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M. V. Sanchez-Villarejo, I. Almansa, R. Lopez-Pedrajas, M. Muriach, M. Miranda, J. M. Genoves, J. M. Barcia, F. J. Romero Gomez; Naltrexone Restores Partially Changes in Retinal Function Induced by Chronic Alcohol Consumption. Invest. Ophthalmol. Vis. Sci. 2010;51(13):3316.
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Chronic consumption of alcohol is highly prevalent in our society. Dependence and abuse of alcohol are the mental illness more abundant in America. Naltrexone is an agent that blocks opioid receptors, and its use in animal models induces a decrease of the dopamine levels in the nucleus accumbens. Indeed, it has showed naltrexone decreases alcohol reinforcement. We studied possible changes in the retinal function after chronic ethanol exposure in adult rats, and the capacity of the naltrexone to prevent these changes.
Sixteen Sprague-Dawley rats received ethanol diet Lieber-De Carli during six weeks, whereas other group was treated with control diet. Half the control and ethanol animals were administered with naltrexone from day 28 to. Retinal function was assessed by electroretinogram (ERG) and evoked visual potential (VEP). The reduced glutathione (GSH) concentration and glutathione peroxidase activity was measured in eye in order to study the glutathione metabolism.
Ethanol increased ERG a-wave latency and decreased ERG b-wave and VEP amplitudes. However, naltrexone only improved ERG a-wave latency, even decreased by itself VEP amplitude in control animals. No change was observed in glutathione content and glutathione peroxidase activity was not altered in any case.
Retinal function may be affected by exposure to ethanol as demonstrated by changes in the ERG and VEP, naltrexone was able to prevent them only partially.
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