A
Anton Sebastian in A Dictionary of the History of Medicine, 2018
Action Potential The basis for the electrical wave that passes through a muscle or a nerve when it is stimulated. Demonstrated at the Paris Academy by Carlo Matteucci (1811–1868) in 1842. He observed that the leg of a frog twitched when it was placed on another frog leg which was electrically stimulated. In the same year Emil du Bois Reymond (1818–1896) detected electrical changes in injured muscle during contraction and this transient measurable electrical change was named action potential. The resting potential and the action potential in healthy nerves were recorded by a physiologist, Sir Alan Lloyd Hodgkin (b 1914) of Banbury, England and Andrew Fielding Huxley (b 1917) of London in 1939. Their dependency on sodium concentration was demonstrated by Sir Bernard Katz (b 1911) in 1949.
ENTRIES A–Z
Philip Winn in Dictionary of Biological Psychology, 2003
A stereotyped change in electrical potential across the MEMBRANE of a neuron or muscle cell as a result of stimulation. The occurrence of an action potential is dependent on the cell being depolarized (see DEPOLARIZATION) past the point called the THRESHOLD. Once the threshold is reached, a positive feedback loop initiates a sequence of depolarization and repolarization that is independent of the initial cause. This allows an action potential to maintain the same amplitude as it travels (or propagates) along the cell membrane. In the case of neurons, this property allows information to be encoded in terms of the rate of firing of action potentials. This information can then be carried without change from one part of the nervous system to another via the neuron's axon. An action potential is also called a spike. The simultaneous occurrence of many action potentials in a peripheral nerve or muscle is recorded as a COMPOUND ACTION POTENTIAL.
Solving The Mystery Of The Nerve Impulse
Andrew P. Wickens in A History of the Brain, 2014
Hodgkin and Katz also discovered another feature of the axon’s depolarisation that would later turn out to be crucial for understanding how an action potential was initiated. Put simply, they showed the action potential was only set into motion if the axon’s initial resting value (i.e. –45 millivolts) was raised by another 15 millivolts (i.e. to about –30 millivolts). Thus, –30 millivolts was the critical threshold value for the action potential to be generated. As Hodgkin and Katz had already shown, this was the point where the membrane would lower its resistance to sodium, thereby setting into motion the train of events reversing the voltage inside the cell from negative to positive. In fact, Hodgkin and Katz were to demonstrate two types of sodium flow into the cell. A fairly gentle one producing the threshold (or trigger) for the action potential to occur; and a second more intense one responsible for causing the rapid depolarisation of the axon to about +40 millivolts.
Toxic effect of acetamiprid on Rana ridibunda sciatic nerve (electrophysiological and histopathological potential)
Published in Drug and Chemical Toxicology, 2019
Yusuf Çamlıca, Salih Cüfer Bediz, Ülkü Çömelekoğlu, Şakir Necat Yilmaz
Nerve signals are transmitted by action potentials, which are rapid changes in cell membrane potential from the resting or depolarized state. Measurements of action potential parameters provide information about membrane signal transmission. We measured amplitude and area values from compound action potential recordings and a decrease on both values was observed. Our electrophysiological findings indicate axonal neuropathy as defined by Aminoff (1998). According to our knowledge, there is no study investigating the effect of acetamiprid on CNAPs of vertebrate peripheral nerves. In addition, Akbas et al. (2014) investigated the effects of imidacloprid, a neonicotinoid insecticide, on the action potential of the frog sciatic nerve and found that different doses of imidacloprid (1, 10 and 100 µM) significantly reduced the action potential amplitude and area compared with those of control nerves. Our electrophysiological results are consistent with the results reported by Akbas et al. (2014) for imidacloprid.
QT shortening: a proarrhythmic safety surrogate measure or an inappropriate indicator of it?
Published in Current Medical Research and Opinion, 2022
Amy Tanti, Benjamin Micallef, Janis Vella Szijj, Anthony Serracino-Inglott, John-Joseph Borg
Within excitable cardiac cells, an electrical stimulus causes the transmembrane voltage to experience a brief change known as an action potential (AP)1. The action potential duration (APD) is defined as the amount of time in which the voltage remains elevated above the resting membrane voltage2. The QT interval represents the time of ventricular activity and is measured from the beginning of the QRS complex to the end of the T wave and reflects the APD3. The QT interval should be corrected for heart rate (QTc) to enable comparison with reference values3. The QTc is normally between 350 and 460 milliseconds (ms) and is considered abnormally short if <350 ms4. Concern is emerging about the pro-arrhythmic risk associated with QT interval shortening and congenital short QT syndrome has been recognized as a congenital clinical entity that may trigger potentially fatal tachyarrhythmias5. Hyperfunction of the delayed rectifier potassium current or hypofunction of the calcium current result in a shortening of the repolarization period, an increase in transmural dispersion of repolarization and cause short QT interval, short atrial and ventricular effective refractory periods, and, as a result increase susceptibility to arrhythmias6.
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).
Related Knowledge Centers
- Anterior Pituitary
- Beta Cell
- Depolarization
- Membrane Potential
- Saltatory Conduction
- Endocrine System
- Muscle Cell
- Cell
- Neuron
- Cell–Cell Interaction