A Comparison of the Effects of Ischaemia on Tissue Flow, Electrical Activity and Extracellular Potassium Ion Concentration in Cerebral Cortex of Baboons

1977 ◽  
Vol 5 (1) ◽  
pp. 158-160 ◽  
Author(s):  
ANTHONY J. STRONG ◽  
MICHELE J. GOODHARDT ◽  
NEIL M. BRANSTON ◽  
LINDSAY SYMON
Keyword(s):  
Cerebral Cortex ◽  
Electrical Activity ◽  
Potassium Ion ◽  
Ion Concentration ◽  
Extracellular Potassium

scholarly journals In Vivo Neocortical [K]o Modulation by Targeted Stimulation of Astrocytes

2021 ◽  
Vol 22 (16) ◽  
pp. 8658
Author(s):  
Azin EbrahimAmini ◽  
Shanthini Mylvaganam ◽  
Paolo Bazzigaluppi ◽  
Mohamad Khazaei ◽  
Alexander Velumian ◽  
...  
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Potassium Ion ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Spreading Depolarization ◽  
Potential Tool ◽  
Stimulation Of

A normally functioning nervous system requires normal extracellular potassium ion concentration ([K]o). Throughout the nervous system, several processes, including those of an astrocytic nature, are involved in [K]o regulation. In this study we investigated the effect of astrocytic photostimulation on [K]o. We hypothesized that in vivo photostimulation of eNpHR-expressing astrocytes leads to a decreased [K]o. Using optogenetic and electrophysiological techniques we showed that stimulation of eNpHR-expressing astrocytes resulted in a significantly decreased resting [K]o and evoked K responses. The amplitude of the concomitant spreading depolarization-like events also decreased. Our results imply that astrocytic membrane potential modification could be a potential tool for adjusting the [K]o.

Quantitative Characterization of Epicardial Wave Fronts During Regional Ischemia and Elevated Extracellular Potassium Ion Concentration

10.1114/1.136 ◽  
1998 ◽  
Vol 26 (6) ◽  
pp. 1010-1021 ◽  
Author(s):  
Bonnie B. Punske ◽  
Wayne E. Cascio ◽  
Connie Engle ◽  
H. Troy Nagle ◽  
Leonard S. Gettes ◽  
...  
Keyword(s):  
Potassium Ion ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Wave Fronts ◽  
Quantitative Characterization ◽  
Regional Ischemia

scholarly journals High extracellular potassium ion concentration attenuates the blockade action of ketanserin on Kv1.3 channels expressed in xenopus oocytes

2008 ◽  
Vol 121 (24) ◽  
pp. 2584-2591
Author(s):  
Zhen-tao LIANG ◽  
Xian-pei WANG ◽  
Qiu-tang ZENG ◽  
Yu-hua LIAO ◽  
An-ruo ZOU ◽  
...  
Keyword(s):  
Xenopus Oocytes ◽  
Potassium Ion ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Kv1.3 Channels

scholarly journals Potassium Ion Homeostasis and Mitochondrial Redox Activity in Brain: Relative Changes as Indicators of Hypoxia

1988 ◽  
Vol 8 (2) ◽  
pp. 155-162 ◽  
Author(s):  
Stephen J. Milito ◽  
Cesar N. Raffin ◽  
Myron Rosenthal ◽  
Thomas J. Sick
Keyword(s):  
Cerebral Cortex ◽  
Ion Transport ◽  
Ion Homeostasis ◽  
Anaerobic Capacity ◽  
Potassium Ion ◽  
Redox Activity ◽  
Mammalian Brain ◽  
Critical Threshold ◽  
Extracellular Potassium ◽  
Neuronal Activation

This study was directed at relating ion transport and mitochondrial redox activity during hypoxia, as a step toward definition of brain oxygen sufficiency. To accomplish this, extracellular potassium ion activity (K+o) was recorded by ion-selective microelectrodes while reduction/oxidation (redox) ratios of cytochrome oxidase (cytochrome a,a3) were monitored by reflection spectrophotometry in cerebral cortex of rats anesthetized with pentobarbital. In normoxia, neuronal activation by direct cortical stimulation produced transient oxidation of cytochrome a,a3 and elevation of K+o. Moderate hypoxia (Pao2 above 50 mm Hg) resulted in reduction of cytochrome a,a3 but only slight elevation of K+o. At this level of hypoxia, cytochrome a,a3 continued to respond to neuronal activation with transient shifts toward oxidation and rates of K+o reaccumulation were unchanged from control. When Pao2 was further decreased below a critical threshold, stimulus-provoked oxidative responses of mitochondrial reactants were replaced by shifts toward reduction, but rates of reaccumulation of K+, spilled into the extracellular space by neuronal activation, remained unchanged. Only during severe hypoxia (Pao2 less than 20 mm Hg) was it possible in some animals to record a slowing in the reaccumulation of K+o without provocation of spreading cortical depression. These data indicate that ion transport activity in cerebral cortex is more refractory to hypoxia than is mitochondrial redox functioning. They suggest an in vivo parallel to the “cushioning” effect of mitochondria in vitro, in which oxygen consumption remains constant despite fluctuations in oxygenation and redox ratios, and also that there may be a greater anaerobic capacity to provide energy for ion transport in mammalian brain than has previously been appreciated.

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