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Physiology of Excitable Cells
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The Nernst equation calculates the potential difference that any ion would produce if the membrane was permeable to it. This is given by the equation: Where E ion = equilibrium potential for the particular ion
Computational Neuroscience and Compartmental Modeling
Published in Bahman Zohuri, Patrick J. McDaniel, Electrical Brain Stimulation for the Treatment of Neurological Disorders, 2019
Bahman Zohuri, Patrick J. McDaniel
The resulting charge displacement creates a potential difference that opposes this flow. The membrane potential at which there is no net flux of the ion is the equilibrium potential (or reversal potential) Ek, represented by a battery in series with the conductance. In the absence of synaptic input, current injection, or spontaneous firing of action potentials, Vm will approach a steady state rest potential Erest, typically in the range of -40 to −100 mV. This is determined by the condition that there is no net current flow into the cell from the various types of ion channels.
Nervous System
Published in Sarah Armstrong, Barry Clifton, Lionel Davis, Primary FRCA in a Box, 2019
Sarah Armstrong, Barry Clifton, Lionel Davis
The RMP is approximately −85 mV in muscles and −70 mV in nerves and can be calculated for a given ion at equilibrium (where the net ion movement is zero) with the Nernst equation: where E = equilibrium potential of the ion, R = universal gas constant, T = absolute temperature, Z = valency of the ion, F = Faraday's constant and Co/Ci = extracellular/intracellular ion concentration
Why do platelets express K+ channels?
Published in Platelets, 2021
Joy R Wright, Martyn P. Mahaut-Smith
GIRK channels (Kir3.0 family) are G-protein-gated inwardly rectifying potassium channels. The rectification displayed by these channels results in an increase in conductance as the membrane is hyperpolarized. Thus, when activated, GIRK channels are very effective at shifting the membrane potential toward the equilibrium potential for K+ (≈-90 mV). Structurally, GIRK channels are tetrameric complexes consisting of 4 GIRK subunits 1–4, whereby each subunit comprises two transmembrane helices on either side of a pore-forming helix [59]. GIRK channel gating requires the presence of phosphatidylinositol 4,5 bisphosphate (PIP2), and interaction is sensitive to intracellular pH, sodium levels and arachidonic acid [60]. The channels are also modulated by Gα and Gβγ G-protein subunits, and GIRK channels have been reported to be present with GPCRs in macromolecular complexes [61].
Non-thermal membrane effects of electromagnetic fields and therapeutic applications in oncology
Published in International Journal of Hyperthermia, 2021
Peter Wust, Ulrike Stein, Pirus Ghadjar
We assume that every channel act like a diode because ions can only be directed along the electrochemical gradient. Our example (Figure 4) shows a huge Ca2+ gradient between the extracellular concentration of 1.3 mmol/l and intracellular concentration of only 100 nmol/L (>10,000-fold). Then, the equilibrium (Nernst) potential for Ca2+ is UCa ≈ 250 mV, which is far from the typical membrane potential of –60 mV. This electrochemical gradient is enormous, causing a strong tendency for calcium influx and intracellular calcium overload if the calcium channel is open. Instead, in the case of potassium, the K+ equilibrium (Nernst) potential of UK = –95 mV is below the membrane potential of 60 mV. Therefore, K+ ions flow from intracellular to extracellular to bring the membrane potential nearer to the K+ equilibrium potential. Thus, a potassium channel acts like a diode with the forward direction from intra- to extracellular.
A major interspecies difference in the ionic selectivity of megakaryocyte Ca2+-activated channels sensitive to the TMEM16F inhibitor CaCCinh-A01
Published in Platelets, 2019
Kirk A. Taylor, Martyn P. Mahaut-Smith
Under the ionic conditions of Figure 1, the equilibrium potential for both Na+ and Cl− is 0mV and thus Ca2+-activated currents may reflect movement of cations and/or anions. Following reduction of external chloride (gluconate substitution), 100µM [Ca2+]i evoked large A01-sensitive currents in each species (Figure 2A). Strikingly, Erev shifted in HELs (+37.2 ± 2.1mV) and rat MKs (+33.5 ± 2.7mV), whereas mouse MK currents continued to reverse close to 0mV (Figure 2B). Under low [Cl−]o conditions ENa = 0mV and ECl = +85.7mV, indicating that the underlying conductance displays greater permeability to Cl− compared to other ions in HELs and rat MK, but not in the mouse MK. A lower, yet significant, permeability to cations or large anions may explain why the shift of Erev was less than that expected for a perfectly Cl–-selective conductance, as reported previously for Cl− channels in human platelets [29,30].