scholarly journals Influence of changes in external potassium and chloride ions on membrane potential and intracellular potassium ion activity in rabbit ventricular muscle

1976 ◽  
Vol 256 (3) ◽  
pp. 663-689 ◽  
Author(s):  
Harry A. Fozzard ◽  
Chin Ok Lee
Keyword(s):  
Membrane Potential ◽  
Chloride Ions ◽  
Potassium Ion ◽  
Ventricular Muscle ◽  
Intracellular Potassium ◽  
Ion Activity ◽  
External Potassium ◽  
Rabbit Ventricular Muscle

Effects of abamectin on intracellular potassium ion activity and membrane potential in dipteran skeletal muscle

1993 ◽  
Vol 37 (1) ◽  
pp. 49-55
Author(s):  
Elizabeth M. Fitzgerald ◽  
Jason Curry ◽  
Mustafa B. A. Djamgoz
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Potassium Ion ◽  
Intracellular Potassium ◽  
Ion Activity

scholarly journals Responses of Regularly-Firing Aplysia R3-R13 Neurones to Normoxia and Hypoxia

1983 ◽  
Vol 107 (1) ◽  
pp. 1-8
Author(s):  
PHILIP E. COYER
Keyword(s):  
Steady State ◽  
Membrane Resistance ◽  
Chloride Ions ◽  
Membrane Potentials ◽  
Potassium Ion ◽  
Ion Permeability ◽  
Intracellular Potassium ◽  
Permeability Changes ◽  
Goldman Equation ◽  
Ion Activities

1. Exposure of 10 R3-R13 neurones to a 115-min period of hypoxia resulted in depolarization of their membrane potentials (EM) from a mean of −46.9±3.1 to −20.8±4.4mV (S.E.). 2. Intracellular potassium ion activities (aiK) decreased significantly from 118.9±5.1 to 67.7±8.5mM-K+. This is equivalent to a change in EK from −70.9 mV to −54.5 mV, which is insufficient to account for depolarization of approximately 26 mV. 3. During reoxygenation of the saline surrounding the ganglion, there was a continued depolarization of EM to −11.5 ± 3.2 mV and progressive fall in aiK to 49.2 ± 4.9 mM. 4. Decreases in the membrane slope resistance were also observed in these depolarizing neurones. The depression in resistance remained irreversible for as long as experiments were conducted. 5. Computations of PNa/PK ratios were made using a steady-state calculation. Increases in the PNa/PK ratio from 0.030 to 0.045 were observed during hypoxic depolarization using a modification of the Goldman equation which neglects the contribution of chloride ions. Subsequent depolarization and loss of aiK during reoxygenation elevated this value to 0.183. Whether or not the observed depression of the membrane resistance is linked to a change in either the sodium or potassium ion permeability is unknown. Release of neuro transmitter and related permeability changes cannot be ruled out as an effect of hypoxia.

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.

scholarly journals Reversible changes in the intracellular potassium ion activities and membrane potentials of Aplysia L2-L6 neurones in response to normoxia and hypoxia

1983 ◽  
Vol 102 (1) ◽  
pp. 79-92
Author(s):  
P. E. Coyer ◽  
J. H. Halsey ◽  
E. R. Strong
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Membrane Potentials ◽  
Potassium Ion ◽  
Intracellular Potassium ◽  
Goldman Equation ◽  
Ion Activities

1. Exposure of 7 L2-L6 neurones to hypoxia for 65 min resulted in hyperpolarization of the membrane potential (EM) from a mean of −49.1 +/− 2.1 to −54.1 +/− 3.6 mV (S.E.). 2. Intracellular potassium ion activities (aiK) increased significantly from 137.7 +/− 4.0 to 155.6 +/− 3.4 mM-K+. This is equivalent to a change in EK from −74.2 mV commensurate with the observed hyperpolarization of 5 mV. 3. The reversibility of these responses was noted by reoxygenating the solution surrounding the ganglion for a period of 55 min. 4. In another group (n = 7) of L2-L6 neurones, the responses in aiK, EM, and EK were slower, although following hypoxia for 90–110 min, similar changes in the levels of these membrane phenomena were recorded. 5. PNa/PK ratios were computed for both L2-L6 groups of neurones using a modified version of the Goldman equation. There were only slight decreases in this ratio with hypoxia, which were not significantly different from the control (normoxia). Therefore, we conclude that this period of hypoxia is capable of stimulating the sodium pump of these cells since the membrane potentials seem to hyperpolarize according to the increase in aiK. However, tonic release of neurotransmitter, which could hyperpolarize these neurones and attract intracellular potassium, cannot be ruled out as an effect of hypoxia.

Effects of intracellular potassium and sodium injections on the inhibitory postsynaptic potential

1964 ◽  
Vol 160 (979) ◽  
pp. 181-196 ◽  
Keyword(s):  
Spinal Cord ◽  
Membrane Potential ◽  
Cell Membrane ◽  
Direct Evidence ◽  
Equilibrium Potential ◽  
Ionic Mechanism ◽  
Half Time ◽  
Intracellular Potassium ◽  
Postsynaptic Potential ◽  
Almost All

Two barrels of double microelectrodes have been filled with different salts so that the electrophoretic injection of Na + and K + ions could be investigated in alternating sequence on the same motoneuron in the cat spinal cord. The effects of these injections on the mechanism generating the IPSP were evaluated by determining the equilibrium potential for the IPSP (the E IPSP ), i. e. the membrane potential at which the IPSP is zero. Such determinations have been made every 5 to 10 s after ion injections and have provided the most direct evidence of the ionic mechanism generating the IPSP . Comparison of the Na + and K + ion injections shows that the former injection always displaced the E IPSP much farther in the depolarizing direction and that recovery was much slower, with a half-time of 70 to 120 s, in contrast to about 20 s after the K + injection. In the discussion and evaluation of these results it was postulated that almost all of the displacement of the E IPSP in the depolarizing direction was due to the increased intracellular Cl - concentration, the (Cl - ) i . Under normal conditions a high (Cl - ) i declines by diffusional exchange across the cell membrane with a half-time of about 20 s, but this decline is much slower when the internal potassium is depleted. An explanation of this difference will be given in the following paper.

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.

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