Overview
- IISc researchers report in Cell Reports that a defined lateral hypothalamic neuron population activated by acute stress directly modulates itch in genetically engineered mice.
- Artificial activation of these neurons reduced scratching in both chloroquine-induced and psoriasis-like models, while silencing them abolished stress-driven itch relief, establishing necessity and sufficiency.
- Anterograde tracing mapped projections to key brainstem nodes involved in itch control, with targeted experiments identifying the periaqueductal gray as the predominant mediator.
- The same stress-sensitive neurons became hyper-excitable in psoriasis-like chronic inflammation and failed to suppress itch, providing a neural basis for stress-related worsening of persistent pruritus.
- The work remains preclinical in mice, activation also produced anxiety-like behavior, and the team plans molecular characterization and tests of additional stress modalities to inform future therapies.