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The role of colinergic nicotinic receptors from hipoccampus in ethanol reinstatement in mice

Grant number: 18/02889-9
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): May 01, 2018
Effective date (End): December 31, 2018
Field of knowledge:Biological Sciences - Pharmacology - Neuropsychopharmacology
Principal Investigator:Fabio Cardoso Cruz
Grantee:Roberta Ayumi Maeda
Home Institution: Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil
Associated research grant:13/24986-2 - The role of neuronal ensembles in context-induced reinstatement of ethanol seeking: pharmacogenetic, optogenetic and molecular investigation, AP.JP

Abstract

Drug addiction is a global public health problem. According to World Health Organization, ethanol is the substance of abuse most consumed worldwide. There are evidences that reinforcing substances can be studied using conditioned place preference (CPP) in rodents. CPP reinstatement protocol can also be used as a relapse model in animals. Ethanol mechanism of action involves the activation of the mesocorticolimbic dopaminergic system and the extended amygdala. Therefore, like other substances of abuse, ethanol is able to activate ventral tegmental area (VTA) dopaminergic neurons promoting dopamine release in the nucleus accumbens (NAc). Similarly, studies demonstrate that VTA nicotinic receptors activation induce dopamine release in the NAc that appears to be mediated primarily by alpha4 beta2 receptors. Thus, the purpose of the present study is to investigate the role of cholinergic nicotinic receptors, such as alpha4 beta2, from hippocampus in the reinstatement of CPP induced by ethanol. To do so, we will perform hippocampal neurons phenotyping that are involved in CPP induced by ethanol. Also, this study aim to investigate the involvement of hippocampal cholinergic nicotinic receptors, such as alpha4 beta2, in the CPP reinstatement induced by ethanol through varenicline central injection - a partial cholinergic nicotinic receptors agonist.