• Shaila Hameed.
• 1 Department of Physiology, King's College London, London, UK.
• Mol Pain. 2019 Jan 1; 15: 17448069198588011744806919858801.

AbstractChronic pain is a significant unmet medical problem. Current research regarding sodium channel function in pathological pain is advancing with the hope that it will enable the development of isoform-specific sodium channel blockers, a promising treatment for chronic pain. Before advancements in the pharmacological field, an elucidation of the roles of Nav1.7 and Nav1.8 in the pathophysiology of pain states is required. Thus, the aim of this report is to present what is currently known about the contributions of these sodium channel subtypes in the pathophysiology of neuropathic and inflammatory pain. The electrophysiological properties and localisation of sodium channel isoforms is discussed. Research concerning the genetic links of Nav1.7 and Nav1.8 in acquired neuropathic and inflammatory pain states from the scientific literature in this field is reported. The role of Nav1.7 and Nav1.8 in the generation and maintenance of abnormal neuronal electrogenesis and hyperexcitability highlights the importance of these channels in the development of pathological pain. However, further research in this area is required to fully elucidate the roles of Nav1.7 and Nav1.8 in the pathophysiology of pain for the development of subtype-specific sodium channel blockers.

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