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      Consumo de alcohol en ratas adolescentes tratadas con reserpina y fluoxetina Translated title: Alcohol consumption in adolescent rats treated with reserpine and fluoxetine

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          Abstract

          RESUMEN Si bien se ha estudiado el vínculo entre los trastornos de estado de ánimo y el consumo de alcohol, tanto en humanos como en animales, todavía no es del todo claro cómo se da esta relación, y menos aún durante la adolescencia. La administración de reserpina, un depletor de monoaminas, es un modelo ampliamente utilizado en roedores adultos para inducir comportamientos asociados a depresión, pero se desconoce su utilidad en otras etapas del desarrollo. En este trabajo validamos este modelo en ratas adolescentes y posteriormente estudiamos el consumo de alcohol en estos animales, así como su modulación por antidepresivos. En el experimento 1 se administró reserpina (0.0 o 1.0 mg/kg, durante 4 días, IP) a ratas Wistar machos de 30 días. El consumo de alcohol fue evaluado luego de observar comportamientos asociados a depresión e indagar indicadores neuroendocrinos de esta patología. En el experimento 2 los animales recibieron reserpina, seguida por el antidepresivo fluoxetina (0.0 o 10.0 mg/kg, durante 4 días, IG), y luego se evaluó el consumo de alcohol. Los resultados mostraron que la reserpina aumentó significativamente los comportamientos asociados a depresión y alteró los niveles de dopamina en la corteza insular y de hormonas tiroideas en sangre. En la prueba de consumo de alcohol los animales deprimidos, pero no los controles, mostraron un incremento en el consumo a través de los días. El segundo experimento replicó parcialmente este perfil, y no se observó un efecto significativo del antidepresivo en el consumo de alcohol. Los resultados indican que la reserpina es útil para modelar en ratas adolescentes comportamientos asociados a depresión. Se encontró una relación entre este estado y el consumo de alcohol, que no se pudo revertir con antidepresivos.

          Translated abstract

          ABSTRACT The relationship between mood disorders and alcohol consumption has been studied in humans and animals, although it is still not fully clear how this relationship unfolds, much less during adolescence. The administration of reserpine -a monoamine depletor- is an approach traditionally used in adult rodents to induce depression-associated behaviours, but its usefulness in other developmental stages is still unknown. In this study, this model was evaluated in adolescent rats in order to study alcohol consumption, as well as its modulation by antidepressants in these animals. In Experiment 1, 30 day-old male Wistar rats were treated with reserpine (0.0 or 1.0 mg/kg, for4 days, IP). Alcohol consumption was tested after observing depression-associated behaviours and assessing neuroendocrine indicators of this pathology. In Experiment 2, the rats were administered reserpine followed by an antidepressant (fluoxetine, 0.0 or 10.0 mg/kg, for 4 days, IG). Alcohol consumption was then tested. The results showed that reserpine significantly increased depression-associated behaviours and altered insular dopamine and thyroid hormone levels. Alcohol consumption tests showed that reserpine-treated animals -but not control animals- increased their consumption throughout the days. The second experiment partially replicated this profile, and no significant effect of antidepressants was observed in alcohol consumption. The results show that reserpine is instrumental in modelling depression-associated behaviours in adolescent rats. A relationship was found between this condition and alcohol intake, which could not be reversed by antidepressants.

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          Most cited references 73

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          To successfully negotiate the developmental transition between youth and adulthood, adolescents must maneuver this often stressful period while acquiring skills necessary for independence. Certain behavioral features, including age-related increases in social behavior and risk-taking/novelty-seeking, are common among adolescents of diverse mammalian species and may aid in this process. Reduced positive incentive values from stimuli may lead adolescents to pursue new appetitive reinforcers through drug use and other risk-taking behaviors, with their relative insensitivity to drugs supporting comparatively greater per occasion use. Pubertal increases in gonadal hormones are a hallmark of adolescence, although there is little evidence for a simple association of these hormones with behavioral change during adolescence. Prominent developmental transformations are seen in prefrontal cortex and limbic brain regions of adolescents across a variety of species, alterations that include an apparent shift in the balance between mesocortical and mesolimbic dopamine systems. Developmental changes in these stressor-sensitive regions, which are critical for attributing incentive salience to drugs and other stimuli, likely contribute to the unique characteristics of adolescence.
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            Modeling of human neuropsychiatric disorders in animals is extremely challenging given the subjective nature of many symptoms, the lack of biomarkers and objective diagnostic tests, and the early state of the relevant neurobiology and genetics. Nonetheless, progress in understanding pathophysiology and in treatment development would benefit greatly from improved animal models. Here we review the current state of animal models of mental illness, with a focus on schizophrenia, depression and bipolar disorder. We argue for areas of focus that might increase the likelihood of creating more useful models, at least for some disorders, and for explicit guidelines when animal models are reported.
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              Dopamine (DA) is considered crucial for the rewarding effects of drugs of abuse, but its role in addiction is much less clear. This review focuses on studies that used PET to characterize the brain DA system in addicted subjects. These studies have corroborated in humans the relevance of drug-induced fast DA increases in striatum [including nucleus accumbens (NAc)] in their rewarding effects but have unexpectedly shown that in addicted subjects, drug-induced DA increases (as well as their subjective reinforcing effects) are markedly blunted compared with controls. In contrast, addicted subjects show significant DA increases in striatum in response to drug-conditioned cues that are associated with self-reports of drug craving and appear to be of a greater magnitude than the DA responses to the drug. We postulate that the discrepancy between the expectation for the drug effects (conditioned responses) and the blunted pharmacological effects maintains drug taking in an attempt to achieve the expected reward. Also, whether tested during early or protracted withdrawal, addicted subjects show lower levels of D2 receptors in striatum (including NAc), which are associated with decreases in baseline activity in frontal brain regions implicated in salience attribution (orbitofrontal cortex) and inhibitory control (anterior cingulate gyrus), whose disruption results in compulsivity and impulsivity. These results point to an imbalance between dopaminergic circuits that underlie reward and conditioning and those that underlie executive function (emotional control and decision making), which we postulate contributes to the compulsive drug use and loss of control in addiction.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Journal
                suma
                Suma Psicológica
                Suma Psicol.
                Fundación Universitaria Konrad Lorenz (Bogotá, , Colombia )
                0121-4381
                June 2017
                : 24
                : 1
                : 67-77
                Affiliations
                Córdoba orgnameInstituto de Investigación Médica M. y M. Ferreyra Argentina
                Montevideo Montevideo orgnameUniversidad de la República orgdiv1Facultad de Veterinaria Uruguay
                Article
                S0121-43812017000100067
                10.1016/j.sumpsi.2016.12.002

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 76, Pages: 11
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