The stimulus
Alan Weiss in The Electroconvulsive Therapy Workbook, 2018
Familiarity with some of the basic principles of neuronal physiology is important in understanding the electrical stimulus applied in ECT. The action potential, illustrated in Figure 5.4.2, is the basic mechanism by which electrical energy travels along a neuronal axon. Action potentials are generated by specific voltage-gated ion channels embedded within the cell membrane that are shut when the membrane potential is near the resting potential. Following a stimulus they rapidly open, allowing sodium ions to rush into the neuron, which has a relative negative charge compared to the outside, changing the electrochemical gradient increasing the membrane potential causing more channels to open. The process continues rapidly until all of the ion channels have opened causing a large increase in membrane potential. The sodium ion channels close and they are actively transported out of the membrane. Potassium channels are then activated and there is an outward flow of potassium ions returning the electrochemical gradient back to the resting state after a transient negative shift during which the plasma membrane is incapable of firing. The sodium and potassium gated ion channels open and close as the membrane reaches the threshold potential in response to a signal from another neuron (Guyton and Hall, 2016).
Physiology of excitable cells
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal in Principles of Physiology for the Anaesthetist, 2015
Nerve signals are transmitted by rapid changes in membrane potentials called action potentials. An action potential occurs with a sudden change from a negative resting potential to a positive membrane potential and almost equally returns to the resting membrane potential. During the course of an action potential, voltage-gated sodium and potassium channels are activated and inactivated. The voltage-gated sodium channels are instantaneously activated when the threshold potential (−65 mV) is reached and cause a 5000-fold increase in sodium conductance. Then, an inactivation process closes the sodium channel within a fraction of a millisecond. The onset of the action potential also activates the voltage-dependent potassium channels, which begin to open more slowly. Shortly after the action potential is initiated, the sodium channels become inactivated and any amount of excitatory signal cannot open the inactivation gates – the absolute refractory period. In the period that follows the absolute refractory period stronger than normal stimuli can initiate an action potential, and this is known as the relative refractory period.
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.
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.
Neuroscience for the mental health clinician
Published in Neuropsychological Rehabilitation, 2019
The book is aimed by and large at psychiatrists, but I think it will be helpful to any clinician interested in neuroscience, and to any neurorehabilitation clinician who feels uncomfortable by a lack of a good grounding in how the brain works. The book does not expect too much prior knowledge. The early chapters, for example on neuroanatomy, neurotransmission or genetics, start at the beginning. If you want to be reminded of some of the basic principles of the function of the nervous system then you will find it here, written in language that is plain speaking and easily understood. For example, the workings of the excitable membrane, why neurons have a potential gradient and what happens during an action potential, are clearly described in a few brief pages. And this is followed by brief descriptions of messenger systems within the cell and more detailed discussion of neurotransmitters and their receptors.
Efficient simulations of stretch growth axon based on improved HH model
Published in Neurological Research, 2023
Xiao Li, Xianxin Dong, Xikai Tu, Hailong Huang
In summary, the novel model accurately reproduced axonal excitement elicited by mechanical traction stimulation. When the axon segment is stimulated again, the conduction velocity increases as the axon length and diameter grow. The development of axons enables the induction of action potentials in a shorter period of time. For identically lengthened axon segments with different diameters, the larger the diameter, the faster the signal conduction from the center to both sides. The new model takes into account the possibility of mechanical constraint and axon bundle tensile development. This approach may be utilized to optimize neural tissue culture input parameters, reduce mechanical force-induced injury to neural tissue, and produce a more successful neural tissue culture process.
Related Knowledge Centers
- Anterior Pituitary
- Beta Cell
- Depolarization
- Membrane Potential
- Saltatory Conduction
- Endocrine System
- Cell
- Neuron
- Muscle Cell
- Cell–Cell Interaction