scholarly journals Enhancement of procainamide-induced rate-dependent conduction slowing by elevated myocardial extracellular potassium concentration in vivo.

Circulation ◽  
1987 ◽  
Vol 76 (6) ◽  
pp. 1380-1387 ◽  
Author(s):  
W E Cascio ◽  
J R Foster ◽  
J W Buchanan ◽  
T A Johnson ◽  
L S Gettes
Keyword(s):  
Potassium Concentration ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration ◽  
Rate Dependent

Temporal relationship between neurotransmitter release and ion flux during spreading depression and anoxia

1987 ◽  
Vol 65 (5) ◽  
pp. 1105-1110 ◽  
Author(s):  
B. Moghaddam ◽  
J. O. Schenk ◽  
W. B. Stewart ◽  
A. J. Hansen
Keyword(s):  
Dopamine Release ◽  
Temporal Relationship ◽  
Spreading Depression ◽  
Potassium Concentration ◽  
Ionic Composition ◽  
Ion Homeostasis ◽  
Cell Permeability ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration

Brain ion homeostasis is severely perturbed during spreading depression of Leao and during anoxia. The ionic composition of the extracellular space changes abruptly and approaches the intracellular concentrations owing to an increase in cell permeability. In spreading depression, synchronous transmitter efflux caused by a depolarization of the presynaptic terminals has been implicated as a possible mechanism that would explain the concomitant movement of ions. Anoxia, having many features in common with spreading depression, may follow the same mechanism. We have measured the concentrations of extracellular potassium with ion-selective microelectrodes and dopamine by in vivo voltammetry with carbon fiber microelectrodes during spreading depression and anoxia to compare the temporal relationship between the release of dopamine and ion movements in the striatum. There is a pronounced release of dopamine during both spreading depression and anoxia. In spreading depression, the sharp increase of potassium concentration that follows an initial smaller and slower increase of potassium is accompanied by the release of dopamine. In anoxia, the dopamine release clearly precedes the fast rise of extracellular potassium concentration. We conclude that in striatum, there is a pronounced dopamine release during spreading depression and anoxia, but that the relationships between ionic changes and transmitter release for these two phenomena are different and probably reflect different mechanisms.

Increasing Extracellular Potassium Results in Subthalamic Neuron Activity Resembling That Seen in a 6-Hydroxydopamine Lesion

2008 ◽  
Vol 99 (6) ◽  
pp. 2902-2915 ◽  
Author(s):  
Ulf Strauss ◽  
Fu-Wen Zhou ◽  
Jeannette Henning ◽  
Arne Battefeld ◽  
Andreas Wree ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Potassium Concentration ◽  
Neuron Activity ◽  
Extracellular Potassium ◽  
Action Potential Firing ◽  
Extracellular Potassium Concentration ◽  
Potential Firing ◽  
6 Hydroxydopamine

Abnormal neuronal activity in the subthalamic nucleus (STN) plays a crucial role in the pathophysiology of Parkinson's disease (PD). Although altered extracellular potassium concentration ([K+]o) and sensitivity to [K+]o modulates neuronal activity, little is known about the potassium balance in the healthy and diseased STN. In vivo measurements of [K+]o using ion-selective electrodes demonstrated a twofold increase in the decay time constant of lesion-induced [K+]o transients in the STN of adult Wistar rats with a unilateral 6-hydroxydopamine (6-OHDA) median forebrain bundle lesion, employed as a model of PD, compared with nonlesioned rats. Various [K+]o concentrations (1.5–12.5 mM) were applied to in vitro slice preparations of three experimental groups of STN slices from nonlesioned control rats, ipsilateral hemispheres, and contralateral hemispheres of lesioned rats. The majority of STN neurons of nonlesioned rats and in slices contralateral to the lesion fired spontaneously, predominantly in a regular pattern, whereas those in slices ipsilateral to the lesion fired more irregularly or even in bursts. Experimentally increased [K+]o led to an increase in the number of spontaneously firing neurons and action potential firing rates in all groups. This was accompanied by a decrease in the amplitude of post spike afterhyperpolarization (AHP) and the amplitude and duration of the posttrain AHP. Lesion effects in ipsilateral neurons at physiological [K+]o resembled the effects of elevated [K+]o in nonlesioned rats. Our data suggest that changed potassium sensitivity due to conductivity alterations and delayed clearance may be critical for shaping STN activity in parkinsonian states.

Disorders of potassium homeostasis

2010 ◽  
pp. 3831-3845 ◽  
Author(s):  
J Firth
Keyword(s):  
Membrane Potential ◽  
Potassium Concentration ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Normal Range ◽  
Critical Determinant ◽  
Potassium Homeostasis ◽  
Extracellular Potassium Concentration

The normal range of potassium concentration in serum is 3.5 to 5.0 mmol/litre and within cells it is 150 to 160 mmol/litre, the ratio of intracellular to extracellular potassium concentration being a critical determinant of cellular resting membrane potential and thereby of the function of excitable tissues....

Theoretical analysis of parameters leading to frequency modulation along an inhomogeneous axon

1976 ◽  
Vol 39 (4) ◽  
pp. 909-923 ◽  
Author(s):  
I. Parnas ◽  
S. Hochstein ◽  
H. Parnas
Keyword(s):  
Potassium Concentration ◽  
Single Step ◽  
Repetitive Firing ◽  
Extracellular Potassium ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Extracellular Potassium Concentration ◽  
Spike Shape ◽  
Single Spike ◽  
Low Pass

1. Theoretical computations were conducted on a computer model of a segmented, nonhomogeneous axon to understand the mechanism of frequency block of conduction. 2. The model is based on the Hodgkin-Huxley equations modified in several ways to better describe the cockroach axon. We used cockroach parameters where available. 3. The increase in fiber radius was spread over a series of segments to approximate a taper. We found that a taper allows a larger overall increase in fiber diameter than a single step to be successfully passed. 4. We studied effects on a train of impulses. The modified equations included effects due to changes in extracellular potassium concentration resulting from the repetitive firing of the axon. 5. An increase in diameter which allows a single spike to pass blocks the subsequent impulses in a train at the taper if potassium concentration variability is introduced. This could explain the low-pass filter characteristics of axon constrictions. 6. Results of the model fit well with the experiemental spike shape and height. Data were computed for the refractory period and its dependence on the taper parameters.

Sodium dependence of carnitine transport in isolated perfused adult rat hearts

1983 ◽  
Vol 244 (2) ◽  
pp. H247-H252 ◽  
Author(s):  
T. C. Vary ◽  
J. R. Neely
Keyword(s):  
Potassium Concentration ◽  
Sodium Concentration ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration ◽  
Rat Hearts ◽  
Carrier Mediated Transport ◽  
Physiological Serum ◽  
Carnitine Transport ◽  
Extracellular Sodium ◽  
Carnitine Concentration

In heart muscle, the intracellular carnitine concentration is approximately 40 times higher than the plasma carnitine concentration, suggesting the existence of an active transport process. At physiological serum carnitine concentrations (44 microM), 80% of total myocardial carnitine uptake occurs via a carrier-mediated transport system. The mechanism of this carrier-mediated transport was studied in isolated perfused rat hearts. Carnitine transport showed an absolute dependence on the extracellular sodium concentration. The rate of carnitine transport was linearly related to the perfusate sodium concentration at every perfusate carnitine concentration examined (15-100 microM). Total removal of extracellular sodium completely abolished the carrier-mediated transport. Decreasing the perfusate potassium concentration from a control of 5.9 to 0.6 mM stimulated transport by 35%, whereas increasing the extracellular potassium concentration from 5.9 to 25 mM reduced transport by 60%. The carrier-mediated transport was inversely proportional to the extracellular potassium concentration. Acetylcholine (10(-3) M), isoproterenol (10(-7) M), or ouabain (10(-3) did not alter the rate of carnitine transport. Addition of tetrodotoxin (10(-5) stimulated carnitine transport by about 40%, while gramicidin S (5 X 10(-6) M) decreased uptake by about 18% relative to control. The data provide evidence that carnitine transport by cardiac cells occurs by a Na+-dependent cotransport mechanism that is dependent on the Na+ electrochemical gradient.

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