hNaV1.9 - "High Throughput Pharmacology of NaV1.9 Channels on Nanion’s SyncroPatch 384"
SyncroPatch 384 (a predecessor model of SyncroPatch 384i) application note: (1.6 MB)
Cells kindly provided by Icagen, Inc., USA.
The SCN11A gene encodes the voltage-gated sodium channel NaV1.9 which is predominantly expressed in small-diameter sensory neurons of dorsal root ganglia (DRG) and trigeminal ganglia. NaV1.9 is characterized by slow activation with little depolarization near the resting membrane potential generating a persistent, tetrodotoxin (TTX)-insensitive current which inactivates only slowly. These properties suggest that the conductance mediated by NaV1.9 mainly contributes to amplification of depolarizing responses to subthreshold stimuli leading to lower action potential (AP) firing thresholds and increase in AP firing frequency. The role of hNaV1.9 has yet to be fully elucidated but is proposed to be involved in nociception of inflammatory and neuropathic pain. Several gain-of function mutations in SCN11A have been identified which result in either painful neuropathy or an insensitivity to pain. Given its proposed role in pain perception, NaV1.9 has gained some attention as a potential target for the development of novel pain therapeutics. Here we present high quality data with reliable pharmacology on hNaV1.9 expressing HEK293 cells at a high throughput collected on the SyncroPatch 384. Biophysical properties of NaV1.9 expressed in HEK cells (cells kindly provided by Icagen, Inc., USA) and concentration response curves for three NaV channel blockers are shown, including use-dependence of tetracaine.
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