Examples of using Action potentials in English and their translations into Vietnamese
{-}
-
Colloquial
-
Ecclesiastic
-
Computer
Inactivation only occurs in neurons firing action potentials;
Action potentials are described as"all or nothing" because they are always the same size.
This electrolyte dependent agent also increases action potentials and prolongs the QT interval.
Our neurons carry messages in the form ofelectrical signals called nerve impulses or action potentials.
High doses of nifedipine shortened action potentials significantly more than high-dose amlodipine.
The third-order neurons carry the received signals to the somatosensory cortex, where the signals,in the form of action potentials.
Ajmaline causes action potentials to be prolonged, therefore slowing down firing of the conducting myocytes which ultimately slows the beating of the heart.
For example, the cell membrane potential and the electric currents that flow in nerves and muscles,as a result of action potentials.
Inhibition of this enzyme canmake neurons less prone to fire action potentials, likely through activation of ATP-sensitive potassium channels.[7].
In excitable cells such as neurons, myocytes, and certain types of glia,sodium channels are responsible for the rising phase of action potentials.
Inactivation only occurs in neurons firing action potentials; this means that drugs that modulate fast inactivation selectively reduce the firing in active cells.
If the tip is small enough,such a configuration may allow indirect observation and recording of action potentials from a single cell, termed single-unit recording.
Their goal is to stimulate individual action potentials with millisecond time precision and to control what neurons are stimulated using genetic methods to target channel protein expression.
Many antiepileptic drugs, like carbamazepine or lamotrigine, slow the recovery from inactivation andhence reduce the ability of neurons to fire action potentials.
These neurons communicate with one another with long fibers called axons,which carry trains of signal pulses called action potentials to distant parts of the brain or body and target them to specific recipient cells.
Nerve impulses, or action potentials, are electrochemical impulses that cause neurons to release electrical or chemical signals that initiate an action potential in another neuron.
We have learned that our brains are computers that work using a system of connected brain cells, called neurons,that exchange information using chemical and electric signals called action potentials.
Reducing IKr in myocardial cells prolongs the cardiac action potential and thus prolongs the QT-interval.[1][14] In non-cardiac cells, blocking Ikr has a different effect:it increases the frequency of action potentials.[3].
Areas of study include electrical or electromagnetic fields produced by living cells, tissues or organisms, including bioluminescent bacteria; for example, the cell membrane potential and the electric currents that flow in nerves and muscles,as a result of action potentials.
Even if another stimulus is present, action potential cannot occur again until after complete repolarization.
This leads to hyperpolarization of the cell membrane potential and suppression of action potential transmission of ascending pain pathways.
In neuroscience, it includes measurements of the electrical activity of neurons, and,in particular, action potential activity.
In addition, the axon hillock also has a specialized plasma membrane that contains large numbers of voltage-gated ion channels,since this is most often the site of action potential initiation.
At that site, ACh normally produces electrical depolarization of the postjunctional membrane of motor end-plate,which leads to conduction of muscle action potential and subsequently induces skeletal muscle contraction.
When a nerve impulse or action potential moves along and reaches the end of the axon at its terminal, it triggers a different set of processes.
Amifampridine works by blockingpotassium channel efflux in nerve terminals so that action potential duration is increased.[7] Ca2+ channels can then be open for a longer time and allow greater acetylcholine release to stimulate muscle at the end plate.[6].
But non-spiking neurons are actually quite complicated because they can have input synapses and output synapses all interdigitated,and there's no single action potential that drives all the outputs at the same time.
This results in a disturbance in the artificial membrane potential and leads to a supraventricular tachycardia which induces failure of the pacemaker and death.[14] Thus,it prolongs QT interval of action potential and increases the risk of torsade de pointes.[2].
Prajmaline(Neo-gilurythmal)[1] is a class Ia antiarrhythmic agent[2] which has been available since the 1970s.[3]Class Ia drugs increase the time one action potential lasts in the heart.[4] Prajmaline is a semi-synthetic propyl derivative of ajmaline, with a higher bioavailability than its predecessor.[5] It acts to stop arrhythmias of the heart through a frequency-dependent block of cardiac sodium channels.
Class 1c drugs have a characteristically slow dissociation rate,which will slow the upstroke duration and amplitude of ventricular myocytes' action potential and prolong the PR, QRS and QT intervals of an ECG.[4] Lorcainide also increases the ventricular fibrillation threshold in a dose-dependent fashion.[4] Overall, Lorcainide causes a decrease in tachycardiac events, but also reduced ventricular contractility ejection fraction.