Ehrlich Tumor Induces TRPV1-Dependent Evoked and Non-Evoked Pain-like Behavior in Mice

Author:

Bertozzi Mariana M.ORCID,Saraiva-Santos Telma,Zaninelli Tiago H.,Pinho-Ribeiro Felipe A.,Fattori Victor,Staurengo-Ferrari Larissa,Ferraz Camila R.ORCID,Domiciano Talita P.,Calixto-Campos Cassia,Borghi Sergio M.ORCID,Zarpelon Ana C.,Cunha Thiago M.,Casagrande RubiaORCID,Verri Waldiceu A.ORCID

Abstract

We standardized a model by injecting Ehrlich tumor cells into the paw to evaluate cancer pain mechanisms and pharmacological treatments. Opioid treatment, but not cyclooxygenase inhibitor or tricyclic antidepressant treatments reduces Ehrlich tumor pain. To best use this model for drug screening it is essential to understand its pathophysiological mechanisms. Herein, we investigated the contribution of the transient receptor potential cation channel subfamily V member 1 (TRPV1) in the Ehrlich tumor-induced pain model. Dorsal root ganglia (DRG) neurons from the Ehrlich tumor mice presented higher activity (calcium levels using fluo-4 fluorescent probe) and an increased response to capsaicin (TRPV1 agonist) than the saline-injected animals (p < 0.05). We also observed diminished mechanical (electronic von Frey) and thermal (hot plate) hyperalgesia, paw flinching, and normalization of weight distribution imbalance in TRPV1 deficient mice (p < 0.05). On the other hand, TRPV1 deficiency did not alter paw volume or weight, indicating no significant alteration in tumor growth. Intrathecal injection of AMG9810 (TRPV1 antagonist) reduced ongoing Ehrlich tumor-triggered mechanical and thermal hyperalgesia (p < 0.05). Therefore, the contribution of TRPV1 to Ehrlich tumor pain behavior was revealed by genetic and pharmacological approaches, thus, supporting the use of this model to investigate TRPV1-targeting therapies for the treatment of cancer pain.

Funder

Fundação Araucária

Coordenação de Aperfeicoamento de Pessoal de Nível Superior

São Paulo Research Foundation

Fundação Nacional de Desenvolvimento do Ensino Superior Particular

National Council for Scientific and Technological Development

Publisher

MDPI AG

Subject

General Neuroscience

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