<?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>2954-4122</journal-id>
<journal-title><![CDATA[Archivos de neurociencias (México)]]></journal-title>
<abbrev-journal-title><![CDATA[Arch. Neurocien. (Mex.)]]></abbrev-journal-title>
<issn>2954-4122</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Neurología y Neurocirugía "Manuel Velasco Suárez"]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S2954-41222024000300067</article-id>
<article-id pub-id-type="doi">10.24875/anc.m24000002</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Disminución de la inmunorreactividad a la subunidad &#946;2 del receptor GABAA en un modelo de autismo en ratas]]></article-title>
<article-title xml:lang="en"><![CDATA[Decreased GABAA receptor &#946;2 subunit immunoreactivity in a rat model of autism]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Puig-Lagunes]]></surname>
<given-names><![CDATA[Ángel A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Villada]]></surname>
<given-names><![CDATA[Frida S.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Morgado-Valle]]></surname>
<given-names><![CDATA[Consuelo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Beltran-Parrazal]]></surname>
<given-names><![CDATA[Luis]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Chi-Castañeda]]></surname>
<given-names><![CDATA[Lizbeth D.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López-Meraz]]></surname>
<given-names><![CDATA[María L.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Veracruzana Facultad de Medicina ]]></institution>
<addr-line><![CDATA[Minatitlán ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Veracruzana Instituto de Investigación Cerebral ]]></institution>
<addr-line><![CDATA[Xalapa ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2024</year>
</pub-date>
<volume>29</volume>
<numero>3</numero>
<fpage>67</fpage>
<lpage>73</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2954-41222024000300067&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2954-41222024000300067&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2954-41222024000300067&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Antecedentes: El ácido gamma-aminobutírico (GABA) es el principal neurotransmisor inhibitorio del cerebro; la activación de los receptores GABA tipo A (GABAA) media sus acciones inhibitorias rápidas. Los individuos con trastorno del espectro autista (TEA) presentan anomalías en la expresión de los receptores GABAA en diversas áreas cerebrales. Asimismo, modelos animales de TEA sugieren alteraciones en la neurotransmisión GABAérgica y una desregulación en el equilibrio entre los sistemas inhibitorios y excitatorios.  Objetivo: Investigar la inmunoreactividad a la subunidad &#946;2 del receptor GABAA (GARB2) en el hipocampo, la amígdala y el tálamo de ratas infantes expuestas prenatalmente a ácido valproico (AVP) como modelo de TEA.  Método: Las hembras gestantes se inyectaron con AVP (600mg/Kg, i.p. grupo AVP) durante el día embrionario 12; las ratas control se inyectaron con salina (grupo SS). A los 14 días posnatales, las ratas de ambos grupos se perfundieron con NaCl 0.9% y paraformaldehído 4%, y se obtuvieron secciones cerebrales coronales (40&#956;m de grosor). Se realizó inmunohistoquímica para detectar a GARB2.  Resultados: Se identificó una disminución de la inmunoreactividad a GARB2 en el núcleo amigdaloide lateral, así como en los núcleos talámicos ventral y lateral del grupo AVP en comparación con el grupo SS. No se detectaron diferencias en el hipocampo.  Conclusión: Los hallazgos sugieren que la exposición prenatal al AVP reduce la inmunoreactividad de GARB2 en regiones cerebrales límbicas implicadas en comportamientos socioemocionales, similar a informes previos en individuos con TEA. Nuestros resultados apoyan la implicación del sistema GABAérgico en la patogénesis del TEA.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Background: Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the brain, and activation of GABA type A (GABAA) receptors mediates rapid inhibitory actions. Numerous studies have shown that individuals with autism spectrum disorder (ASD) exhibit abnormalities in the expression of GABAA receptors in several brain areas. In addition, animal models of ASD have suggested alterations in GABAergic neurotransmission and dysregulation of the balance between inhibitory and excitatory systems.  Objective: We investigated the immunolabeling of GABAA receptor &#946;2 subunit (GARB2) in the hippocampus, the amygdala, and the thalamus of infant rats prenatally exposed to valproic acid (AVP) as a model of ASD.  Methods: Pregnant female rats were injected with AVP (600mg/Kg, i.p.) on embryonic day 12; control rats were injected with saline (SS group). On postnatal day 14, rats from both groups were anesthetized, transcardially perfused with 0.9% NaCl and 4% paraformaldehyde, and sequential coronal brain slices (40&#956;m thickness) were obtained. Immunohistochemistry was performed to detect GARB2, and the relative optical density (OD) of immunoreactivity was analyzed.  Results: Our data showed a statistically significant decrease in GARB2 immunoreactivity in the lateral amygdaloid nucleus and the ventral and lateral thalamic nuclei of AVP group when compared to the SS group. No statistically significant differences were found in the hippocampus.  Conclusion: Our findings suggest that prenatal exposure to AVP reduces GARB2 immunoreactivity in limbic brain regions involved in social-emotional behavior, consistent with previous reports in individuals with ASD. These findings support for the involvement of the GABAergic system in the pathogenesis of ASD.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Ácido gamma-aminobutírico]]></kwd>
<kwd lng="es"><![CDATA[Receptor GABAA]]></kwd>
<kwd lng="es"><![CDATA[Autismo]]></kwd>
<kwd lng="es"><![CDATA[Ácido valproico]]></kwd>
<kwd lng="es"><![CDATA[Subunidad &#946;2 del receptor GABAA (GARB2)]]></kwd>
<kwd lng="en"><![CDATA[Gamma-aminobutyric acid]]></kwd>
<kwd lng="en"><![CDATA[GABAA receptor &#946;2 subunit (GARB2)]]></kwd>
<kwd lng="en"><![CDATA[Autism]]></kwd>
<kwd lng="en"><![CDATA[Valproic acid]]></kwd>
<kwd lng="en"><![CDATA[Gamma-aminobutyric acid type A receptor]]></kwd>
</kwd-group>
</article-meta>
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