bioRxiv · 10.1101/2021.02.22.432248
The non-benzodiazepine anxiolytic etifoxine limits the sensory-affective expression of pain following streptozotocin-induced diabetic neuropathy
Abstract
More than 450 million people worldwide suffer from diabetes, or 1 in 11 people. Chronic hyperglycemia degrades patients quality of life and the development of neuropathic pain contributes to the burden of this disease. In this study, we used the mouse model of streptozocin-induced diabetic type 1 neuropathy to assess the analgesic potential of etifoxine. Etifoxine is a prescribed anxiolytic that increases GABAAA receptor function through a direct positive allosteric modulation effect and, indirectly, by stimulating the production of endogenous GABAA receptor positive modulators such as allopregnanolone-type neurosteroids. We show that a curative or preventive treatment strongly and durably reduces mechanical hyperalgesia and anxiety in diabetic neuropathic mice. This analgesic and neuroprotective effect on painful symptoms and emotional comorbidities is promising and should now be clinically evaluated.
Source connections
Explore related subjects
Keep this discovery
Explore connections, maps & timelines
Gazzo, G., Salgado-Ferrer, M., Poisbeau, P.. 2021-02-22. The non-benzodiazepine anxiolytic etifoxine limits the sensory-affective expression of pain following streptozotocin-induced diabetic neuropathy. https://doi.org/10.1101/2021.02.22.432248
Cite the original work for its findings. Save a collection to share your selection of sources.