Ví dụ về việc sử dụng Sodium channels trong Tiếng anh và bản dịch của chúng sang Tiếng việt
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Another gene, SCN11A also affects sodium channels.
Furthermore, AM404 inhibits sodium channels, as do the anesthetics lidocaine and procaine.
In figure 4.16A, the short time constant τmis indicated by the almost simultaneous opening of two sodium channels.
This occurs because calcium ions interact with the exterior surface of sodium channels in the plasma membrane of nerve cells.
This results in a runaway condition whereby the positivefeedback from the sodium current activates even more sodium channels.
When this gene isn't working properly, sodium channels in the brain(which help brain cells function) do not work correctly.
The most intensively studiedtype of voltage-dependent ion channels comprises the sodium channels involved in fast nerve conduction.
As the sodium channels close, sodium ions can no longer enter the neuron, and they are then actively transported back out of the plasma membrane.
There is also an involvement of ion voltagechannel proteins such as VGSC(voltage gated sodium channels) in the chronic pain pathways.
Batrachotoxin binds to and irreversibly opens the sodium channels of nerve cells and prevents them from closing, resulting in paralysis- no antidote is known.
Lacosamide has low potential for drug-drug interactions, and no pharmacokinetic interactions have been found to occur with other(AEDs)that act on sodium channels.
It induces rapid block of the batrachotoxin(BTX)-activated sodium channels of the heart muscle and acts as antagonist to long-gating closures.
Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita,because of its direct effects on muscle membrane and sodium channels.
In excitable cells such as neurons, myocytes,and certain types of glia, sodium channels are responsible for the rising phase of action potentials.
Fast-acting voltage-gated sodium channels(Nav1.5) found in high concentrations in the ventricular myocytes, open at a membrane potential of- 80 mv in typical cardiac rhythm.
Slow inactivation is similar butdoes not produce complete blockade of voltage gated sodium channels, with both activation and inactivation occurring over hundreds of milliseconds or more.
Lacosamide is a functionalized amino acid that produces activity in the maximal electroshock seizure(MES) test, that, like some other antiepileptic drugs(AEDs),are believed to act through voltage-gated sodium channels.
When closing after an action potential, sodium channels enter an"inactivated" state, in which they cannot be made to open regardless of the membrane potential- this gives rise to the absolute refractory period.
Almost all fishes from this family contain tetrodotoxin which is a verypowerful nerve affecting poison that blocks the sodium channels in the nerve cells and can cause death in a very short time period.
Levobupivacaine reversibly binds voltage-gated sodium channels to modulate ionic flux and prevent the initiation and transmission of nerve impulses(stabilizing neuronal membrane), thereby resulting in analgesia and anesthesia.
It blocks nerve conduction in sensory andmotor nerves largely by interacting with voltage sensitive sodium channels on the cell membrane, but also potassium and calcium channels are blocked.
To an extent, how they exert these effects still hasn't been fully explained, but recent studies suggest that the soothing nature of a throat lozengeis due to the interaction of the compounds therein with sodium channels.
A mutation in either of these two geneswill cause an individual to develop dysfunctional sodium channels, which are crucial in the pathway for sending chemical signals in the brain, causing the phenotypic display of myoclonic epilepsy from the individual.
The potassium-sparing diuretics are competitive antagonists that either compete with aldosterone for intracellular cytoplasmic receptor sites,or directly block sodium channels(specifically epithelial sodium channels(ENaC) by amiloride).
Once the action potential is triggered, the depolarization(2)of the neuron activates sodium channels, allowing sodium ions to pass through the cell membrane into the cell, resulting in a net positive charge in the neuron relative to the extracellular fluid.
These are sometimes known as Hodgkin-Huxley sodium channels because they were first characterized by Alan Hodgkin and Andrew Huxley in their Nobel Prize-winning studies of the biophysics of the action potential, but can more conveniently be referred to as NaV channels. .
After the action potential peak is reached, the neuron begins repolarization(3),where the sodium channels close and potassium channels open, allowing potassium ions to cross the membrane into the extracellular fluid, returning the membrane potential to a negative value.
However, the same raised voltage that opened the sodium channels initially also slowly shuts them off, by closing their pores; the sodium channels become inactivated.[32] This lowers the membrane's permeability to sodium relative to potassium, driving the membrane voltage back towards the resting value.
Proxymetacaine is believed to act as an antagonist on voltage-gated sodium channels to affect the permeability of neuronal membranes; how this inhibits pain sensations and the exact mechanism of action of proxymetacaine are, however, unknown.[2].
Disopyramide's Class 1aactivity is similar to that of quinidine in that it targets sodium channels to inhibit conduction.[1][2] Disopyramide depresses the increase in sodium permeability of the cardiac myocyte during Phase 0 of the cardiac action potential, in turn decreasing the inward sodium current.