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Mario Francis Rivera Meza

Profesor Asistente

Universidad de Chile

Santiago, Chile

Líneas de Investigación


Alcoholism; Gene Therapy; Pharmacology; Alcohol intake; Drug Dependence; Gene Therapy of Alcoholism; Mechanisms of Alcohol Addiction; Vectors for Gene Therapy; Farmacologia (Neurofarmacologia); Neuroquimica; Neurociencias; Alcoholism, animal models and interventions in humans; Mechanism of alcohol actions; Gene delivery and phage display libraries

Educación

  •  Químico Farmacéutico, UNIVERSIDAD DE CHILE. Chile, 1998
  •  Doctorado en Farmacología, UNIVERSIDAD DE CHILE. Chile, 2009
  •  Diplomado en Innovación y Docencia Universitaria, UNIVERSIDAD DE CHILE. Chile, 2019

Experiencia Académica

  •   Profesor Asistente Full Time

    UNIVERSIDAD DE CHILE

    Ciencias Químicas y Farmacéuticas

    Santiago, Chile

    2015 - A la fecha

  •   Investigador Postdoctoral Full Time

    UNIVERSIDAD DE CHILE

    Medicina

    Santiago, Chile

    2010 - 2015


 

Article (24)

Activation of mitochondrial aldehyde dehydrogenase (ALDH2) by ALDA-1 reduces both the acquisition and maintenance of ethanol intake in rats=> A dual mechanism?
Fenofibrate -a PPARα agonist- increases alcohol dehydrogenase levels in the liver: implications for its possible use as an ethanol-aversive drug
Gene and cell therapy on the acquisition and relapse-like binge drinking in a model of alcoholism=> translational options.
Molecular modeling of salsolinol, a full Gi protein agonist of the μ-opioid receptor, within the receptor binding site
Silencing brain catalase expression reduces ethanol intake in developmentally-lead-exposed rats.
UFR2709, a Nicotinic Acetylcholine Receptor Antagonist, Decreases Ethanol Intake in Alcohol-Preferring Rats
Erysodine, a competitive antagonist at neuronal nicotinic acetylcholine receptors, decreases ethanol consumption in alcohol-preferring UChB rats.
Acquisition, Maintenance and Relapse-Like Alcohol Drinking=> Lessons from the UChB Rat Line.
Fenofibrate administration reduces alcohol and saccharin intake in rats=> possible effects at peripheral and central levels
Racemic Salsolinol and its Enantiomers Act as Agonists of the mu-Opioid Receptor by Activating the Gi Protein-Adenylate Cyclase Pathway.
(R)-Salsolinol, a product of ethanol metabolism, stereospecifically induces behavioral sensitization and leads to excessive alcohol intake.
Beyond the "First Hit": Marked Inhibition by N-Acetyl Cysteine of Chronic Ethanol Intake But Not of Early Ethanol Intake. Parallel Effects on Ethanol-Induced Saccharin Motivation.
Long-term inhibition of ethanol intake by the administration of an aldehyde dehydrogenase-2 (ALDH2)-coding lentiviral vector into the ventral tegmental area.
PPAR-alpha agonists reduce alcohol drinking: do they act in the brain or in the liver?
The “first hit” against alcohol reinforcement: role of ethanol metabolites.
Overexpression of Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels into the Ventral Tegmental Area Increases the Rewarding Effects of Ethanol in UChB Drinking Rats
Salsolinol, free of isosalsolinol, exerts ethanol-like motivational/sensitization effects leading to increases in ethanol intake.
Gene specific modifications unravel ethanol and acetaldehyde actions.
The alcohol deprivation effect: marked inhibition by anticatalase gene administration into the ventral tegmental area in rats.
Reduction of ethanol consumption in alcohol-preferring rats by dual expression gene transfer.
Reward and relapse: complete gene-induced dissociation in an animal model of alcohol dependence.
Acetaldehyde burst protection of ADH1B*2 against alcoholism: An additional hormesis protection against esophageal cancers following alcohol consumption?
Ethanol as a prodrug: brain metabolism of ethanol mediates its reinforcing effects.
Mechanism of protection against alcoholism by an alcohol dehydrogenase polymorphism: development of an animal model.

BookSection (1)

The Hyperpolarization-Activated Cyclic Nucleotide-Gated Ion Channels in the Rewarding Effects of Ethanol

Proyecto (6)

A common mechanism for alcohol- and nicotine-use disorders: translational options
Pharmacological activation of aldehyde dehydrogenase=> mechanism involved in the reduction of ethanol consumption
A NEW PHARMACOLOGIC STRATEGY FOR THE TREATMENT OF ALCOHOLISM=> STUDIES IN ANIMAL MODELS
REBOUND OF THE OPIATE SYSTEM AS RESPONSIBLE FOR BINGE-DRINKING IN THE ALCOHOL DEPRIVATION EFFECT.
REWARDING MOLECULES GENERATED FROM ETHANOL IN THE BRAIN
GENE SILENCING OF HCN CHANNELS AND ITS EFFECTS ON THE STIMULATING AND REWARDING EFFECTS OF ETHANOL
5
Mario Rivera

Profesor Asistente

Química Farmacológica y Toxicológica

Universidad de Chile

Santiago, Chile