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Neuromuscular Physiology
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Several stimuli, including extreme temperature changes and chemical, mechanical, and electrical stimuli, can cause an excitable membrane to depolarize. A wave of depolarization that occurs along the surface of excitable tissue such as muscle and nerve is termed an AP. The AP is a result of sequential alterations in the membrane potential lasting a fraction of a second. Depolarization of an excitable membrane, such as the neurolemma or sarcolemma, is followed by a rapid return to RMP values. Rapid alterations in membrane permeability for Na+ and K+ are associated with the AP. Alterations in membrane permeability for various ions can be quite rapid and these rapid movements are associated with the opening and closing of ionic gates (channels). These gates, along with electrogenic pumps such as the Na+ / K+ pump, largely control the movement of specific ions across the plasmalemma (13, 33, 108, 125, 127).
Electrophysiologic Evaluation
Published in Jacques Corcos, Gilles Karsenty, Thomas Kessler, David Ginsberg, Essentials of the Adult Neurogenic Bladder, 2020
Melita Rotar, David B. Vodušek
Tests of conduction rely on the principle that the nervous system has excitable membranes and can be depolarized by an electric current. Electrical stimulation (or stimulation using a changing magnetic field, which induces electric currents) can be applied to different parts of the central and peripheral nervous systems (Figure 23.2). The depolarization spreads along the nervous pathways. Thus, the depolarization after stimulation of a sensory nerve can be recorded along the particular afferent pathway. (It also elicits reflex responses.) Stimulation of motor pathways causes activation of striated muscles, which can be recorded as an evoked compound muscle potential.
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 basis of the action potential is that depolarization opens sodium, potassium or calcium channels that are gated by the membrane voltage. The ionic basis of a nerve action potential are described in detail in Chapter 4.
Efficient simulations of stretch growth axon based on improved HH model
Published in Neurological Research, 2023
Xiao Li, Xianxin Dong, Xikai Tu, Hailong Huang
Because neural cells can produce action potentials, a regenerative electrical signal whose amplitude does not fade as it travels down the axon, is capable of transmitting signals over extended distances [19]. Electrical signals play a critical role in the transmission of nerve signals. When the depolarization of the membrane at any point along the axon exceeds a threshold value, an action potential is generated in that region in response to the opening of voltage-gated sodium ion channels. Local depolarization propagates electrically along the axon, forcing surrounding membrane areas to exceed the threshold for generating additional action potentials. As a result of the potential differential between the active and inactive sections of the axonal membrane, depolarization propagates throughout the length of the axon via a ‘local loop’ of current.
Solanaceae glycoalkaloids: α-solanine and α-chaconine modify the cardioinhibitory activity of verapamil
Published in Pharmaceutical Biology, 2022
Szymon Chowański, Magdalena Winkiel, Monika Szymczak-Cendlak, Paweł Marciniak, Dominika Mańczak, Karolina Walkowiak-Nowicka, Marta Spochacz, Sabino A. Bufo, Laura Scrano, Zbigniew Adamski
Calcium ions are crucial for the contraction of all types of muscles. After influx into the cytoplasm, they interact with myofilaments and ultimately allow for interaction between myosin and actin filaments, and thus for muscle contraction. Since they are a trigger and an executor of muscle contractions, their concentration in the sarcoplasm must be strictly regulated. In striated muscles, cell membrane depolarization is a signal that initiates the cascade responsible for muscle contraction. Changes in the cell membrane potential activate and open the L-type calcium channels. Then, the local increase in Ca2+ concentration activates the ryanodine receptor, a sarcoplasmic calcium channel, which releases the next portion of calcium ions into the cytoplasm, which interacts with myofilaments.
Chronic cough: Investigations, management, current and future treatments
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2021
I. Satia, M. Wahab, E. Kum, H. Kim, P. Lin, A. Kaplan, P. Hernandez, J. Bourbeau, L. P. Boulet, S. K. Field
Cough can be under both voluntary and automatic control at the same time, but it is widely recognized that the cough reflex is the archetypal airway defensive reflex to prevent aspiration of foreign bodies or inhalation of noxious chemicals like smoke. The lungs are innervated by two sub-types of the vagus afferent nerve”34 unmyelinated c-fibers and myelinated A-delta fibers projecting sensory nerve terminals to the epithelium and sub-epithelium, respectively. The c-fibers are predominantly chemically sensitive and express ion channels and g-protein coupled receptors on their terminals that, upon activation, allow cations to flow inside resulting in membrane depolarization. The A-delta fibers are mainly mechanosensitive, but also respond to change in pH and osmolarity. Depolarization generates action potentials that are transmitted to the central nervous system. Once the signal reaches the first order synapse in the nucleus tractus solitarius (NTS) and paratrigeminal nuclei, second order neurons relay the signal to the thalamus, and third order neurons to the primary somatosensory cortex. This causes the unpleasant conscious sensation of urge to cough, which if strong enough, will evoke coughing (Figure 2). Importantly, cough is also under voluntary control and recent evidence suggests the presence of descending inhibitory control neurons that inhibit impulses arriving at the brainstem, thus limiting the urge to cough40,50 (Figure 3).