<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0185-3325</journal-id>
<journal-title><![CDATA[Salud mental]]></journal-title>
<abbrev-journal-title><![CDATA[Salud Ment]]></abbrev-journal-title>
<issn>0185-3325</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0185-33252015000300167</article-id>
<article-id pub-id-type="doi">10.17711/SM.0185-3325.2015.024</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[¿La exposición crónica al alcohol induce neurodegeneración en el Sistema Nervioso Central de la rata?]]></article-title>
<article-title xml:lang="en"><![CDATA[Does chronic alcohol exposure induce neurodegeneration in the rat Central Nervous System?]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hernández-Fonseca]]></surname>
<given-names><![CDATA[Karla]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Martinell]]></surname>
<given-names><![CDATA[Paula]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Reyes-Guzmán]]></surname>
<given-names><![CDATA[Cosette]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Méndez]]></surname>
<given-names><![CDATA[Milagros]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz Subdirección de Investigaciones Clínicas Departamento de Neuroquímica]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>MX</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2015</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2015</year>
</pub-date>
<volume>38</volume>
<numero>3</numero>
<fpage>167</fpage>
<lpage>176</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0185-33252015000300167&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0185-33252015000300167&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0185-33252015000300167&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Antecedentes: La exposición crónica al alcohol se asocia con procesos neurotóxicos y neurodegenerativos relacionados con disfunciones cognitivas y de memoria. El daño inducido por alcohol depende de los patrones de consumo de etanol. La exposición prolongada al alcohol induce daño en distintas regiones cerebrales (cortezas prefrontal, perirrinal, entorrinal y parahipocampal, tálamo, hipotálamo, hipocampo y cerebelo) en pacientes alcohólicos y modelos animales de alcoholismo. Sin embargo, no se han estudiado las regiones cerebrales asociadas con el circuito de reforzamiento y recompensa de drogas de abuso.Objetivo: Investigar si la exposición crónica al alcohol induce daño neurodegenerativo en el cerebro de la rata, en particular en el sistema mesocorticolímbico y la amígdala.Método: Ratas Wistar macho fueron expuestas a etanol (10% v/v) o agua por consumo oral durante 30 días y se les privó de la droga por 0, 24 y 48h. Los animales fueron sacrificados y se les extrajo la sangre troncal y el cerebro. Para evaluar el daño neurodegenerativo, se utilizó el marcador fluorescente Fluoro-Jade B. La concentración de alcohol en sangre se determinó por espectrofotometría.Resultados: Se observó un escaso número de células positivas a Fluoro-Jade en las cortezas piriforme y frontal de asociación, el caudado-putamen y el tálamo dorsal. No se encontraron diferencias entre el tratamiento crónico o la privación de alcohol versus el grupo control.Discusión y conclusión: La exposición crónica al alcohol no indujo neurodegeneración en las condiciones utilizadas en este estudio. Probablemente, las concentraciones de alcohol en sangre alcanzadas durante el tratamiento no fueron suficientes para inducir muerte celular.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Background: Chronic alcohol exposure is associated to neurotoxic and neurodegenerative mechanisms that lead to several cognitive and memory dysfunctions. Alcohol-induced damage depends on ethanol consumption patterns. Prolonged alcohol exposure induces damage in distinct brain regions (prefrontal, perirhinal, entorhinal and parahippocampal cortices, thalamus, hypothalamus, hippocampus and cerebellum) in both alcoholic patients and animal models of alcoholism. However, brain areas of the drug reinforcement and reward circuit have not been investigated.Objective: To investigate if chronic alcohol exposure induces neurodegenerative damage in the rat brain, particularly in the mesocorticolimbic system and the amygdala.Method: Male Wistar rats were exposed to ethanol (10% v/v) or water by oral consumption during 30 days. In another set of experiments, animals similarly treated with ethanol were withdrawn from the drug for 24 and 48 h. At the end of the treatments, animals were sacrificed, whole blood samples were obtained and the brains were removed. A fluorescence marker (Fluoro-Jade B) was used to assess neurodegenerative damage in the brain. Blood alcohol concentration was evaluated by spectrophotometry.Results: We observed a low number of Fluoro-Jade B positive cells in different brain regions, including the piriform cortex, frontal cortex of association, caudate-putamen and dorsal thalamus. No differences were found between chronic alcohol or ethanol withdrawn groups versus control animals.Discussion and conclusion: Our results suggest that chronic alcohol exposure does not induce neurodegeneration under the present experimental conditions. Alcohol blood concentrations attained during treatment may not be sufficient to induce cell death.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Alcohol]]></kwd>
<kwd lng="es"><![CDATA[etanol]]></kwd>
<kwd lng="es"><![CDATA[tratamiento crónico]]></kwd>
<kwd lng="es"><![CDATA[daño celular]]></kwd>
<kwd lng="es"><![CDATA[neurodegeneración]]></kwd>
<kwd lng="en"><![CDATA[Alcohol]]></kwd>
<kwd lng="en"><![CDATA[ethanol]]></kwd>
<kwd lng="en"><![CDATA[chronic treatment]]></kwd>
<kwd lng="en"><![CDATA[cell damage]]></kwd>
<kwd lng="en"><![CDATA[neurodegeneration]]></kwd>
</kwd-group>
</article-meta>
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