Scientists identify brain circuit for chronic pain transition

Researchers at the University of Colorado Boulder have pinpointed a brain region called the caudal granular insular cortex, or CGIC, that acts as a switch turning acute pain into chronic pain. In animal studies, disabling this circuit prevented chronic pain from developing or reversed it once established. The findings, published in the Journal of Neuroscience, open paths to new treatments beyond opioids.

A team led by Linda Watkins, a distinguished professor of behavioral neuroscience at the University of Colorado Boulder, studied the CGIC in rats with sciatic nerve injuries. They used advanced chemogenetic methods and fluorescent proteins to track and silence specific neurons. Shutting down the CGIC pathway stopped pain signals from persisting after the injury healed, eliminating symptoms like allodynia, where light touch feels painful. Watkins stated, 'If this crucial decision maker is silenced, chronic pain does not occur. If it is already ongoing, chronic pain melts away.'

Liittyvät artikkelit

Illustration of mitochondria transferring from glia to neurons to reduce nerve pain in neuropathy models.
AI:n luoma kuva

Duke-led Nature study links glia-to-neuron mitochondria transfer to reduced nerve pain in neuropathy models

Raportoinut AI AI:n luoma kuva Faktatarkistettu

Duke University researchers report that boosting the transfer of healthy mitochondria from support cells to sensory neurons reduced pain-like behaviors in mouse models of diabetic and chemotherapy-related peripheral neuropathy, an approach they say could address a root driver of nerve pain rather than simply blocking pain signals.

Researchers have identified a specific group of neurons in the amygdala that plays a central role in anxiety and social withdrawal. By restoring normal activity in this circuit, they reversed anxiety-related behaviors in mice. The findings point to a potential new target for treating emotional disorders.

Raportoinut AI

Researchers have uncovered a neural signal involving the TRPV4 molecule that tells the brain when scratching an itch has provided enough relief. Experiments in mice showed that without this signal, scratching episodes become prolonged even as overall frequency drops.

University of Oklahoma scientists report that the hormone FGF21 reduces body weight in obese mice by acting on a hindbrain pathway—centered on the nucleus of the solitary tract and area postrema—that relays signals to the parabrachial nucleus. The team says the mechanism overlaps anatomically with brain regions implicated in GLP-1 drugs, but appears to promote weight loss mainly by increasing metabolic rate rather than primarily suppressing food intake.

Raportoinut AI Faktatarkistettu

Researchers in Germany have developed an AI-based imaging and analysis system that can map nerves, immune cells, and dozens of organs across intact, transparent mice. In experiments on diet-induced obesity, the tool flagged structural damage in branches of the trigeminal (facial sensory) nerve alongside broad immune-cell changes, and the team reported related molecular signatures in human trigeminal tissue from people with obesity.

Tämä verkkosivusto käyttää evästeitä

Käytämme evästeitä analyysiä varten parantaaksemme sivustoamme. Lue tietosuojakäytäntömme tietosuojakäytäntö lisätietoja varten.
Hylkää