Correlational data suggests that learned associations are encoded within sparsely distributed patterns of neurons called neuronal ensembles that are selectively activated during learned behaviors. Until recently it has been difficult to prove that neuronal ensembles mediate learned behaviors because both traditional pharmacological and lesion methods, and newer optogenetic and chemo genetic methods alter activity of neurons regardless of whether they were selectively activated or not during learned behaviors. Additionally, previous studies on synaptic and molecular alterations induced by learning did not distinguish between behaviorally activated and non-activated neurons. Based on these considerations, we propose to combine some methodologies, considered as state-of-art (overlap, optogenetic regulation, causal role experiments, c-Fos::teop-Cre and LacZ rats) to assess different aspects of ensemble-specific neuroadaptations in different brain areas in context-induced reinstatement of alcohol seeking. Understanding the role of these neuronal ensembles in behavior and the ways that repeated drug administration alters them will help us to understand how drugs of abuse produce the learned behaviors associated with addiction. Here, we will investigate context-specific sets of neurons, so-called neuronal ensembles that are involved to alcohol self-administration training context or extinction context. For that, we will use the pharmacogenetic (beta-galactosidase) and optogenetic protein (channel rhodopsin), in these neuronal ensembles, to selectively inhibite the memories associated with alcohol taking or extinction of alcohol seeking.
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