<?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>0188-6266</journal-id>
<journal-title><![CDATA[Acta universitaria]]></journal-title>
<abbrev-journal-title><![CDATA[Acta univ]]></abbrev-journal-title>
<issn>0188-6266</issn>
<publisher>
<publisher-name><![CDATA[Universidad de Guanajuato, Dirección de Investigación y Posgrado]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0188-62662022000100123</article-id>
<article-id pub-id-type="doi">10.15174/au.2022.3350</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Determinación teórica de la función del complejo canal de K+ dependiente de Ca2+ de alta conductancia / receptor inositol trifosfato (BK/IP3-R) en dos condiciones de actividad epiléptica]]></article-title>
<article-title xml:lang="en"><![CDATA[Theoretical determination of the function of the large conductance Ca2+-activated K+ channel / inositol triphosphate complex (BK/IP3-R) under two conditions of epileptic activity]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez Bonilla]]></surname>
<given-names><![CDATA[María Eugenia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Reyes Monreal]]></surname>
<given-names><![CDATA[Marleni]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Quintero Pérez]]></surname>
<given-names><![CDATA[Jessica]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez Escalera]]></surname>
<given-names><![CDATA[Miguel]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Reyes Lazalde]]></surname>
<given-names><![CDATA[Arturo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Benemérita Universidad Autónoma de Puebla Facultad de Ciencias Biológicas Laboratorio de Biología Interactiva]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Benemérita Universidad Autónoma de Puebla Escuela de Artes Plásticas y Audiovisuales ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Benemérita Universidad Autónoma de Puebla Facultad de Medicina Escuela de Fisioterapia]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>00</month>
<year>2022</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>00</month>
<year>2022</year>
</pub-date>
<volume>32</volume>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0188-62662022000100123&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0188-62662022000100123&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0188-62662022000100123&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen Actualmente, se estudian los procesos epileptogénicos a dos niveles: redes neuronales y propiedades intrínsecas de la neurona. Sin embargo, poco se sabe sobre los mecanismos celulares que determinan el cese de la actividad epiléptica en neuronas. En este trabajo se propone a la función del complejo BK/IP3-R como parte de uno de estos mecanismos. Para probarlo, se realizó un estudio teórico. Se desarrollaron dos simuladores de epileptogénesis en una neurona silente: (1) por mutación del canal de sodio dependiente de voltaje (NaV 1.2) y (2) por incremento de K+ externo. En estas condiciones el complejo BK/IP3-R bloqueó la actividad epiléptica en la neurona con NaV 1.2 mutado y bloqueó o provocó una pausa del estado epiléptico en la neurona con alto K+ externo. Estos resultados confirman un posible mecanismo de protección del complejo BK/IP3-R en condiciones anómalas como epilepsia. Su eficacia podría variar significativamente según el tipo de epilepsia.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Currently, epileptogenic processes are studied at two levels: neural networks and intrinsic properties of the neuron. However, little is known about the cellular mechanisms that determine the cessation of the epileptic activity in neurons. In this work, the role of the BK/IP3-R complex is proposed as part of one of these mechanisms. To prove it, a theoretical study was carried out. Two simulators of epileptogenesis were developed in a silent neuron: (1) by mutation of the voltage-gated sodium channel (NaV 1.2), and (2) by increase of external K+. Under these conditions the BK/IP3-R complex blocked epileptic activity in the neuron with muted NaV 1.2 and blocked or caused a pause of status epilepticus in the high external K+ neuron. These results confirm a possible mechanism of protection of the BK/IP3-R complex in abnormal conditions such as epilepsy. Its efficacy could vary significantly depending on the type of epilepsy.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Epilepsia]]></kwd>
<kwd lng="es"><![CDATA[simuladores electrofisiológicos]]></kwd>
<kwd lng="es"><![CDATA[complejo BK/IP3-R]]></kwd>
<kwd lng="es"><![CDATA[canales BK]]></kwd>
<kwd lng="en"><![CDATA[Epilepsy]]></kwd>
<kwd lng="en"><![CDATA[electrophysiological simulators]]></kwd>
<kwd lng="en"><![CDATA[BK/IP3-R complex]]></kwd>
<kwd lng="en"><![CDATA[BK channels]]></kwd>
</kwd-group>
</article-meta>
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