Chronic pain stemming from hypersensitivity to slight touch is often caused by injury or inflammation. This is a common and debilitating medical condition. Since the type of sensory neurons responsible for this persistent pain after injury and the molecular pathways involved are both unknown, patient treatment is limited to mitigating pain. However, Seal et al. have identified a specific subset of sensory neurons that express a rare transporter molecule called VGLUT3. This transporter enables neurons to release an excitatory neurotransmitter, glutamate. Researchers engineered mice that lack VGLUT3 and discovered that these mice no longer display injury-induced pain hypersensitivity. Conversely, researchers produced a different strain of mice that express VGLUT3 normally, but only in neurons that also emit a traceable green light. The VGLUT3-expressing neurons responded normally to light touch however, after injury, these neurons produced pain signals under similar conditions. This discovery suggests that drugs targeting the VGLUT3 pathway may inhibit the transmission of pain associated with hypersensitivity following injury.
Written by M.R.
