Neuropathic pain syndromes are caused by a genetic modification that affects peripheral nerve fibres. Therapy of these syndromes is challenging as treatment is often unsatisfactory. Mutations of the voltage-gated sodium channel Nav1.7 lead to the chronic pain syndrome erythromelalgia. The role of this ion channel in action potential generation in human peripheral nerves has not been elucidated so far and novel pain therapeutics targeting this channel only provide minor pain relief for the patients.
In our current study (https://journals.lww.com/pain/Abstract/publishahead/The_role_of_Nav1_7_in_human_nociceptors__insights.98752.aspx), we investigated human stem cell-derived sensory neurons to show that Nav1.7 defines the activation threshold of these neurons. Mutations can lower this threshold, leading to neuronal hyperexcitability and to intolerable pain attacks. We show why an inhibition of this channel probably does not help and why the newly developed analgesics are therefore insufficient to reduce the patients’ suffering.
Here you can find a video describing our work: