<?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>0188-9532</journal-id>
<journal-title><![CDATA[Revista mexicana de ingeniería biomédica]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. mex. ing. bioméd]]></abbrev-journal-title>
<issn>0188-9532</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Mexicana de Ingeniería Biomédica]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0188-95322021000200102</article-id>
<article-id pub-id-type="doi">10.17488/rmib.42.2.2</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Theoretical Study of the Function of the IP3 Receptor/BK Channel Complex in a Single Neuron]]></article-title>
<article-title xml:lang="es"><![CDATA[Estudio Teórico de la Función del Complejo Receptor-IP3/Canales BK en Neurona Única]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez-Bonilla]]></surname>
<given-names><![CDATA[M. E.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Reyes-Monreal]]></surname>
<given-names><![CDATA[M.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Quintero-Pérez]]></surname>
<given-names><![CDATA[J.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pérez-Escalera]]></surname>
<given-names><![CDATA[M. F.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Reyes-Lazalde]]></surname>
<given-names><![CDATA[A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Benemérita Universidad Autónoma de Puebla  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>08</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>08</month>
<year>2021</year>
</pub-date>
<volume>42</volume>
<numero>2</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0188-95322021000200102&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0188-95322021000200102&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0188-95322021000200102&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[ABSTRACT Large conductance calcium-activated potassium (BK) channels carry out many functions in the central nervous system. These channels open in response to increased cytosolic calcium ([Ca2+]cyt) concentration. The influx of calcium ions to the cytosol can occur through voltage-gated calcium channels (VGCCs) on the plasma membrane and/ or through IP3 receptors (IP3-Rs) and ryanodine receptors (RyRs) on the endoplasmic reticulum membrane. The BK channel/IP3-R/RyR interaction has been widely reported in smooth muscle but scarcely investigated in relation to neurons. The aim of this study was to theoretically explore the function of the BK/IP3-R complex by means of a computational model of a neuron that replicates the interaction between the release of Ca2+ from the endoplasmic reticulum (through IP3-Rs) and the opening of the BK channels. The mathematical models are based on the Hodgkin-Huxley formalism and the Goldbeter model. These models were implemented on Visual Basic® and differential equations were solved numerically. Distinct conditions were contemplated for BK conductance and the efflux of endoplasmic Ca2+ to the cytosol. An abrupt rise in [Ca2+]cyt (&#8805; 5 &#956;M) and short duration (spark) was found to activate BK channels and either pause or stop the action potential train.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[RESUMEN Los canales de potasio activados por calcio de gran conductancia (canales BK) cumplen múltiples funciones en el sistema nervioso central. Estos canales se abren en respuesta al incremento de la concentración de calcio citosólico ([Ca2+]cyt). La entrada de Ca2+ puede ocurrir a través de canales de calcio dependientes de voltaje (VGCCs) localizados en la membrana plasmática y por eflujo de Ca2+ del retículo endoplásmico (ER) causado por 1,4,5-Trifosfato (IP3) o rianodina (RyR). La interacción BK/IP3/RyR ha sido ampliamente estudiada en músculo liso, pero escasamente en neuronas. El objetivo de este estudio fue explorar teóricamente la función del complejo BK/IP3-R mediante un modelo computacional de una neurona que replica la interacción entre la liberación de Ca2+ del retículo endoplásmico (a través de IP3-Rs) y la apertura de los canales BK. Los modelos matemáticos se basan en el formalismo de Hodgkin-Huxley y el modelo de Goldbeter. Estos modelos fueron implementados en Visual Basic® y las ecuaciones diferenciales fueron resueltas por métodos numéricos. Se contemplaron distintas condiciones para la conductancia del canal BK y la salida de Ca2+ endoplásmico al citosol. Los resultados muestran que un incremento abrupto de [Ca2+] cyt (&#8805; 5 &#956;M) y de corta duración (spark) activa los canales BK y producen una pausa o detiene el tren de potenciales de acción.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[BK channels]]></kwd>
<kwd lng="en"><![CDATA[IP3 receptor]]></kwd>
<kwd lng="en"><![CDATA[Ca2+ microdomains]]></kwd>
<kwd lng="en"><![CDATA[Single-neuron simulations]]></kwd>
<kwd lng="en"><![CDATA[SERCA pump]]></kwd>
<kwd lng="es"><![CDATA[BK channels]]></kwd>
<kwd lng="es"><![CDATA[IP3 receptor]]></kwd>
<kwd lng="es"><![CDATA[Ca2+ microdomains]]></kwd>
<kwd lng="es"><![CDATA[Single-neuron simulations]]></kwd>
<kwd lng="es"><![CDATA[SERCA pump]]></kwd>
</kwd-group>
</article-meta>
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