Electrophysiology
A. Bakiya, K. Kamalanand, R. L. J. De Britto in Mechano-Electric Correlations in the Human Physiological System, 2021
Biopotentials are generated as a result of the electrochemical activity of the cells that are the components of the nervous, muscular and granular tissue. The electrical activity of the cell is generated via in and out ion movement (K+, Na+ and Cl−) through the cell membrane (Van Drongelen, 2010). Generally, the potentials are in two states (active and resting potential). The active potential is generated when cells are stimulated. The membrane potential when the cell is inactive is the resting potential. At resting state, the potassium ion is more permeable in the cell membrane when compared to the sodium and potassium ion concentrations is higher in the interior of the cell when compared to the exterior of the cell. The diffusion gradient of potassium ion arises toward the exterior of the cell that creates more negative ions in the interior of the cell. At steady or depolarization state, the diffusion gradient of potassium ion is in equilibrium and balanced by the electric field with the polarization voltages of −70 mV (Thakor, 2015; Webster, 1984). If the cells are electrically stimulated, the diffusion gradient of potassium ion increases and diffuse toward the interior of the cells that creates more potential. If the active potentials reach +40 mV, the permeability of the potassium ion decreases and the sodium ion increases causing resting potential. This cycle produces the several cellular potentials called as action potentials (Yazıcıoğlu et al., 2009; Thakor, 2015).
The cardiac myocyte: excitation and contraction
Neil Herring, David J. Paterson in Levick's Introduction to Cardiovascular Physiology, 2018
The resting potential is the result of a high intracellular K+ concentration (140 mM) relative to extracellular K+ (4 mM), in combination with open K+-permeable channels in the resting cell membrane. The membrane also has Na+ and Ca2+ chan-nels, but these are mostly closed at negative potentials. By contrast, a specific type of K+ channel, the inwardly rectifying channel (Kir), is partly in the open state at negative potentials. (Mammals have a bewildering variety of K+ channels, with at least 7 genes for inward rectifiers, 12 genes for voltage-acti-vated K+ channels and 5 genes for Ca2+-activated K+ channels.) Since intracellular K+ concentration is ~35 times higher than extracellular K+ concentration (Table 3.1), K+ tends to diffuse out of the cell through the Kir channels, creating a resting out-ward current of K+ ions, iKir (or iK+). The negative intracellular ions, mainly organic phosphates and charged proteins, cannot accompany the K+ ions because the cell membrane is imperme-able to them (Figure 3.5). Consequently, the outward leak of K+ ions quickly creates a tiny separation of charge, which leaves the cell interior negative with respect to the exterior. The elec-trical charge on a single ion is very large so just one excess neg-ative intracellular ion per 1015 ion pairs is enough to generate a resting potential of −80 mV (see equation 3.1a). This minute imbalance is far too tiny to be detected by chemical analysis.
Hypothalamic Control Centers
Nate F. Cardarelli in The Thymus in Health and Senescence, 2019
The firing rate of SCN neurons is higher during the light period.151 Resting potential is about −60 mV.152 Action potentials evoked by synaptic activation are sometimes followed by up to three small fast potentials. Firing can be at a constant low rate with fixed interspike intervals (unlike most central neurons).153 Such activity can be interrupted by anesthetics, such as sodium pentabarbatone.153 SCN neurons require extracellular Ca++ to fire spontaneously;154 thus lack of calcium ion leads to a low firing rate and abolition of diurnal rhythm.151 Andrew found calcium to be critical for the fire bursts of action potentials that facilitate hormonal release from magnocellular neuroendocrine cells.155
Effect of pulsed millisecond current magnetic field on the proliferation of C6 rat glioma cells
Published in Electromagnetic Biology and Medicine, 2019
Wenjun Xu, Jinru Sun, Yangjing Le, Jingliang Chen, Xiaoyun Lu, Xueling Yao
Since ions inside and outside the cell membrane are different in excitable tissues, such as the nuclei of muscles, there is a certain potential difference inside and outside the membrane, which is referred to as the membrane potential. The resting potential of different cells is variable. The potential of human neurons is −86 mV and is −90 to −80 mV for ventricular myocytes; for sinoatrial node cells, it is −70 to 40 mV, and is generally maintained at around −70 mV (Cifra et al., 2011). From the perspective of electricity, a living body is a complex volume conductor composed of a myriad of cells. Each cell consists of a cell membrane, a cytoplasm and a nucleus. The extracellular fluid between cells has the same electrical conductivity as the cytoplasm, which is equivalent to resistance, and the low leakage characteristics of the cell membrane can be equivalent to a capacitor (Kotnik et al., 2012). Simulation results show that the cell membrane can be equivalent to a low-pass filter and is a place where weak low-frequency magnetic fields interact (Chenguo et al., 2008). Organelle membranes such as the mitochondrial membrane and nuclear membrane can be equivalent to band-pass filters, and the intermediate frequency component is more likely to pass through the organelle membrane. The opening of calcium channels can also be affected by the ELF magnetic field (Koch et al., 2003; Yan, 2007).
After-effect induced by microwave radiation in human electroencephalographic signal: a feasibility study
Published in International Journal of Radiation Biology, 2018
Maie Bachmann, Laura Päeske, Andreas A. Ioannides, Jaanus Lass, Hiie Hinrikus
Low-level microwave radiation, rotating dipolar water molecules, can reduce hydrogen bonds, decrease viscosity and increase diffusion (Hinrikus et al. 2018). Neuronal resting conditions are determined by balance between diffusion driven jD and electric field driven jE ions currents density through a cell membrane (Malmivuo and Plonsey 1995) D is diffusion coefficient, ∇c is ions concentration gradient, c is ions concentration, q is an ion charge and E is electric field strength. The resting potential U or Nernst potential can be determined from the equation above (Malmivuo and Plonsey 1995) ci is intracellular and co is extracellular ions concentration.
Ketogenic diet: overview, types, and possible anti-seizure mechanisms
Published in Nutritional Neuroscience, 2021
Mohammad Barzegar, Mohammadreza Afghan, Vahid Tarmahi, Meysam Behtari, Soroor Rahimi Khamaneh, Sina Raeisi
Two-pore domain potassium (K2P) channels, also known as potassium leak channels, are a major and distinct subclass of the potassium channel superfamily. They have been discovered in a wide variety of mammalian cells including neurons, myocytes, glia, and many different types of epithelial cells. These channels are structurally different from most other classes of potassium channels which form a functional tetramer. It has been shown that each subunit of K2P channels has two pore-forming regions and four trans-membrane segments, and thus, they form functional dimers. Functionally, these channels are spontaneously active leading to continuous efflux of potassium ions through the cell membrane which is necessary for setting a hyperpolarized resting potential of the cell membrane. Therefore, K2P channels may directly influence the duration and frequency of action potential firings [56,58–60]. These channels can be also modulated by a variety of physical, chemical and natural factors including voltage, temperature, mechanical pressure, protons (pH), and volatile anesthetics. It has been suggested that K2P channels may also be activated by ketone bodies and certain fatty acids as well [59,61]. Thus, KD-induced raises in blood ketone bodies and fatty acids as well may regulate neuron membrane excitability by activating K2P channels, and this can be assumed as another probable anticonvulsant mechanism of KD.