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.

scholarly journals The thalamic low-threshold Ca 2+ potential: a key determinant of the local and global dynamics of the slow (<1 Hz) sleep oscillation in thalamocortical networks

2011 ◽  
Vol 369 (1952) ◽  
pp. 3820-3839 ◽  
Author(s):  
Vincenzo Crunelli ◽  
Adam C. Errington ◽  
Stuart W. Hughes ◽  
Tibor I. Tóth
Keyword(s):  
Action Potential ◽  
Slow Oscillation ◽  
Global Dynamics ◽  
Action Potential Firing ◽  
Local And Global Dynamics ◽  
Up States ◽  
Potential Firing ◽  
Low Threshold

During non-rapid eye movement sleep and certain types of anaesthesia, neurons in the neocortex and thalamus exhibit a distinctive slow (<1 Hz) oscillation that consists of alternating UP and DOWN membrane potential states and which correlates with a pronounced slow (<1 Hz) rhythm in the electroencephalogram. While several studies have claimed that the slow oscillation is generated exclusively in neocortical networks and then transmitted to other brain areas, substantial evidence exists to suggest that the full expression of the slow oscillation in an intact thalamocortical (TC) network requires the balanced interaction of oscillator systems in both the neocortex and thalamus. Within such a scenario, we have previously argued that the powerful low-threshold Ca 2+ potential (LTCP)-mediated burst of action potentials that initiates the UP states in individual TC neurons may be a vital signal for instigating UP states in related cortical areas. To investigate these issues we constructed a computational model of the TC network which encompasses the important known aspects of the slow oscillation that have been garnered from earlier in vivo and in vitro experiments. Using this model we confirm that the overall expression of the slow oscillation is intricately reliant on intact connections between the thalamus and the cortex. In particular, we demonstrate that UP state-related LTCP-mediated bursts in TC neurons are proficient in triggering synchronous UP states in cortical networks, thereby bringing about a synchronous slow oscillation in the whole network. The importance of LTCP-mediated action potential bursts in the slow oscillation is also underlined by the observation that their associated dendritic Ca 2+ signals are the only ones that inform corticothalamic synapses of the TC neuron output, since they, but not those elicited by tonic action potential firing, reach the distal dendritic sites where these synapses are located.

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, 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)

scholarly journals Blood to Brain Sodium Transport and Interstitial Fluid Potassium Concentration during Early Focal Ischemia in the Rat

1991 ◽  
Vol 11 (3) ◽  
pp. 466-471 ◽  
Author(s):  
Gerald P. Schielke ◽  
Hylan C. Moises ◽  
A. Lorris Betz
Keyword(s):  
Sodium Transport ◽  
Interstitial Fluid ◽  
Potassium Concentration ◽  
Capillary Endothelium ◽  
Extracellular Potassium ◽  
Sprague Dawley ◽  
Ischemic Tissue ◽  
The Right

During partial ischemia, sodium and potassium ions exchange across the blood–brain barrier, resulting in a net increase in cations and brain edema. Since this exchange is likely mediated by specific transporters such as Na,K–ATPase in the capillary endothelium and because brain capillary Na,K–ATPase activity is stimulated by increased extracellular potassium in vitro, this study was designed to determine if the rate of blood to brain sodium transport is increased in ischemic tissue having an elevated interstitial fluid potassium concentration ([K]ISF) in vivo. Sprague-Dawley rats were studied between 2–3 h after occlusion of the right middle cerebral artery. To identify where cortical tissue with an elevated [K]ISF could be sampled for transport studies, the regional pattern of cerebral blood flow and [K]ISF was obtained in a group of 17 rats using hydrogen clearance and potassium-selective microelectrode techniques. We observed severely elevated [K]ISF (> 10 m M) when CBF was less than 20 ml 100 g−1 min−1 and mildly elevated levels at CBF between 20–45 ml 100 g−1 min−1. In a second group of seven rats, permeability-surface area products (PS products) for 22Na and [3H]α-aminoisobutyric acid ([3H]AIB) were determined in ischemic cortex with elevated [K]ISF and in nonischemic cortex. The PS products for AIB were similar in both tissues (2.2 ± 0.7 and 2.1 ± 0.4 μl/g/min) while the PS products for sodium was significantly increased in the ischemic tissue (1.5 ± 0.2 and 2.4 ± 1.1 μl/g/min). This study demonstrates that blood to brain sodium transport is increased in ischemic tissue at early times before the BBB is disrupted. Stimulation of the Na,K pumps in the capillary endothelium by elevated [K]ISF may mediate this effect.

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.

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