Changes of Extracellular Potassium in Rat Cerebellar Cortex Indicate a Reduced Na-K-Pump Activity during Acute and Chronic Li-Application

1981 ◽  
pp. 231-234
Author(s):  
G. ten Bruggencate ◽  
A. Ullrich ◽  
P. Baierl
Keyword(s):  
Cerebellar Cortex ◽  
Extracellular Potassium ◽  
Pump Activity

Sodium-potassium pump inhibitors increase neuronal excitability in the rat hippocampal slice: role of a Ca2+-dependent conductance

1987 ◽  
Vol 57 (2) ◽  
pp. 496-509 ◽  
Author(s):  
M. McCarren ◽  
B. E. Alger
Keyword(s):  
Hippocampal Slice ◽  
Neuronal Excitability ◽  
Pyramidal Cells ◽  
Input Resistance ◽  
Extracellular Potassium ◽  
Gamma Aminobutyric Acid ◽  
Extracellular Potassium Concentration ◽  
Spike Threshold ◽  
Pump Activity ◽  
Voltage Dependent

We have used the rat hippocampal slice preparation as a model system for studying the epileptogenic consequences of a reduction in neuronal Na+-K+ pump activity. The cardiac glycosides (CGs) strophanthidin and dihydroouabain were used to inhibit the pump. These drugs had readily reversible effects, provided they were not applied for longer than 15-20 min. Hippocampal CA1 pyramidal cells were studied with intracellular recordings; population spike responses and changes in extracellular potassium concentration ([K+]o) were also measured in some experiments. This investigation focused on the possibility that intrinsic neuronal properties are affected by Na+-K+ pump inhibitors. The CGs altered the CA1 population response evoked by an orthodromic stimulus from a single spike to an epileptiform burst. Measurements of [K+]o showed that doses of CGs sufficient to cause bursting were associated with only minor (less than 1 mM) changes in resting [K+]o. However, the rate of K+ clearance from the extracellular space was moderately slowed, confirming that a decrease in pump activity had occurred. Intracellular recording indicated that CG application resulted in a small depolarization and apparent increase in resting input resistance of CA1 neurons. Although CGs caused a decrease in fast gamma-aminobutyric acid mediated inhibitory postsynaptic potentials (IPSPs), CGs could also enhance the latter part of the epileptiform burst induced by picrotoxin, an antagonist of these IPSPs. Since intrinsic Ca2+ conductances comprise a significant part of the burst, this suggested the possibility that Na+-K+ pump inhibitors affected an intrinsic neuronal conductance. CGs decreased the threshold for activation of Ca2+ spikes (recorded in TTX and TEA) without enhancing the spikes themselves, indicating that a voltage-dependent subthreshold conductance might be involved. The action of CGs on Ca2+ spike threshold could not be mimicked by increasing [K+]o up to 10 mM. A variety of K+ conductance antagonists, including TEA, 4-AP, Ba2+ (in zero Ca2+), and carbachol were ineffective in preventing the CG-induced threshold shift of the Ca2+ spike. The shift was also seen in the presence of a choline-substituted low Na+ saline. Enhancement of a slow inward Ca2+ current is a possible mechanism for the decrease in Ca2+ spike threshold; however, it is impossible to use the Ca2+ spike as an assay when testing the effects of blocking Ca2+ conductances. Therefore, we studied the influence of CGs on the membrane current-voltage (I-V) curve, since persistent voltage-dependent conductances appear as nonlinearities in the I-V plot obtained under current clamp.(ABSTRACT TRUNCATED AT 400 WORDS)

Alkaline and acid transients in cerebellar microenvironment

1983 ◽  
Vol 49 (3) ◽  
pp. 831-850 ◽  
Author(s):  
R. P. Kraig ◽  
C. R. Ferreira-Filho ◽  
C. Nicholson
Keyword(s):  
Neuronal Activity ◽  
Cerebellar Cortex ◽  
Stimulus Frequency ◽  
Ringer Solution ◽  
Weak Acid ◽  
Ion Concentration ◽  
Extracellular Potassium ◽  
Base Line ◽  
Extracellular Potassium Concentration ◽  
The Brain

1. Extracellular pH (pHo) was measured in the cerebellar cortex of the rat using a recently developed liquid membrane ion-selective micropipette (ISM). pHo was determined during stimulus-evoked neuronal activity, elevated extracellular potassium concentration, [K+]o, spreading depression (SD), and complete ischemia. In many experiments [K+]o was simultaneously determined. 2. A train of local surface stimuli (LOC) produced an initial alkaline shift in pHo from a base line of 7.20-7.30 to 7.25-7.35. This was followed by a long-lasting acid phase that reached a plateau of 7.05-7.15 after 64 s of stimulation. pHo decrease was related to stimulus frequency, intensity, and duration. 3. Superfusion with Ringer solution containing manganese ions rapidly abolished parallel fiber-induced Purkinje cell synaptic depolarization together with the alkaline shifts while enhancing the acid shifts. 4. Superfusion of the cerebellar cortex with Ringer solution containing increasingly elevated [K+] progressively lowered pHo to a plateau of 6.95-7.05. The acidification occurred in the presence of ouabain but was reversed on return to the normal [K+]o or with the addition of the glycolytic blocker, fluoride. Stimulus-evoked alkaline shifts were enhanced by K+-Ringer superfusion. These experiments suggested that the acid shift was due to the metabolic production of an anion, possibly lactate. 5. Elevation of [K+]o above 8-12 mM often produced oscillation in pHo and [K+]o with a period of about 40 s. Sometimes these oscillations ended in a spontaneous SD or SD could be evoked by stimulation. Under these conditions of raised [K+]o, the SD consisted of a very pronounced alkaline transient followed by a small, long-lasting acid shift. When SD was induced by conditioning the cerebellum with proprionate or lowered NaCl, the alkaline phase was reduced and the acid enhanced. 6. Complete ischemia began with a progressive decrease of pHo and rise in [K+]o. When [K+]o reached 12 mM, a second more rapid rise in [K+]o to 40 mM or more occurred. This was correlated with 0.1-0.2 pHo transient increase similar to that seen during SD. pHo eventually reached a plateau of 6.60-6.80, close to neutrality. 7. Superfusion with Ringer solution containing acetazolamide immediately altered pHo homeostasis by increasing base-line pHo by about 0.10 and enhanced the induced pHo changes. These results suggest that carbonic anhydrase (CA) is important for acute buffering of the brain extracellular microenvironment. 8. The above results were interpreted in terms of changes in extracellular strong ion concentration differences ( [SID]o), extracellular concentration of total weak acid ( [Atot]o) and partial pressure of CO2 (Pco2) in the brain microenvironment. The results indicate that neuronal activity produces changes in many of the constituents of the microenvironment.

scholarly journals Effects of extracellular calcium and potassium on the sodium pump of rat adrenal glomerulosa cells

2001 ◽  
Vol 280 (1) ◽  
pp. C119-C125 ◽  
Author(s):  
Douglas R. Yingst ◽  
Joanne Davis ◽  
Rick Schiebinger
Keyword(s):  
Sodium Pump ◽  
Calcium Influx ◽  
Calcium Ionophore ◽  
Extracellular Calcium ◽  
Intracellular Free Calcium ◽  
Free Calcium ◽  
Extracellular Potassium ◽  
A 23187 ◽  
Pump Activity ◽  
Glomerulosa Cells

Because the activity of the sodium pump (Na-K-ATPase) influences the secretion of aldosterone, we determined how extracellular potassium (Ko) and calcium affect sodium pump activity in rat adrenal glomerulosa cells. Sodium pump activity was measured as ouabain-sensitive 86Rb uptake in freshly dispersed cells containing 20 mM sodium as measured with sodium-binding benzofluran isophthalate. Increasing Ko from 4 to 10 mM in the presence of 1.8 mM extracellular calcium (Cao) stimulated sodium pump activity up to 165% and increased intracellular free calcium as measured with fura 2. Increasing Ko from 4 to 10 mM in the absence of Cao stimulated the sodium pump ∼30% and did not increase intracellular free calcium concentration ([Ca2+]i). In some experiments, addition of 1.8 mM Cao in the presence of 4 mM Ko increased [Ca2+]i above the levels observed in the absence of Cao and stimulated the sodium pump up to 100%. Ca-dependent stimulation of the sodium pump by Ko and Cao was inhibited by isradipine (10 μM), a blocker of L- and T-type calcium channels, by compound 48/80 (40 μg/ml) and calmidizolium (10 μM), which inhibits calmodulin (CaM), and by KN-62 (10 μM), which blocks some forms of Ca/CaM kinase II (CaMKII). Staurosporine (1 μM), which effectively blocks most forms of protein kinase C, had no effect. In the presence of A-23187, a calcium ionophore, the addition of 0.1 mM Cao increased [Ca2+]i to the level observed in the presence of 10 mM Ko and 1.8 mM Cao and stimulated the sodium pump 100%. Ca-dependent stimulation by A-23187 and 0.1 mM Cao was not reduced by isradipine but was blocked by KN-62. Thus, under the conditions that Ko stimulates aldosterone secretion, it stimulates the sodium pump by two mechanisms: direct binding to the pump and by increasing calcium influx, which is dependent on Cao. The resulting increase in [Ca2+]i may stimulate the sodium pump by activating CaM and/or CaMKII.

Changes in extracellular potassium accumulation produced by opioids and naloxone in frog spinal cord: Relation to changes of Na/1b-K pump activity

1985 ◽  
Vol 59 (3) ◽  
pp. 285-290 ◽  
Author(s):  
Eva Sykova ◽  
I. Hájek ◽  
A. Chvátal ◽  
N. Kříž ◽  
Galina I. Diatchkova
Keyword(s):  
Spinal Cord ◽  
Extracellular Potassium ◽  
Potassium Accumulation ◽  
Frog Spinal Cord ◽  
Pump Activity

Extracellular potassium in rat cerebellar cortex during acute and chronic lithium application

1980 ◽  
Vol 192 (1) ◽  
pp. 287-290 ◽  
Author(s):  
Axel Ullrich ◽  
Peter Baierl ◽  
Gerrit ten Bruggencate
Keyword(s):  
Cerebellar Cortex ◽  
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
Sign in / Sign up

Export Citation Format

Share Document