Examples of 'voltage-gated' in a sentence
Meaning of "voltage-gated"
voltage-gated (verb) - a term used in biology and physiology to describe channels or proteins that open or close in response to changes in the membrane potential or voltage across a cell membrane
How to use "voltage-gated" in a sentence
Basic
Advanced
voltage-gated
Voltage-gated calcium channels are made up of several subunits.
This peptide targets voltage-gated potassium channels.
Voltage-gated sodium channels are inactivated.
Neurons contain a variety of voltage-gated ion channels.
The voltage-gated sodium channels are the classic targets of lidocaine.
This syndrome is caused by antibodies to voltage-gated calcium channels.
They also inhibit voltage-gated calcium channels in insect neurons.
Excitable cells in living organisms have voltage-gated ion channels.
Voltage-gated ion channels open upon depolarization of the cell membrane.
This wave causes a plurality of voltage-gated sodium channels to open.
Voltage-gated ion channels open and close in response to membrane potential.
Typical action potentials are initiated by voltage-gated sodium channels.
Voltage-gated sodium channels are believed to play a critical role in pain signaling.
The protein encoded by this gene is a voltage-gated potassium channel subunit.
Thus, voltage-gated sodium channel blockers may be useful as anticonvulsant agents.
See also
In certain embodiments, the second compound inhibits voltage-gated sodium channels.
It affects the gating of voltage-gated sodium channels and calcium channels.
Voltage-gated sodium channel blockers have clinical uses in addition to pain.
It has been shown to block the voltage-gated sodium channels at picomolar concentrations.
It does this through stabilization of the inactive state of voltage-gated sodium channels.
Pyrethroids affect the voltage-gated sodium channels in vertebrates and non - vertebrates.
Compounds of the invention are useful as antagonists of voltage-gated sodium ion channels.
The brevetoxins bind to voltage-gated sodium channels, important structures of cell membranes.
Compounds of the invention are useful as antagonists of voltage-gated calcium ion channels.
In order to characterize voltage-gated channels, the equations are fit to voltage clamp data.
In certain embodiments, the first compound inhibits voltage-gated sodium channels.
Mutations in voltage-gated sodium channels are responsible for several monogenic epilepsy syndromes.
It is also important to stress the involvement of voltage-gated sodium channels in trigeminal neuralgia.
Voltage-gated sodium channels are transmembrane proteins which cause sodium permeability to increase.
The action potentials arise by the voltage-gated sodium and potassium channels.
Nonselective voltage-gated sodium channel blockade is responsible for LAs toxic properties.
This depolarizes the β cells and causes voltage-gated calcium channels to open.
The blockade of voltage-gated sodium channels represents the primary action of those agents.
Action potentials are generated by the activation of certain voltage-gated ion channels.
In one embodiment, the voltage-gated ion channels are sodium or calcium ion channels.
Tetrodotoxin binds to what is known as site 1 of the fast voltage-gated sodium channel.
Lamotrigine blocks voltage-gated sodium channels and inhibits glutamate and aspartate release.
The selectivities of these channels may be relatively weak in comparison to voltage-gated channels.
The voltage-gated sodium channels play a key role in the mechanism of neuronal excitability.
It remains unknown how exactly kalkitoxin binds to the voltage-gated sodium channel.
These voltage-gated ion channels allow for rapid depolarization throughout the cell.
The mechanism of toxicity is through the blockage of fast voltage-gated sodium channels.
Voltage-gated sodium channels are involved in the propagation of a nerve impulse across the neuron.
It is further envisaged that the receptor may be a ligand - or voltage-gated ion channel.
These rapid reversals are mediated by voltage-gated ion channels found in the plasma membrane.
This peripheral nerve hyperexcitability is mediated by antibodies that target voltage-gated potassium channels.
Pyrethroids act as neurotoxics on voltage-gated sodium channels by slowing their activation and inactivation properties.
In yet other embodiments, the first compound inhibits voltage-gated calcium channels.
These voltage-gated channels are sodium and potassium specific and only allow one through.
This change in the cell 's membrane potential causes voltage-gated calcium channels to close.
