Optimising a difficult Nav1.8 cell line assay for automated patch-clamp screening

Poster Description

The TTX-resistant sodium channel Nav1.8 is expressed in peripheral sensory nociceptors and is implicated in a range of inflammatory and visceral pain conditions such as irritable bowel syndrome (IBS)1. Nav1.8 channel function in sensory neurons changes after injury or inflammation, with a redistribution from the soma to axons and upregulated activity through inflammatory mediators and signalling pathways. This is thought to underlie increased neuronal excitability and a greater role of Nav1.8 currents in persistent, repetitive and ectopic action potential firing in inflammatory and visceral pain. Several gain-of-function mutations in Nav1.8 have also been detected in human patients suffering from small fibre neuropathy (SFN), offering similar genetic target validation and clinical population for personalised medicine approaches seen with Nav1.7 mutations in primary erythmelalgia, paroxysmal extreme pain and SFN patients.

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