Explore chapters and articles related to this topic
X-Nuclei MRI and Energy Metabolism
Published in Guillaume Madelin, X-Nuclei Magnetic Resonance Imaging, 2022
The membrane Na+ and K+ permeabilities are controlled by the voltage-gated Na+ and K+ channels, respectively. The open probability of the Na+ and K+ channels is both voltage-dependent and time-dependent. The depolarization starts only when the membrane potential reaches a threshold potential of about –55 mV (induced by some electrical stimulus), at which some voltage-gated Na+ channels open rapidly. When the potential reaches about +40 mV, the Na+ channels close and the K+ channels open more slowly to repolarize the membrane, and leading to a short hyperpolarization phase before the membrane reached its resting value. The Na+/K+-ATPase is responsible for re-establishing the resting membrane potential by pumping out 3 Na+ and pumping in 2 K+ using hydrolysis of ATP as a source of energy for its mechanism.
Monolithic Device Models
Published in Wai-Kai Chen, Analog and VLSI Circuits, 2018
Bogdan M. Wilamowski, Guofu Niu, John Choma, Stephen I. Long, Nhat M. Nguyen, Martin A. Brooke
where it is essential to remember that the drain saturation voltage, Vdsat, is now given by Equation 1.129. It is clear that Msat in Equation 1.129 is properly viewed as a drain saturation voltage correction factor in a short channel (indeed, deep submicron) environment. Because of Equation 1.135, the square of Msat can be accorded the stature of a current correction factor pertinent to short channel drain currents in the saturation regime. The dependence on parameter α of these correction factors is displayed in the plots submitted in Figure 1.33. The indicated correction factors are significant. For example, consider α = 2, which might typically represent a gate–source voltage, Vgs, that is about a volt over the threshold potential. The curves in the figure at hand suggest an approximate 38% reduction in the drain saturation voltage predicted by the simple long channel model, which corresponds to α = 0, as well as about a 62% attenuation of the corresponding drain saturation current.
Physiological basis and concepts of electromyography
Published in Kumar Shrawan, Mital Anil, Electromyography in Ergonomics, 2017
The principle of action potential propagation along an excitable fiber is illustrated in Figure 2.5. It is assumed that the left side of the schematically represented muscle fiber is excited. In this state the inner surface of the muscle fiber membrane is positive in relation to the outer surface. In the non-excited area in the right-hand section of the diagram the polarity is reversed. As can be seen from Figure 2.5, a potential gradient exists between the excited and the non-excited areas on account of the difference in the charge distribution. The difference in the potential results in a local circuit current. As the arrows in Figure 2.5 indicate, in the unexcited area the current passes the membrane in an outward direction. An outward current leads – as was shown for the stimulus current in Figure 2.4 – to membrane depolarization in a narrowly defined area. The depolarization is sufficient for the threshold potential to be reached, thus inducing excitation in the previously non-excited area. As a result, an action potential occurs there, too. In the example shown in Figure 2.5 the front of excitation moves to the right. This newly initiated action potential may, in turn, excite a point further to the right along the membrane. In the manner described in the above, an excitation produced at one point on a muscle fiber can spread over the entire muscle fiber.
A bulk-driven, buffer-biased, gain-boosted amplifier for biomedical signal enhancement
Published in Cogent Engineering, 2019
Sarin Vijay Mythry, D. Jackuline Moni
When neurons depolarize, Na+ (sodium) channels rapidly open and shift the membrane potential towards the equilibrium potential of sodium. As leakage channels are open at rest, there is a balance between leakage currents and Na+ channels opened at depolarization, but at a specific point, Na+ current exceeds the leakage current, membrane potential at this state is called the threshold potential. However, as Na+ depolarization opens voltage gated K+ channels; the membrane potential overshoots 0 mV and then rapidly returns to resting membrane potential after a transient undershoot. This rapid change occurs over several milliseconds and is called as an Action potential (or commonly as Sodium spike) and this propagates along the length of the axon. At the axon terminal, the spike provides Ca2+ opening depolarization and the resultant release of neurotransmitters which excite another neuron and thereby communicating information (Sadock et al., 0000). Figure 4 depicts the depolarization and repolarization wave in a nerve cell (Sadock et al., 0000).
A Cross-layer based mapping for spiking neural network onto network on chip
Published in International Journal of Parallel, Emergent and Distributed Systems, 2018
The main computational unit is spiking neuron in SNNs. Based on different implementation complexity and biological accuracy, various neuron models have been proposed, such as Hodgkin–Huxley [34], Izhikevich [35], and leaky integrate-and-fire (LIF) [36] neuron models. Among them the LIF neuron model is popular in hardware implementation of SNNs for its biological plausibility and computational efficiency. In this paper, LIF model presented in [36] is used. The current membrane potential value is summed with corresponding synaptic weight values while receiving spikes from pre-neurons. The neuron emits a spike when the membrane potential exceeds the threshold potential value, and then its membrane potential reset to the resting potential. The membrane potential can be described as (1).