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Samples in periodicals archive:
Pyrethroid insecticides: ste-reospecific allosteric interaction with the batrachotoxinin-A benzoate binding site of mammalian voltage-sensitive sodium channels.
The mechanism of action is not known, but in vitro studies suggest that lamotrigine inhibits voltage-sensitive sodium channels, thus stabilizing neuronal membranes and modulating presynaptic release of excitatory neurotransmitters such as glutamate and aspartate.
2 Lamotrigine is structurally unrelated to any other AED therapy currently available, and is believed to act through use-dependent blockade of voltage-sensitive sodium channels.
Anticonvulsants and Voltage-Sensitive Ion Channels Neurotransmitter release from presynaptic nerve terminals is linked to both voltage-sensitive sodium channels (VSSC) and voltage-sensitive calcium channels (VSCC) (figure).
Brevetoxins, unique activators of voltage-sensitive sodium channels, bind to specific sites in rat brain synaptosomes.
These lipid-soluble polyether toxins, like the ciguatoxins, exert their toxicity by activating voltage-sensitive sodium channels (1).
Lamotrigine, a novel anticonvulsant, appears to have diverse mechanisms of action, including inhibition of the release of the excitatory neurotransmitter glutamate, calcium channel blockade, and an effect on voltage-sensitive sodium channels, which are believed to play a role in bipolar disorder.
html Brevetoxins are lipid-soluble, polyether, marine toxins that have an excitatory action on voltage-sensitive sodium channels (1).