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Possible involvement of the endocannabinoid signaling in the treatment-resistant behaviors induced in flinders sensitive line rats by exposure to a traumatic stressor

Grant number: 19/27458-3
Support type:Scholarships abroad - Research Internship - Scientific Initiation
Effective date (Start): April 01, 2020
Effective date (End): July 31, 2020
Field of knowledge:Biological Sciences - Pharmacology - Neuropsychopharmacology
Principal researcher:Sabrina Francesca de Souza Lisboa
Grantee:Arthur Alves Coelho
Supervisor abroad: Gregers Wegener
Home Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Research place: Aarhus University, Denmark  
Associated to the scholarship:19/12830-4 - Evaluation of the possible facilitation of the conditioned fear extinction response after trauma by drugs that modulate the endocannabinoid signaling, BP.IC


Stress exposure has been closely associated with the development of several psychiatric conditions, such as depression and post-traumatic stress disorder (PTSD). Stress causes several neuroimmunoendocrine axis dysfunctions, leading to biomolecular and behavioral changes. Some changes that occur in PTSD include decreased endocannabinoid signaling in brain regions such as the hippocampus, medial prefrontal cortex, and amygdala. In addition, there is also evidence of alterations in the immune system. There is a strong relationship between PTSD and depression. Both conditions are treated with antidepressant and psychological counseling, although the majority will not achieve remission. Moreover, recent studies have shown that the comorbidity increases the chance of treatment-resistant depression development, making treatment even more difficult. Based on this, we hypothesized that association between depression and PTSD may also generate resistance to the treatment of PTSD-related behaviors, such as the deficit of fear memory extinction. We suggest that decreased endocannabinoid signaling and increased proinflammatory signaling may be involved in this process. Therefore, we intend to combine a genetic rat model of depression to a PTSD paradigm to evaluate if there is resistance to facilitation of fear extinction by a conventional antidepressant treatment, and if this is correlated with alteration in endocannabinoid and immune molecules expression in the brain. Moreover, we will investigate whether a drug that increases endocannabinoid signaling via cannabinoid CB1 receptors, but blocks vanilloid TRPV1 receptors, could facilitate fear extinction. (AU)

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