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Neurons
Published in Nassir H. Sabah, Neuromuscular Fundamentals, 2020
The AHP can have some important modulating effects on neuronal firing. The larger the hyperpolarization, the longer it will take the membrane to return to the resting level and to subsequently depolarize to threshold. The AHP is thus involved in setting the minimum rate of steady firing. If [Ca2+]i builds up after the initiation of a train of APs, the frequency of the APs in the train will decrease with time due to the hyperpolarization resulting from Ca2+-activated SK channels. This decrease in frequency is known as spike frequency adaptation (SFA). The steady frequency of repetitive firing will then depend on the strength of the AHP. A larger build-up of [Ca2+]i can lead to a hyperpolarization that is strong enough to terminate the train of APs. As the hyperpolarization subsides, the neuron can fire again leading to another burst of APs and so on. Controlling the AHP can thus cause the neuron to switch between repetitive firing of single APs and repetitive bursts.
Introduction to Noninvasive Therapies
Published in Robert B. Northrop, Non-Invasive Instrumentation and Measurement in Medical Diagnosis, 2017
An ECT stimulation (or a tDCS) session's intensity is generally specified as the electrode current, rather than a voltage. That is, the ECT or tDCS source generator must be a current, rather than a voltage source. If a low output-impedance voltage source was used, the actual current through the brain could be individually highly variable because of the variability of the impedances of the two electrodes, the underlying scalp tissue, the skull, the meninges, the cerebrospinal fluid, and, of course, the brain tissue in the subjects. Presumably, it is the voltages induced in the brain volume conductor caused by the ECT current densities interacting with the brain tissue impedances therein that are important. We traditionally think of neurons responding to voltages across their membranes at their spike generator loci (SGLs). The normal DC resting potential (EMF) across a neural membrane is about 60 mV, inside negative. Thus, any electrical stimulus (such as ECT pulses) that causes the transmembrane potential to momentarily become less negative, that is, go in a positive direction, can bring an SGL closer to its transmembrane voltage firing threshold where it can generate an action potential, sending one or more nerve impulses down its axon to either stimulate or inhibit other target neurons. Prolonged neural depolarization can also be the result of local changes in the concentrations of extracellular cations (e.g., Na+, K+, Ca++) and anions (e.g., Cl−) caused by the mobility of these ions in the transient ECT-caused electric field in the brain. Note that conversely, induced hyperpolarization of a nerve's SGL membrane will inhibit a neuron's propensity to fire in response to an excitatory input stimulus. Of course, ions in the brain also migrate in the DC field set up during tDCS.
Force Generation Mechanism of Skeletal Muscle Contraction
Published in Yuehong Yin, Biomechanical Principles on Force Generation and Control of Skeletal Muscle and their Applications in Robotic Exoskeleton, 2020
The change of membrane potential is dominated by the open and close of ion channels. When a specific channel is open, driven by transmembrane and chemical potential, the ions inside (outside) the membrane spread quickly to the opposite side of the membrane, leading to the change of charge concentration across the membrane and accordingly the change of membrane potential. There are two types of ion channels, namely the receptor type and voltage-sensitive type. The former opens when binding with specific acceptor, and the latter opens when the membrane potential rises. The voltage-sensitive Na+ channel and K+ channel play a key role in the generation and spread of AP. There are two significant potentials for the neuron membrane: the resting potential (about −80 mV) and the threshold potential (about −70 mV). The excitation in the soma of motoneuron raises the membrane potential near the axon (depolarization), thus opening the high-density voltage-sensitive Na+ channels here. The inward flow of Na+ brings about the further rise of the membrane potential. When the membrane potential is higher than the threshold potential, the opening of the numerous Na+ channels leads to a huge leap in the membrane potential (tens of mV). However, there is a delay in the opening of K+ channels compared to that of Na+ channels. Thus, after the jump of the membrane potential, K+ ions start to flow out due to the opening of K+ channels, so this current is called delayed rectifier K+ current. This makes the membrane potential decrease to the resting potential (repolarization) or even lower than the resting potential temporarily (hyperpolarization). The waveform of a typical AP is illustrated in Figure 1.4a. When one AP bursts, the adjacent Na+ and K+ channels will open in series, transferring the AP to the distal end of axon. It should be noted that inactivation mechanism exists for the voltage-sensitive Na+ and K+ channels; i.e., when AP is generated somewhere on the membrane, there is a refractory period for the ion channels lasting for several milliseconds (ms), which is also called absolute deactivation period. Then, the threshold potential would decrease exponentially with time, and the unidirectional conduction of AP is also guaranteed by the inactivation mechanism. However, if there are continuous intensive excitations somewhere on the membrane (membrane potential is constantly high), back propagation of AP would occur. There is another significant kind of ion channel on the membrane, the active type ion channel or the ion pump. The ion pump would consume the energy of ATP and transport ions across the membrane against the concentration gradient to maintain the transmembrane ion concentration difference at the resting potential.
Does anodal tDCS improve basketball performance? A randomized controlled trial
Published in European Journal of Sport Science, 2022
Jitka Veldema, Arne Engelhardt, Petra Jansen
TDCS consists of the application of a low-intensity direct current that flows between two electrodes (anode and cathode) (Giordano et al., 2017; Herrmann, Rach, Neuling, & Strüber, 2013; Nasseri, Nitsche, & Ekhtiari, 2015). One of the electrodes is positioned over the target area (the active electrode), the other (the reference electrode) over another cranial or extracranial position. Anodal stimulation (the anode over the target area) induces a depolarization of cortical neurons and thereby an increase of cortical excitability. Cathodal stimulation (the cathode over the target area) induces hyperpolarization and decreases cortical excitability (Giordano et al., 2017; Herrmann et al., 2013; Nasseri et al., 2015). The amount and the duration of the neurophysiological changes depend on current density and stimulation duration (Nitsche & Paulus, 2007). The available data shows that current intensities of at least 0.6 mA and stimulation durations of at least 3 minutes are needed to induce changes in motor cortex excitability that outlast the stimulation period. TDCS stimulation with a current intensity of 1 mA and a stimulation duration of 5 or 7 minutes evokes short-term changes of cortical excitability that last for 10–15 minutes after the stimulation itself. For long-term changes in motor cortex excitability (1 hour or more) a current intensity of 1 mA should be applied for at least 11 minutes (Nitsche & Paulus, 2007).
Mechanism of peripheral nerve modulation and recent applications
Published in International Journal of Optomechatronics, 2021
Heejae Shin, Minseok Kang, Sanghoon Lee
Neurons are activated by an external stimulus above the threshold or by commands from the brain or the spinal cord. And when activated, voltage-gated Na+ channels located at the membrane are opened. In the case of Na+, since the concentration outside the cell is higher than that inside the cell, the Na+ ions rush into the cell as soon as the channel is opened, reducing the voltage polarity between inside and outside the cell. This process is called depolarization. When the depolarization process is finished, the voltage-gated Na+ channel is closed again and the voltage-gated K+ channel is opened. In the case of K+, since the concentration inside the cell is higher than the concentration outside the cell, K+ ions are released to the outside of the cell as soon as the channel is opened, and the potential within the cell gradually becomes relatively negative (repolarization), and later, a potential value lower than the resting membrane potential is obtained (hyperpolarization). After that, when the membrane potassium permeability returns to the resting state value, the membrane potential returns to the resting membrane potential value (Figure 1(d)). Due to the initial diffusion of Na+, the voltage-gated Na+ channel located next to it is also opened and the above process is repeated. Through this process, the action potential propagates along the entire axon, and at the end of the neuron (axon terminal), the specific type and amount of neurotransmitter are released based on the information of action potential.[16,17]
Emerging memristive neurons for neuromorphic computing and sensing
Published in Science and Technology of Advanced Materials, 2023
Zhiyuan Li, Wei Tang, Beining Zhang, Rui Yang, Xiangshui Miao
The working process of biological neurons involves complex ion dynamics processes. The neuronal membrane serves as a barrier between the external environment and the neuronal cytoplasm, across which various ion exchange processes take place. These processes are in turn governed by voltage-dependent opening and closing of ion channels (e.g. Na+ and K+ ion channels) [46,47]. As illustrated in Figure 1(b), an action potential can normally be roughly divided into four segments: resting potential, depolarization, repolarization, and hyperpolarization. Initially, the neuron is in a resting potential (usually ~−70 mV), the membrane potential maintains a constant charge gradient (Na+/K+ pump). When incoming spikes induce the membrane potential to reach the threshold of the neuron (usually ~−55 mV), Na+ ion channels are activated, and the rapid influx of Na+ ions results in depolarization of the membrane potential. Then, the voltage-gated K+ ions channels determine physiological processes of repolarization and hyperpolarization. Ion pumps allow K+ ions to flow out of the cell membrane, the membrane potential decreases rapidly, until it reaches a new resting state when the outward of K+ ions balance the inward of Na+ ions. This spike generation process is an all-or-none event, a spike generates when its membrane potential exceeds the threshold; Otherwise, the membrane potential boosting lasts for a short time without leading to spike generation. Note that after the neuron emitting an action potential, it remains nonresponsive to subsequent stimuli for a certain period of time, called as the refractory period.