scholarly journals Evidence that compromised K+ spatial buffering contributes to the epileptogenic effect of mutations in the human kir4.1 gene (KCNJ10)

Glia ◽  
2011 ◽  
Vol 59 (11) ◽  
pp. 1635-1642 ◽  
Author(s):  
Nadia Nabil Haj-Yasein ◽  
Vidar Jensen ◽  
Gry Fluge Vindedal ◽  
Georg Andreas Gundersen ◽  
Arne Klungland ◽  
...  
Keyword(s):  
Spatial Buffering

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.

scholarly journals Reaccumulation of [K+]o in the toad retina during maintained illumination.

1984 ◽  
Vol 84 (3) ◽  
pp. 475-504 ◽  
Author(s):  
H Shimazaki ◽  
B Oakley
Keyword(s):  
Differential Equations ◽  
Glial Cells ◽  
Time Course ◽  
Subretinal Space ◽  
Light Onset ◽  
Müller Glial Cells ◽  
Isolated Retina ◽  
Steady Level ◽  
Spatial Buffering ◽  
Toad Bufo

Using K+-selective microelectrodes, [K+]o was measured in the subretinal space of the isolated retina of the toad, Bufo marinus. During maintained illumination, [K+]o fell to a minimum and then recovered to a steady level that was approximately 0.1 mM below its dark level. Spatial buffering of [K+]o by Müller (glial) cells could contribute to this reaccumulation of K+. However, superfusion with substances that might be expected to block glial transport of K+ had no significant effect upon the reaccumulation of K+. These substances included blockers of gK (TEA+, Cs+, Rb+, 4-AP) and a gliotoxin (alpha AAA). Progressive slowing of the rods' Na+/K+ pump (perhaps caused by a light-evoked decrease in [Na+]i) also could contribute to this reaccumulation of K+ by reducing the uptake of K+ from the subretinal space. As evidence for a major contribution by this mechanism, treatments designed to prevent such slowing of the pump reversibly blocked reaccumulation. These treatments included superfusion with 2 microM ouabain, or lowering [K+]o, PO2, or temperature. It is likely that such treatments inhibit the pump, increase [Na+]i, and attenuate any light-evoked decrease in [Na+]i. The results are consistent with the following hypothesis. At light onset, the decrease in rod gNa will reduce the Na+ influx and the resulting rod hyperpolarization will reduce the K+ efflux. In combination with these reduced passive fluxes, the continuing active fluxes will lower both [K+]o and [Na+]i, which in turn will inhibit the pump. In support of this hypothesis, the solutions to a pair of coupled differential equations that model changes in both [K+]o and [Na+]i match quantitatively the time course of the observed changes in [K+]o during and after maintained illumination for all stimuli examined.

scholarly journals Neuromodulation of astrocytic K+ clearance

2019 ◽  
Author(s):  
Alba Bellot-Saez ◽  
Orsolya Kékesi ◽  
Yuval Ben-Abu ◽  
John W. Morley ◽  
Yossi Buskila
Keyword(s):  
Network Activity ◽  
Oscillatory Behaviour ◽  
Kir Channels ◽  
Neuronal Network Activity ◽  
Synergistic Mechanism ◽  
Synchronous Network ◽  
Clearance Process ◽  
Spatial Buffering ◽  
Parallel Activation ◽  
The Impact

ABSTRACTPotassium homeostasis is a fundamental requirement for normal brain function. Therefore, effective removal of excessive K+ accumulation from the synaptic cleft during neuronal activity is paramount. Astrocytes, one of the most common subtype of glial cells in the brain, 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+]°) or impairments of the astrocytic clearance mechanism effect the resonance and oscillatory behaviour of both individual and networks of neurons recorded from C57/BL6 mice of both sexes. 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 behaviour, on the astrocytic clearance process. Our results suggest that some neuromodulators (5-HT; NA) affect astrocytic spatial buffering via gap-junctions, while others (DA; Histamine) 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 recruitment of neurons into ensamble of networks to maximise the synchronous network activity.Significance statementNeuromodulators are known to mediate changes in network oscillatory behaviour and thus impact on brain states. In this study we show that certain neuromodulators directly affect distinct stages of astrocytic K+ clearance, promoting neuronal excitability and network oscillations through parallel activation of both neurons and astrocytes, thus establishing a synergistic mechanism to maximise the synchronous network activity.

Local temperatures inferred from plant communities suggest strong spatial buffering of climate warming across Northern Europe

2013 ◽  
Vol 19 (5) ◽  
pp. 1470-1481 ◽  
Author(s):  
Jonathan Lenoir ◽  
Bente Jessen Graae ◽  
Per Arild Aarrestad ◽  
Inger Greve Alsos ◽  
W. Scott Armbruster ◽  
...  
Keyword(s):  
Plant Communities ◽  
Climate Warming ◽  
Northern Europe ◽  
Spatial Buffering

scholarly journals Expression of Kir2.1 Inward Rectifying Potassium Channels in Optic Nerve Glia: Evidence for Heteromeric Association with Kir4.1 and Kir5.1

Neuroglia ◽  
2018 ◽  
Vol 1 (1) ◽  
pp. 176-187 ◽  
Author(s):  
Csilla Brasko ◽  
Arthur Butt
Keyword(s):  
Optic Nerve ◽  
Potential Role ◽  
Large Family ◽  
Knock Out ◽  
Kir Channels ◽  
Spatial Buffering ◽  
Knock Out Mice ◽  
Sites Of Action ◽  
The Brain ◽  
Heteromeric Association

Inward rectifying potassium (Kir) channels comprise a large family with diverse biophysical properties. A predominant feature of central nervous system (CNS) glia is their expression of Kir4.1, which as homomers are weakly rectifying channels, but form strongly rectifying channels as heteromers with Kir2.1. However, the extent of Kir2.1 expression and their association with Kir4.1 in glia throughout the CNS is unclear. We have examined this in astrocytes and oligodendrocytes of the mouse optic nerve, a typical CNS white matter tract. Western blot and immunocytochemistry demonstrates that optic nerve astrocytes and oligodendrocytes express Kir2.1 and that it co-localises with Kir4.1. Co-immunoprecipitation analysis provided further evidence that Kir2.1 associate with Kir4.1 and, moreover, Kir2.1 expression was significantly reduced in optic nerves and brains from Kir4.1 knock-out mice. In addition, optic nerve glia express Kir5.1, which may associate with Kir2.1 to form silent channels. Immunocytochemical and co-immunoprecipitation analyses indicate that Kir2.1 associate with Kir5.1 in optic nerve glia, but not in the brain. The results provide evidence that astrocytes and oligodendrocytes may express heteromeric Kir2.1/Kir4.1 and Kir2.1/Kir5.1 channels, together with homomeric Kir2.1 and Kir4.1 channels. In astrocytes, expression of multiple Kir channels is the biophysical substrate for the uptake and redistribution of K+ released during neuronal electrical activity known as ‘potassium spatial buffering’. Our findings suggest a similar potential role for the diverse Kir channels expressed by oligodendrocytes, which by way of their myelin sheaths are intimately associated with the sites of action potential propagation and axonal K+ release.

scholarly journals Genetic and Physiological Evidence That Oligodendrocyte Gap Junctions Contribute to Spatial Buffering of Potassium Released during Neuronal Activity

2006 ◽  
Vol 26 (43) ◽  
pp. 10984-10991 ◽  
Author(s):  
D. M. Menichella ◽  
M. Majdan ◽  
R. Awatramani ◽  
D. A. Goodenough ◽  
E. Sirkowski ◽  
...  
Keyword(s):  
Gap Junctions ◽  
Neuronal Activity ◽  
Physiological Evidence ◽  
Spatial Buffering
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