Project: To study the participation of environmental pollutants in vulnerability to addiction in animal models.
Linked Target: To study whether environmental contaminants can facilitate the incidence of addictive behaviors in laboratory animals.
General description: Addiction is currently recognized as a neurobiological disease where repetitive abuse of psychoactive substances corrupts the normal reward circuitry. Psychoactive substances are all those chemical substances that can modify mood, sleep/wakefulness, activity level, etc. Environmental factors such as acute or chronic stress affect this dopaminergic reward system and increase the risk of psychoactive substance use and relapse. Various studies support the idea that exposure to environmental pollution can contribute to cognitive and psychiatric disorders, some associate exposure to environmental pollution and substance abuse. Likewise, the use of pesticides in agriculture is related to several CNS disorders associated with dopaminergic neurotransmission, such as Parkinson's disease and Attention Deficit/Hyperactivity Disorder. Dopamine (DA) is the critical neurotransmitter in the reward circuit that mediates substance abuse, thus exposure to certain environmental neurotoxins could influence the development of drug addiction. For decades our Laboratory studied the neurotoxic effects of the herbicide 2,4-Dichlorophenoxyacetic acid (2,4-D) in animal models. He was the first to demonstrate that chronic exposure to 2,4D induced behavioral and neurochemical changes associated with the modification of dopaminergic neurotransmission. For some years now, he has also been studying the long-term effects of cocaine in an animal model that makes it possible to identify the neuroadaptations that would underlie the behavioral changes observed in addiction, allowing the behavioral changes to be related to the molecular ones. He was the first to describe the participation of the Wnt/B-catenin signaling pathway in long-term neuroadaptations induced by cocaine and stress. Suggesting that this signaling pathway has an important role in vulnerability to the effect of drugs. This evidence has directed our interest towards the study of the impact of environmental pollutants, especially the herbicide 2,4-D, widely used in our country, on vulnerability to the development of addiction. For this, we will use this model that allows us to identify the neuroadaptions induced by cocaine, in rats previously exposed to environmental contaminants through food and thus be able to evaluate: 1) if the exposure to environmental contaminants in the evaluated periods produces an increase in the response to cocaine known as sensitization; 2) whether environmental pollutants produce alterations in dopaminergic neurotransmission in brain areas involved in addiction; 3) if effectors of the Wnt signaling pathways are involved in this increase in vulnerability; 4) whether exposure to environmental pollutants induces behavioral changes.
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Director: Cintia N. Konjuh
Members: Alejandra M. Pacchioni, Alejandrina Funes, Abraham Ramírez, Lucía Trossero.
Spaces/Institutions/Academic Units: Faculty of Biochemical and Pharmaceutical Sciences (UNR)
Contact
ckonjuh@fbioyf.unr.edu.ar