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They act by binding to fast sodium channels from within (in an open state).
These toxins are thought to operate by opening sodium channels.
Other hainantoxins bind at site 3 of the sodium channels.
Inhibitors of sodium channels have also been found in this venom.
The class I antiarrhythmic agents interfere with the sodium channel.
The sodium channels close at the peak of the action potential, while potassium continues to leave the cell.
The actions of these two drugs are mediated principally through sodium channels.
After a short while, the open sodium channels inactivate and become refractory.
As sodium channels close calcium provides current to maintain the potential around 20 mV.
A minor effect on sodium channels at higher concentrations has also been seen, but these effects appear to vary between species.
This results in an elevated probability for sodium channels to open, leading to depolarisation.
Interaction with potassium and sodium channels has been proposed.
The fast sodium channels are voltage-dependent and have a very important role in cardiac action potential as explained above.
Due to the change in the activation the sodium channel will open at smaller depolarisations.
Sodium channel blockers are used in the treatment of cardiac arrhythmia.
Voltage-gated sodium channels found in mammals can be divided into three types: Nav1.
Sodium channels are typically targeted for the prevention of focal seizures.
The sodium channel is a membrane protein with a hydrophilic interior.
A remotely related group of atracotoxins operate by opening sodium channels.
In addition, BcTx1 slows down the activation of sodium channels.
In addition it captures the sodium channels at a closed state which speeds up inactivation.
This region is characterized by having an incredibly high concentration of voltage-activated sodium channels.
Saxitoxin has been used in molecular biology to establish the function of the sodium channel.
Tricyclic antidepressants may also have effects on sodium channels.
Cessation of spontaneous activity is associated with sodium channel inactivation (Na1.4).
In chromosome-3-linked patients, sodium ion channels do not turn off soon enough, so sodium-channel blocking agents might be required.
The structure periodicity may also regulate the sodium ion channels in axons.
It affects voltage-gated sodium ion channels leading to an increased duration of its opening.
This gene encoded a different regulatory protein, which provided a sodium ion channel on the surface of heart cells.
Upon the opening of the eyes, these cells begin to shed their sodium ion channels and become non-spiking neurons.
The drug riluzole is a neuroprotective drug that blocks sodium ion channels.
Phaiodotoxin acts on voltage-dependent sodium ion channels of insects.
The sodium is only able to pass into the membrane through sodium ion channels distributed along the axon.
The positive feedback of the rising phase slows and comes to a halt as the sodium ion channels become maximally open.
Lidocaine and Novocaine belong to a class of local anesthetics which block sodium ion channels.
It affects voltage-dependent sodium ion channels and blocks the synaptic transmission in the central nervous system.
In addition to these opioidergic and anticholinergic effects, it has local anesthetic activity related to its interactions with sodium ion channels.
Note that it is not linear, indicating that the sodium ion channel is voltage-dependent.
As the membrane potential is increased, sodium ion channels open, allowing the entry of sodium ions into the cell.
By blocking the inactivation of sodium ion channels, α-scorpion toxins prolong action potentials.
They bind to specific sodium ion channels in cell membranes, the receptor sites involved in activation and inactivation.
The structural basis for the selectivity of these toxins for insects over the mammalian sodium ion channels is still largely unknown.
In insects it opens sodium ion channels in neurons, causing them to fire spontaneously, which leads to spasms and eventual death.
Woolf is particularly interested in certain abnormal sodium ion channels that are only expressed in sensory neurons that have been damaged.
It uses Na-H antiport, Na-glucose symport, sodium ion channels (minor).
The Na1.5 is a sodium ion channel protein that in humans is encoded by the SCN5A gene.
By binding to voltage-dependent sodium ion channels and potassium channels, they cause sialorrhea, lacrimation and rhinorrhea.
Veratridine is a steroid-derived alkaloid from plants in the Liliaceae family that functions as a neurotoxin by activating sodium ion channels.
Dr. Albuquerque said malfunctions of sodium ion channels may play a role in abnormal heart rhythms and many neurological diseases, such as amyotrophic lateral sclerosis.
Any deformation in the corpuscle causes action potentials to be generated by opening pressure-sensitive sodium ion channels in the axon membrane.
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