Pain management by chemogenetic control of sensory neurons

Cell Rep Med. 2023 Dec 19;4(12):101338. doi: 10.1016/j.xcrm.2023.101338.

Abstract

In this study, Perez-Sanchez et al.1 developed a chemogenetic method aimed at alleviating pain in mouse models while dampening excitability in human sensory neurons. This analgesic effect was attained through the introduction of human α7 nicotinic acetylcholine receptor and glycine receptor pore domain via virus-mediated expression in sensory neurons, forming a chloride channel. The activation of this channel was made possible by specific agonists. This study highlights the potential for treating clinical pain by gene therapy.

Publication types

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Animals
  • Humans
  • Mice
  • Pain / drug therapy
  • Pain Management*
  • Sensory Receptor Cells*
  • alpha7 Nicotinic Acetylcholine Receptor / agonists
  • alpha7 Nicotinic Acetylcholine Receptor / physiology

Substances

  • alpha7 Nicotinic Acetylcholine Receptor