Effect of carbachol on spontaneous transmitter release from rat motor nerve endings depending on extracellular potassium concentration

1985 ◽  
Vol 16 (4) ◽  
pp. 370-373
Author(s):  
E. E. Nikol'skii
Keyword(s):  
Transmitter Release ◽  
Potassium Concentration ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration

Transmitter release induced by a ‘factor’ in rabbit serum

1974 ◽  
Vol 187 (1087) ◽  
pp. 235-241 ◽  
Keyword(s):  
Complement System ◽  
Transmitter Release ◽  
Motor Nerve ◽  
Nerve Endings ◽  
Rabbit Serum ◽  
Nerve Terminals ◽  
The Complement System ◽  
The Way

Non-heated rabbit serum causes massive transmitter release from motor nerve endings. The effect is not observed after heating the serum, in the way usually done to destroy complement. It seems that serum may be acting on the nerve terminals by a mechanism involving the complement system in the absence of antibody.

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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