“The current opioid crisis emphasizes the need for nonaddictive pain treatments. Here Perez-Sanchez and colleagues evaluated whether direct inhibition of pain-related hyperactivity in sensory neurons could be such a targeted pain treatment strategy. The authors expressed PSAM4-GlyR, a chemogenetic system based on the human nicotinic acetylcholine and glycine receptors, in mouse sensory neurons. PSAM4-GlyR activation with the FDA-approved drug varenicline inhibited sensory neurons and improved acute, inflammatory, and neuropathic pain-related behaviors in mice. PSAM4-GlyR activation also inhibited human-derived sensory neurons and normalized hyperactivity in sensory neurons derived from a patient with erythromelalgia, a condition characterized by burning pain. Although further validation in human pain models is needed, these results suggest the potential of PSAM4-GlyR in gene therapy for pain treatment.” — Daniela Neuhofer, Editor’s Summary
Read more on “A humanized chemogenetic system inhibits murine pain-related behavior and hyperactivity in human sensory neurons” via Science Translational Medicine.
Family Medicine Residency Site: Abbotsford-Mission 