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)

Effect of Extracellular Potassium on the Transport of Sodium and Potassium in Rat Thymocytes

1981 ◽  
Vol 61 (3) ◽  
pp. 307-312 ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton
Keyword(s):  
Potassium Concentration ◽  
Extracellular Potassium ◽  
Sodium Influx ◽  
Potassium Efflux ◽  
Sodium Efflux ◽  
Extracellular Potassium Concentration ◽  
External Potassium ◽  
Potassium Influx ◽  
Sodium And Potassium

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro. 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.

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.

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.

Long-term Adaptations of Sabella Giant Axons to Hyposmotic Stress

1978 ◽  
Vol 75 (1) ◽  
pp. 253-263
Author(s):  
J. E. TREHERNE ◽  
Y. PICHON
Keyword(s):  
Sea Water ◽  
Potassium Concentration ◽  
Resting Potential ◽  
Sodium Permeability ◽  
Bathing Medium ◽  
Appreciable Change ◽  
Axon Membrane ◽  
Giant Axons

Reprint requests should be addressed to Dr Treherne. Sabella is a euryhaline osmoconformer which is killed by direct transfer to 50% sea water, but can adapt to this salinity with progressive dilution of the sea water. The giant axons were adapted to progressive dilution of the bathing medium (both in vivo and in vitro) and were able to function at hyposmotic dilutions (down to 50%) sufficient to induce conduction block in unadapted axons. Hyposmotic adaptation of the giant axon involves a decrease in intracellular potassium concentration which tends to maintain a relatively constant resting potential during adaptation despite the reduction in external potassium concentration. There is no appreciable change in the intracellular sodium concentration, but the relative sodium permeability of the active membrane increases during hyposmotic adaptation. This increase partially compensates for the reduction in sodium gradient across the axon membrane, during dilution of the bathing media, by increasing the overshoot of the action potentials recorded in hyposmotically adapted axons.

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....

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