scholarly journals Extracellular Potassium Ion Activity During PGO Spike in Cat Lateral Geniculate Nucleus

SLEEP ◽  
1982 ◽  
Vol 5 (3) ◽  
pp. 213-217 ◽  
Author(s):  
Toyohiko Satoh ◽  
Makoto Sakagucci ◽  
Kunihiro Eguchi
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Potassium Ion ◽  
Extracellular Potassium ◽  
Lateral Geniculate ◽  
Ion Activity

scholarly journals Inhibition of Glycolysis Alters Potassium Ion Transport and Mitochondrial Redox Activity in Rat Brain

1988 ◽  
Vol 8 (6) ◽  
pp. 857-865 ◽  
Author(s):  
Cesar N. Raffin ◽  
Thomas J. Sick ◽  
Myron Rosenthal
Keyword(s):  
Ion Transport ◽  
Iodoacetic Acid ◽  
Potassium Ion ◽  
Redox Activity ◽  
Extracellular Potassium ◽  
Potassium Ion Transport ◽  
Ion Activity ◽  
Inhibition Of Glycolysis ◽  
Glycolytic Inhibitor ◽  
Active Processes

To examine the relationships between brain glycolysis, ion transport, and mitochondrial reduction/oxidation (redox) activity, extracellular potassium ion activity (K+0) and redox shifts of cytochrome oxidase (cytochrome a,a3) were recorded previous to and during superfusion of rat cerebral cortex with the glycolytic inhibitor iodoacetic acid (IAA). IAA produced oxidation of cytochrome a,a3, increased local oxygenation, increased K+0, and, in response to neuronal activation, slowed rates of K+0 reaccumulation. Rates of rereduction of cytochrome a,a3, after the oxidation of this cytochrome by stimulation, were also slowed by IAA. These effects of IAA demonstrate the dependence of K+0 reaccumulation on the integrity of glycolysis, support the concept that active processes are involved in brain ion transport, and suggest a link between ATP supplied by glycolysis and ion transport activity. These data are also compatible with the suggestion that residual dysfunctions after brain ischemia result from derangements in glycolytic functioning rather than from limitations in oxygen availability or oxidative metabolic activity.

Enhancement during REM sleep of extracellular potassium ion activity in the reticular formation

1979 ◽  
Vol 174 (1) ◽  
pp. 180-183 ◽  
Author(s):  
Toyohiko Satoh ◽  
Kazushige Watabe ◽  
Kunihiro Eguchi
Keyword(s):  
Reticular Formation ◽  
Rem Sleep ◽  
Potassium Ion ◽  
Extracellular Potassium ◽  
Ion Activity

Intracellular potassium ion activity in resting and stimulated mouse pancreas and submandibular gland

1979 ◽  
Vol 204 (1154) ◽  
pp. 99-104 ◽  
Keyword(s):  
Submandibular Gland ◽  
Marked Decrease ◽  
Potassium Ion ◽  
Pancreatic Acinar Cells ◽  
Extracellular Potassium ◽  
Potassium Ions ◽  
Mouse Pancreas ◽  
Intracellular Potassium ◽  
Ion Activity ◽  
Ion Activities

Intracellular potassium ion activities ( a i K + ) and membrane potentials were measured with double-barrelled, potassium-specific microelectrodes in superfused mouse pancreas and submandibular gland. Stimulation with the cholinergic agonist bethanechol caused a marked decrease in a i K + in the submandibular gland, whereas no change in a i K + could be detected in the pancreas. This indicates that bethanechol increases the permeability of the cell membranes to potassium ions in the submandibular gland but not in the pancreas. Pancreatic acinar cells hyperpolarized promptly when the extracellular potassium ion activity was restored after a prolonged period of potassium deprivation. In comparison, the recovery of a i K + was a slow process. This finding gives support to the view that the hyperpolarization is due to electrogenic sodium pumping.

Sign in / Sign up

Export Citation Format

Share Document