IndraLab

Statements


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"Furthermore, TTX effectively inhibited Nav1.7 activity and reduced cell invasion by up to 50%."

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"The “TTX-sensitive channels” includes Nav1.1–1.4, Nav1.6 and Nav1.7 that can be blocked by nanomolar concentrations of TTX."

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"Figure 2B shows all the 16 wells imaged by objective 1 from a zebra sentinel plate with alternating columns of wells containing a Nav1.7 blocker tetrodotoxin (TTX; 1 μM) as a positive control and dimethylsulfoxide (DMSO; 0.15%) as a negative vehicle control."

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"The authors have noted in preliminary work that tetrodotoxin (TTX), which inhibits NaV1.7 and several other TTX-sensitive sodium channels, has differential effects on nociceptors, dramatically reducing their excitability under certain conditions but not under others."

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"The current subsets identified by TTX have been demonstrated to depend on specific voltage-gated sodium channels (VGSC): TTX-sensitive (TTX-S) sodium channels, such as Nav1.1, Nav.1.3, Nav1.6 and Nav1.7 which are blocked by TTX at nanomolar concentrations, and TTX-resistant (TTX-R) sodium channels, such as Nav1.8 and Nav1.9 which are blocked by TTX only at micromolar concentrations (Dib-Hajj et al., 2009)."

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"While both tetrodotoxin and PF-05089771 potently blocked Nav1.7, they lacked or only had modest subtype specificity against Nav1.2 (Figure 3B)."

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"Hainantoxin-III is a selective antagonist of neuronal tetrodotoxin-sensitive voltage-gated sodium channels; wherein it suppresses Nav1.7 current amplitude without altering any activation, inactivation, and repriming kinetics (Liu et al., 2013)."

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"High levels (0.5 M) of TTX can produce complete Nav1.7 block in wild type DRG neurons that also leads to opioid upregulation; but TTX at five times the IC50 for Nav1.7 could prevent enhanced encephalin expression."