Dagnino et al 2020 Kinin and reserpine.pzfx

Fibromyalgia-like models in mice induced by reserpine opened a new avenue to better understand the molecular mechanism behind this complex better and incapacitate pain syndrome. Kinin B1 receptor (B1R) contributes to mechanical allodynia and acute coping behavior in mice under inflammatory and immunological conditions. The present study added new results that confirm a recently published study by Brusco et al. (2019). This study replicated our previous data where amine depletion induced by reserpine significantly decreased the dopamine and serotonin levels in prefrontal cortex (PFC), hippocampus (HPC), and spinal cord of mice. The animals submitted to the reserpine fibromyalgia model also showed a decrease of paw withdrawal threshold (PWT) and increased the immobility time in the forced swimming test (FST). The genetic deletion of B1R or pharmacological blockade by selective kinin B1R antagonist R-715 (acute i.p. treatment) counteracted the mechanical allodynia and increased immobility time induced by reserpine. However, neither pharmacological nor genetic inhibition of B1R reversed the monoamine depletion. Our data confirm that reserpine induced a fibromyalgia-like phenotype in mice and the role of B1R on the acute coping behavior and nociception modulation.