<?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>S0185-33252016000100047</article-id>
<article-id pub-id-type="doi">10.17711/SM.0185-3325.2015.067</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Neurobiología de la depresión mayor y de su tratamiento farmacológico]]></article-title>
<article-title xml:lang="en"><![CDATA[Neurobiology of major depression and its pharmacologic treatment]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cruzblanca Hernández]]></surname>
<given-names><![CDATA[Humberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Lupercio Coronel]]></surname>
<given-names><![CDATA[Patricia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Collas Aguilar]]></surname>
<given-names><![CDATA[Jorge]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Castro Rodríguez]]></surname>
<given-names><![CDATA[Elena]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad de Colima Centro Universitario de Investigaciones Biomédicas ]]></institution>
<addr-line><![CDATA[Colima Col.]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>02</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>02</month>
<year>2016</year>
</pub-date>
<volume>39</volume>
<numero>1</numero>
<fpage>47</fpage>
<lpage>58</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0185-33252016000100047&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0185-33252016000100047&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0185-33252016000100047&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen:  INTRODUCCIÓN: La depresión mayor (DM) se debe a la interacción de factores ambientales, genéticos y epigenéticos, que atenúan la transmisión monoaminérgica en el cerebro. Sin embargo, poco se conoce sobre los mecanismos fisiopatológicos que subyacen a ella.  OBJETIVO: Proponer una visión integral sobre la fisiopatología de la DM y los mecanismos de acción de los fármacos antidepresivos.  MÉTODO: Se empleó la base PubMed para la búsqueda bibliográfica. La mayoría son investigaciones experimentales y estudios de genética molecular o de imágenes cerebrales en humanos.  RESULTADOS: La DM se asocia con: i) menor volumen de la corteza cingulada anterior; ii) hiper-metabolismo del área Cg25; iii) menor expresión del receptor 5-HT1A; iv) mayor expresión de la monoamino oxidasa A. Algunos polimorfismos están asociados a la fisiopatología. El estrés crónico reduce la expresión del 5-HT1A. Los antidepresivos atenúan el hiper-metabolismo del área Cg25, estimulan la neurogénesis y activan la vía del AMPc. Encontramos que la imipramina aumenta y reduce la expresión de    G  &#945; s y    G  &#945; z, respectivamente (datos sin publicar).  DISCUSIÓN Y CONCLUSIÓN: El déficit en la transmisión monoaminérgica puede deberse a: i) el polimorfismo G1463A en el gen de la enzima hTPH2 que reduce la síntesis de serotonina; ii) el polimorfismo C(-1019)G en el gen del receptor 5-HT1A, aumentando su transcripción en el rafé e implicando menor liberación del neurotransmisor; iii) mayor degradación de las monoaminas. La menor expresión del receptor 5-HT1A se discute considerando su acción inhibitoria en la corteza prefrontal. Los cambios en la expresión de    G  &#945; s y    G  &#945; z coinciden con la estimulación de la vía del AMPc.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract:  INTRODUCTION: The major depressive disorder (MDD) arises from the interaction of environmental, genetic and epigenetic factors, producing a deficit in monoaminergic transmission within the brain. However, our understanding of its pathophysiology is quite limited.  OBJECTIVE: To reach an integrative view of the MDD pathophysiology, as well as the mechanisms of action of antidepressant drugs.  METHOD: We used the PubMed database to search for the documents by using the appropriate key words. Most of them are experimental research and molecular genetics and brain imaging studies in humans.  RESULTS: The pathophysiology of MDD is characterized by: i) shrinkage of the cingulate anterior cortex; ii) hyper-metabolism of the Cg25 area; iii) lower expression of the 5-HT1A receptor; iv) enhanced expression of monoamine oxidase A. Besides, certain gene polymorphisms are strongly linked to the pathophysiology, and there is evidence that 5-HT1A receptor expression is reduced by psychological stress. Antidepressants reverse the hyper-metabolic state of Cg25, stimulate neurogenesis and the cAMP pathway. We found that imipramine increases and reduces the expression of    G  &#945; s and    G  &#945; z, respectively (data no published).  DISCUSSION AND CONCLUSION: The disruption in monoaminergic transmission could be mediated by: i) the G1463A hTPH2 polymorphism that reduces the serotonin synthesis; ii) the C(-1019)G 5-HT1A polymorphism that increases the receptor expression in the dorsal rafe, and reduces serotonin release; iii) an increase in monoamine degradation. The reduced 5-HT1A expression is discussed considering its inhibitory properties in the prefrontal cortex. The effects of imipramine on    G  &#945; s and    G  &#945; z are in agreement with the antidepressant-induced stimulation of the cAMP pathway.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Depresión mayor]]></kwd>
<kwd lng="es"><![CDATA[fármacos antidepresivos]]></kwd>
<kwd lng="es"><![CDATA[serotonina]]></kwd>
<kwd lng="es"><![CDATA[estrés]]></kwd>
<kwd lng="es"><![CDATA[neuronas]]></kwd>
<kwd lng="en"><![CDATA[Major depression]]></kwd>
<kwd lng="en"><![CDATA[antidepressant drugs]]></kwd>
<kwd lng="en"><![CDATA[serotonin]]></kwd>
<kwd lng="en"><![CDATA[stress]]></kwd>
<kwd lng="en"><![CDATA[neurons]]></kwd>
</kwd-group>
</article-meta>
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