The post-traumatic stress disorder (PTSD) may develop after exposure to severe trauma, resulting in debilitating symptoms such as difficulty in extinguishing aversive memories. The main therapy is cognitive-behavioral in order to facilitate the extinction of those memories. However, despite the severity of PTSD, this therapy, as well as pharmacotherapy, which may be associated with cognitive-behavioral therapy, are ineffective in many patients. In addition, pharmacotherapy is quite limited. These facts demonstrate the need to identify mechanisms altered by trauma that could serve as biomarkers and thus indicate new therapeutic targets to be explored. The neuroimmune and endocannabinoid (ECB) systems are altered in response to trauma in humans and animals. There is evidence of interactions between these systems in the modulation of stress responses, such as activation of microglia cells and changes in synaptic plasticity, which may result in synaptic dysfunction. One of the changes in the microglia that could contribute to these effects is the activation of the NLRP3 inflammassoma. The aim of this project is to evaluate if the pharmacological intervention in the ECB system associated with the extinction process 7 days after exposure to a potential traumatic event in mice is able to facilitate the extinction process and if there is alteration of the molecules of the ECB system and of the NLRP3 inflammassoma.
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