20-1724, also increased IKR conductance in these neurons. 4. 5-HT and forskolin modulated other ion conductances as well in all of these cultured neurons.

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