| Grant number: | 15/02397-0 |
| Support Opportunities: | Regular Research Grants |
| Start date: | February 01, 2016 |
| End date: | July 31, 2018 |
| Field of knowledge: | Biological Sciences - Pharmacology - Neuropsychopharmacology |
| Principal Investigator: | Rosana Camarini |
| Grantee: | Rosana Camarini |
| Host Institution: | Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil |
| City of the host institution: | São Paulo |
Abstract
Environmental enrichment (EE) allows to study the influence of the environment in response to various manipulations, including the treatment of drug abuse. Our laboratory has shown that the EE is able to prevent and reverse the behavioral sensitization to ethanol in mice, and this was accompanied by decreased of Brain Derived Neurotrophic Factor (BDNF) in the prefrontal cortex of animals. One of the likely properties of the EE may involve its action on stress pathway. Stress plays a key role in addiction and relapse, and several studies indicate that ethanol is able to activate the HPA axis and increase levels of stress-related hormones such as CRF and corticosterone. This work aims to study the effects of EE on behavioral parameters (anxiety, depression, memory), on gene expression of Bdnf in the prefrontal cortex, and evaluate the role of the signaling pathway of BDNF on the protective effect of EE on ethanol-induced behavioral sensitization in the prefrontal cortex. The levels of oxytocin, distribution and quantification of OT receptors will also be assessed, as well as the conditioned place preference (CPP) to ethanol and to social stimuli under EE condition, and the role of the oxytocin on those parameters. Excessive drinking (relapse) of alcohol after a period of abstinence is a major feature of the process of addiction. Positive environmental conditions can help minimize cravings and withdrawal symptoms, however, negative conditions such as stress, may play a role in vulnerability to relapse. This study will also evaluate whether the EE modifies ethanol consumption after periods of abstinence and after stress. (AU)
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