<?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>1665-5044</journal-id>
<journal-title><![CDATA[Revista mexicana de neurociencia]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. mex. neurocienc.]]></abbrev-journal-title>
<issn>1665-5044</issn>
<publisher>
<publisher-name><![CDATA[Academia Mexicana de Neurología A.C.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1665-50442021000200067</article-id>
<article-id pub-id-type="doi">10.24875/rmn.20000050</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[The role of GABA neurotransmitter in the human central nervous system, physiology, and pathophysiology]]></article-title>
<article-title xml:lang="es"><![CDATA[El papel del neurotransmisor GABA en el sistema nervioso central humano, fisiología, y fisiopatología]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ochoa-de la Paz]]></surname>
<given-names><![CDATA[Lenin D.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Gulias-Cañizo]]></surname>
<given-names><![CDATA[Rosario]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ruíz-Leyja]]></surname>
<given-names><![CDATA[Estela D´Abril]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sánchez-Castillo]]></surname>
<given-names><![CDATA[Hugo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Parodí]]></surname>
<given-names><![CDATA[Jorge]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Nacional Autónoma de México School of Medicine ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Hospital Dr. Luis Sánchez Bulnes  ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad Anáhuac México  ]]></institution>
<addr-line><![CDATA[Huixquilucan State of Mexico]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Universidad Nacional Autónoma de México Faculty of Psychology Laboratorio de Neuropsicofarmacología y Estimación Temporal]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,Universidad Mayor School of Sciences ]]></institution>
<addr-line><![CDATA[Temuco ]]></addr-line>
<country>Chile</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>04</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>04</month>
<year>2021</year>
</pub-date>
<volume>22</volume>
<numero>2</numero>
<fpage>67</fpage>
<lpage>76</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-50442021000200067&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-50442021000200067&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-50442021000200067&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract GABA is the main inhibitory neurotransmitter of the central nervous system (CNS) and one of the most abundant neurotransmitters in mammals is distributed in most areas of the brain and participates in 40% of the inhibitory synapses of adult vertebrates. It is produced in the CNS, through the decarboxylation of glutamic acid, catalyzed by glutamic acid decarboxylase (GAD). GABA exerts its inhibitory effect through two types of specific receptors, GABAA (ionotropic) and GABAB (metabotropic), which show different pharmacological, structural, and molecular differences. Even though GABA plays a key role in the physiology of the CNS modulating different processes, also is involved in some pathologies, furthermore, is a target for several therapeutics drugs. For instance, GABA has important involvement in sleep cycle regulation, and for decades benzodiazepines and gaboxadol have been prescribed for the treatment of insomnia. In epilepsy disease, the pharmacological and gene expression studies suggest a role in the prevention of seizures by blocking the regulation of GABAA receptors with specific antagonists. In depression and anxiety, studies indicate changes in the regulation of the genes which encoding GABA receptors. In the same way, GABA receptors have been associated with alcoholism and premenstrual syndrome. In conclusion, experimental evidence suggests, that the same subtype of GABA receptors showed a different pattern of cellular population and subcellular expression in different areas of the brain, modulating the excitability, and neuronal synchronization in different affection pathologies and conditions in humans.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen El GABA es el principal neurotransmisor inhibitorio en el sistema nervioso central (SNC) y uno de los más abundantes en mamíferos; se distribuye en diferentes áreas del cerebro y participa en el 40% de las sinápsis de vertebrados adultos. Su síntesis se realiza en el SNC a través de la descarboxilación del ácido glutámico por acción de la descarboxilasa del ácido glutámico (GAD). El efecto ihibitorio de GABA se ejerce a través de dos tipos de receptores específicos: GABAA (ionotrópicos) y GABAB (metabotrópicos), los cuales presentan características farmacológicas, estructurales y moleculares diferentes. A pesar de que GABA participa de manera importante regulando diferentes procesos en el SNC, también está involucrado en algunas patologías, por lo que sus receptores son un blanco terapéutico. Por ejemplo, GABA participa en la regulación del ciclo del sueño, y por décadas las benzodiazepinas y el gaboxadol se han prescrito para el tratamiento del insomnio. En epilepsia, estudios farmacológicos y de expresión génica sugieren una participación en la prevención de las crisis al bloquear los receptores GABAA con antagonistas específicos. En el caso de la depresión y ansiedad, estudios indican cambios en la regulación de genes que codifican para los receptores a GABA. En este mismo sentido, los receptores a GABA también se han asociado al alcoholismo y al síndrome premenstrual. En conclusión, la evidencia experimental sugiere que el mismo subtipo de receptor a GABA presenta patrones diferentes en las poblaciones celulares y en su expresión subcelular en diferentes áreas del cerebro, modulando la excitabilidad y sincronización neuronal en diferentes condiciones y afecciones patológicas en humanos.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Human]]></kwd>
<kwd lng="en"><![CDATA[GABA]]></kwd>
<kwd lng="en"><![CDATA[GABA receptors]]></kwd>
<kwd lng="en"><![CDATA[Central nervous system]]></kwd>
<kwd lng="en"><![CDATA[Physiology]]></kwd>
<kwd lng="en"><![CDATA[Pathophysiology]]></kwd>
<kwd lng="es"><![CDATA[Humano]]></kwd>
<kwd lng="es"><![CDATA[GABA]]></kwd>
<kwd lng="es"><![CDATA[Receptores GABA]]></kwd>
<kwd lng="es"><![CDATA[CNS]]></kwd>
<kwd lng="es"><![CDATA[Fisiología]]></kwd>
<kwd lng="es"><![CDATA[Patofisiología]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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