Loss of Glutaminase 1 in Small Sensory Neurons Prevents Nerve Injury Induced Mechanical Allodynia: Insights From Conditional Knockout Mice
We generated a transgenic mouse with a specific deletion of the Gls1 gene in Nav1.8-expressing neurons to assess the role of peripheral GLS1 in pain transmission. GLS1 is not required for physiological pain but is essential for the development of mechanical allodynia after nerve injury. GLS1 is upregulated in nociceptors following nerve injury, suggesting enhanced glutamate signalling. Taken together, results suggest that targeting GLS1 expression in neuropathic conditions could be a potential therapeutic strategy.
Authors
- Carolina Roza (ORCID: https://orcid.org/0000-0001-5757-9066)
- Elsa Cisneros (ORCID: https://orcid.org/0000-0003-0584-7107)
- A.B. Martínez-Padilla (ORCID: https://orcid.org/0000-0002-4150-0349)
- Javier Márquez (ORCID: https://orcid.org/0000-0003-3317-3963)
- Miguel Á. Huerta (ORCID: https://orcid.org/0000-0003-2842-0085)
Institutions
- Universidad de Granada (ES)
- Universidad de Alcalá (ES)
- Instituto de Investigación Biosanitaria de Granada (ES)
- Universidad Internacional De La Rioja (ES)
- Instituto de Investigación Biomédica de Málaga (ES)
- Universidad de Málaga (ES)
Publication Details
- Journal
- European Journal of Pain
- Published
- 2025-06-24
- DOI
- https://doi.org/10.1002/ejp.70069
- Primary Topic
- Pain Mechanisms and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00
Funders
- Universidad de Alcalá
- Junta de Andalucía