Extracellular Potassium Activity and Axon Excitability

1981 ◽  
pp. 205-208
Author(s):  
Dean O. Smith
Keyword(s):  
Extracellular Potassium

Modification of the Ca2+ influx pattern of the pancreatic beta cell by high extracellular potassium

2015 ◽  
Vol 10 (S 01) ◽  
Author(s):  
N Görgler ◽  
M Willenborg ◽  
K Schumacher ◽  
A Welling ◽  
I Rustenbeck
Keyword(s):  
Beta Cell ◽  
Pancreatic Beta Cell ◽  
Extracellular Potassium

scholarly journals Neuromodulation of Astrocytic K+ Clearance

2021 ◽  
Vol 22 (5) ◽  
pp. 2520
Author(s):  
Alba Bellot-Saez ◽  
Rebecca Stevenson ◽  
Orsolya Kékesi ◽  
Evgeniia Samokhina ◽  
Yuval Ben-Abu ◽  
...  
Keyword(s):  
Oscillatory Behavior ◽  
Network Activity ◽  
Oscillatory Activity ◽  
Extracellular Potassium ◽  
Uptake Mechanism ◽  
Kir Channels ◽  
Neuronal Network Activity ◽  
Clearance Process ◽  
Spatial Buffering ◽  
The Impact

Potassium homeostasis is fundamental for brain function. Therefore, effective removal of excessive K+ from the synaptic cleft during neuronal activity is paramount. Astrocytes play a key role in K+ clearance from the extracellular milieu using various mechanisms, including uptake via Kir channels and the Na+-K+ ATPase, and spatial buffering through the astrocytic gap-junction coupled network. Recently we showed that alterations in the concentrations of extracellular potassium ([K+]o) or impairments of the astrocytic clearance mechanism affect the resonance and oscillatory behavior of both the individual and networks of neurons. These results indicate that astrocytes have the potential to modulate neuronal network activity, however, the cellular effectors that may affect the astrocytic K+ clearance process are still unknown. In this study, we have investigated the impact of neuromodulators, which are known to mediate changes in network oscillatory behavior, on the astrocytic clearance process. Our results suggest that while some neuromodulators (5-HT; NA) might affect astrocytic spatial buffering via gap-junctions, others (DA; Histamine) primarily affect the uptake mechanism via Kir channels. These results suggest that neuromodulators can affect network oscillatory activity through parallel activation of both neurons and astrocytes, establishing a synergistic mechanism to maximize the synchronous network activity.

Epileptiform activity in the hippocampus produced by tetraethylammonium

1990 ◽  
Vol 64 (4) ◽  
pp. 1077-1088 ◽  
Author(s):  
P. A. Rutecki ◽  
F. J. Lebeda ◽  
D. Johnston
Keyword(s):  
Potassium Channel ◽  
Voltage Clamp ◽  
Channel Blocker ◽  
Mossy Fiber ◽  
Reversal Potential ◽  
Evoked Response ◽  
Epileptiform Discharge ◽  
Extracellular Potassium ◽  
Potassium Channel Blocker ◽  
Epileptiform Discharges

1. The epileptiform discharges in the CA3 region of the rat hippocampal slice produced by bath application of the potassium channel blocker tetraethylammonium (TEA) were investigated. The effects of a convulsant (5 mM) and subconvulsant (0.5 mM) concentration of TEA on the mossy fiber-evoked synaptic currents were studied by the use of voltage-clamp techniques to determine whether TEA, like 4-aminopyridine (4-AP), another potassium channel blocker and convulsant, increased both inhibitory and excitatory components of the synaptic response. 2. At extracellular potassium concentrations of 2.5 mM, TEA (5 mM) was found to produce spontaneously occurring epileptiform discharges that could be recorded extracellularly. The intracellular correlate of the epileptiform discharge, the paroxysmal depolarizing shift (PDS), could be reversed in polarity by depolarizing the membrane and was associated with a large increase in membrane conductance. These results suggest that a synaptically mediated potential underlies the generation of the epileptiform discharge. 3. The reversal potential for the PDS was dependent on the time, relative to the extracellularly recorded field discharge, at which the measurement was made. In current clamp the mean reversal potential of the PDS measured at the midpoint of the extracellular discharge was -3.3 +/- 2.9 (SE) mV (n = 9). The reversal potential of the PDS was considerably more negative when measured either before or after the midpoint of the extracellular discharge, suggesting the presence of an inhibitory synaptic component. In voltage clamp similar results were obtained and a large conductance change was found to be associated with the PDS. These results suggest that the synaptic conductance associated with the PDS has both inhibitory and excitatory components. 4. TEA increased significantly the mossy fiber-evoked, early-inhibitory conductance. A convulsant concentration (5 mM) increased the conductance measured 15 ms after the stimulus from 39.7 +/- 8.7 to 87.2 +/- 8.0 nS (n = 6). The reversal potential associated with the conductance depolarized from -68.3 +/- 3.4 to -58.3 +/- 4.0 mV after 5 mM TEA. A subconvulsant concentration of TEA (0.5 mM) also increased the conductance of the mossy fiber-evoked response at 15 ms after the stimulus from 49.5 +/- 3.1 to 63.1 +/- 6.1 nS (n = 4) without an associated shift in reversal potential. 5. The late-inhibitory component of the mossy fiber-evoked response, when present, was increased by 5 mM TEA and unchanged by 0.5 mM TEA. 6. The excitatory mossy fiber-evoked synaptic current was studied in the presence of picrotoxin and was found to be increased and prolonged by 5 mM TEA.(ABSTRACT TRUNCATED AT 400 WORDS)

Extracellular potassium concentration in chronic alumina cream foci of cats

1984 ◽  
Vol 52 (3) ◽  
pp. 421-434 ◽  
Author(s):  
U. Heinemann ◽  
I. Dietzel
Keyword(s):  
Border Zone ◽  
Constant Current ◽  
Extracellular Potassium ◽  
Local Concentration ◽  
Base Line ◽  
Extracellular Potassium Concentration ◽  
Concentration Changes ◽  
K Concentration ◽  
Repetitive Electrical Stimulation ◽  
Normal Cortex

Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.

The role of extracellular potassium transport in computer models of the ischemic zone

2007 ◽  
Vol 45 (12) ◽  
pp. 1187-1199 ◽  
Author(s):  
Mark Potse ◽  
Ruben Coronel ◽  
A.-Robert LeBlanc ◽  
Alain Vinet
Keyword(s):  
Computer Models ◽  
Potassium Transport ◽  
Extracellular Potassium

Effect of elevated potassium on the ion content of mouse astrocytes and neurons

1992 ◽  
Vol 70 (S1) ◽  
pp. S263-S268 ◽  
Author(s):  
H. Steve White ◽  
Sien Yao Chow ◽  
Y. C. Yen-Chow ◽  
Dixon M. Woodbury
Keyword(s):  
Cortical Neurons ◽  
Cell Types ◽  
Mouse Cell ◽  
Ion Concentration ◽  
Cellular Heterogeneity ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Individual Response ◽  
Extracellular Potassium Concentration ◽  
The Brain

Potassium is tightly regulated within the extracellular compartment of the brain. Nonetheless, it can increase 3- to 4-fold during periods of intense seizure activity and 10- to 20-fold under certain pathological conditions such as spreading depression. Within the central nervous system, neurons and astrocytes are both affected by shifts in the extracellular concentration of potassium. Elevated potassium can lead to a redistribution of other ions (e.g., calcium, sodium, chloride, hydrogen, etc.) within the cellular compartment of the brain. Small shifts in the extracellular potassium concentration can markedly affect acid–base homeostasis, energy metabolism, and volume regulation of these two brain cells. Since normal neuronal function is tightly coupled to the ability of the surrounding glial cells to regulate ionic shifts within the brain and since both cell types can be affected by shifts in the extracellular potassium, it is important to characterize their individual response to an elevation of this ion. This review describes the results of side-by-side studies conducted on cortical neurons and astrocytes, which assessed the effect of elevated potassium on their resting membrane potential, intracellular volume, and their intracellular concentration of potassium, sodium, and chloride. The results obtained from these studies suggest that there exists a marked cellular heterogeneity between neurons and astrocytes in their response to an elevation in the extracellular potassium concentration.Key words: astrocytes, neurons, ion concentration, neuronal–glial interactions, mouse, cell culture.

scholarly journals Glutamate, NMDA, and AMPA Induced Changes in Extracellular Space Volume and Tortuosity in the Rat Spinal Cord

2001 ◽  
Vol 21 (9) ◽  
pp. 1077-1089 ◽  
Author(s):  
Lýdia Vargová ◽  
Pavla Jendelová ◽  
Alexandr Chvátal ◽  
Eva Syková
Keyword(s):  
Spinal Cord ◽  
Glutamate Receptor ◽  
Extracellular Space ◽  
Volume Fraction ◽  
Glutamate Release ◽  
Extracellular Potassium ◽  
Receptor Agonists ◽  
Diffusion Parameters ◽  
Glutamate Receptor Agonists ◽  
Cellular Swelling

Glutamate release, particularly in pathologic conditions, may result in cellular swelling. The authors studied the effects of glutamate, N-methyl-d-aspartate (NMDA), and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) on extracellular pH (pHe), extracellular potassium concentration ([K+]e), and changes in extracellular space (ECS) diffusion parameters (volume fraction α, tortuosity λ) resulting from cellular swelling. In the isolated spinal cord of 4-to 12-day-old rats, the application of glutamate receptor agonists induced an increase in [K+]e, alkaline-acid shifts, a substantial decrease in α, and an increase in λ. After washout of the glutamate receptor agonists, α either returned to or overshot normal values, whereas λ remained elevated. Pretreatment with 20 mmol/L Mg++, MK801, or CNQX blocked the changes in diffusion parameters, [K+]e and pHe evoked by NMDA or AMPA. However, the changes in diffusion parameters also were blocked in Ca2+-free solution, which had no effect on the [K+]e increase or acid shift. The authors conclude that increased glutamate release may produce a large, sustained and [Ca2+]e-dependent decrease in α and increase in λ. Repetitive stimulation and pathologic states resulting in glutamate release therefore may lead to changes in ECS volume and tortuosity, affecting volume transmission and enhancing glutamate neurotoxicity and neuronal damage.

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