Extracellular potassium in neuropile and nerve cell body region of the leech central nervous system

1980 ◽  
Vol 87 (1) ◽  
pp. 23-43
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nerve Cell ◽  
Cell Body ◽  
Potassium Concentration ◽  
Rate Of Change ◽  
Body Region ◽  
Extracellular Potassium ◽  
Nerve Cell Body ◽  
Potassium Ions ◽  
Bathing Medium ◽  
Extracellular Potassium Concentration

Potassium-sensitive double-barrelled microelectrodes were used to measure the potassium content of extracellular spaces in leech ganglia, both intact and with the ganglion capsule opened. When the ganglion capsule was opened, the extracellular concentrations of potassium in the ganglion were similar to that of the bathing medium (4 mM). With intact ganglia the extracellular potassium concentration in the neuropile averaged 6.3 +/− 0.7 mM and in the nerve cell body region 5.8 +/− 0.6 mM. The potential measured in these parts of the ganglion was between +2 and −8 mV, averaging −1.9 mV. The change of potassium concentration in the extracellular spaces following increase or decrease in the concentration of potassium ions in the bath declined exponentially. This rate of change, which would be expected of a first-order diffusion process, was found in both the neuropile and the nerve cell body region. In a medium containing 5 × 10(−4) M ouabain, the potassium concentration in both parts of the ganglion increased transiently by an average of 3.8 +/− 1.0 mM in the neuropile and 1.2 +/− 0.4 mM in the nerve cell body region. Negatively charged polyelectrolytes in extracellular spaces of leech ganglia could affect the distribution of potassium ions to give a Donnan distribution. It is also possible, that the endothelial layer influences the extracellular potassium concentration in a ganglion under resting conditions.

Extracellular potassium, volume fraction, and tortuosity in rat hippocampal CA1, CA3, and cortical slices during ischemia

1995 ◽  
Vol 74 (2) ◽  
pp. 565-573 ◽  
Author(s):  
M. A. Perez-Pinzon ◽  
L. Tao ◽  
C. Nicholson
Keyword(s):  
Volume Fraction ◽  
Potassium Concentration ◽  
Extracellular Volume ◽  
Diffusion Method ◽  
Extracellular Potassium ◽  
Bathing Medium ◽  
Extracellular Potassium Concentration ◽  
In Vitro Ischemia ◽  
Anoxic Depolarization

1. An in vitro slice model of ischemia was used to study changes in extracellular potassium concentration and diffusion properties in the stratum pyramidale of CA1 and CA3 regions of the hippocampus and in the cortex of the rat. Slices were submerged in artificial cerebrospinal fluid, and ischemia was induced by removing oxygen and glucose until anoxic depolarization occurred. 2. Extracellular potassium concentration was measured with a valinomycin-based ion-selective microelectrode. The bathing medium contained 5 mM potassium, and in vitro ischemia caused the potassium concentration to rise to 45 mM in CA1, 12 mM in CA3, and 32 mM in cortex. 3. Extracellular volume fraction and tortuosity were determined during normoxic conditions and in vitro ischemia by measuring the diffusion of tetramethylammonium. This cation was iontophoretically released into the extracellular space and its concentration as a function of time determined with an ion-selective microelectrode approximately 100 microns away from the source. 4. During normoxia the volume fraction was 0.14, 0.20, and 0.18, and tortuosity was 1.50, 1.57, and 1.62 in CA1, CA3, and cortex, respectively. These data confirm that the volume fraction of CA1 is smaller than in the two other regions. 5. During ischemia the volume fraction decreased to 0.05, 0.17, and 0.09 in CA1, CA3, and cortex, respectively. Only in CA3 did the tortuosity change significantly by increasing to 1.75. Because of limitations in the time resolution of the diffusion method, the changes in volume fraction and tortuosity during the anoxic depolarization phase of ischemia may have been underestimated.(ABSTRACT TRUNCATED AT 250 WORDS)

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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