<?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>S1665-50442025000600003</article-id>
<article-id pub-id-type="doi">10.24875/rmn.24000062</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Temporal lobe epilepsy and changes in the M-current]]></article-title>
<article-title xml:lang="es"><![CDATA[Epilepsia del lóbulo temporal y cambios en la corriente M]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Solís]]></surname>
<given-names><![CDATA[Hugo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López-Hernández]]></surname>
<given-names><![CDATA[Estela]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Autónoma de México Facultad de Medicina ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2025</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2025</year>
</pub-date>
<volume>26</volume>
<numero>6</numero>
<fpage>190</fpage>
<lpage>196</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-50442025000600003&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-50442025000600003&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-50442025000600003&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Objective: Acquired alterations of ion channel function occur after status epilepticus (SE). Kv7 channels mediate a sustained outward current (IM) that exerts pivotal control over neuronal excitability. Here, we investigate if pilocarpine-induced SE alters M-channel activity by quantifying the IM.  Methods: Hippocampal slices were prepared from adult rats after pilocarpine-induced SE, when the animal was showing 3-5 spontaneous recurrent seizures (SRS) a day. A group of untreated, age-matched rats was used as the control group. Recordings were made using the whole-cell configuration of the patch clamp technique and current clamp mode to measure the membrane time constant.  Results: The IM measured amplitude in CA1 neurons from pilocarpine-SE rats was significantly reduced compared to the control group (control, 208.72 ± 25.49 pA, n = 15; pilocarpine-SE, 49.28 ± 6.17 pA, n = 11; p &lt; 0.05, Student's t). The time constant was 27.7 ± 17.7 msec in the control group and 48.9 ± 5.5 msec in the pilocarpine-SE group, and was significantly different (p &lt; 0.05).  Conclusions: In this study, we demonstrated that the M-current amplitude is significantly reduced in CA1 pyramidal neurons after pilocarpine-SE. Considering the acute damage that SE induces, the silent interval between injury and the onset of spontaneous seizures, and the chronic epileptic state in which the M-current was measured, we can speculate about the lack of homeostatic regulation of the intrinsic properties of neuronal excitability.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Objetivo: Las alteraciones adquiridas en la función de canales iónicos ocurren después del estado epiléptico (SE). Los canales Kv7 determinan una corriente de salida sostenida llamada corriente M (IM), que ejerce un control fundamental sobre la excitabilidad neuronal. Investigamos si el SE inducido por pilocarpina altera la funcionalidad del canal M mediante la cuantificación de la IM.  Métodos: Se prepararon rebanadas de hipocampo de ratas adultas que presentaron de 3 a 5 convulsiones espontáneas recurrentes (SRS) al día, después de haberles provocado el SE por la administración de pilocarpina. Los registros se realizaron con la técnica de fijación de voltaje en la modalidad de registro de toda la célula (whole cell).  Resultados: En neuronas piramidales de la región CA1 del hipocampo de ratas que experimentaron SE, la amplitud de la IM disminuyó significativamente comparada con el grupo control (control, 208.72 ± 25.49 pA, n = 15; pilocarpina-SE, 49.28 ± 6.17 pA, n = 11; p &lt; 0.05, Student's t). Se cuantificó la constante de tiempo (&#964;) de relajación. La &#964; se modificó significativamente (48.9 ± 5.5 mseg en el grupo pilocarpina-SE) con respecto al grupo control (27.7 ± 17.7 mseg).  Conclusiones: En este estudio demostramos que la amplitud de la IM se reduce significativamente en las neuronas piramidales CA1 después del SE provocado por pilocarpina. Al considerar el daño agudo provocado por el SE, el intervalo de silencio entre la lesión, el inicio de las convulsiones espontáneas y el estado epiléptico crónico en el que se midió la IM, nos permite especular sobre la falta de regulación homeostática de algunas de las propiedades intrínsecas de la excitabilidad neuronal.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Hippocampus]]></kwd>
<kwd lng="en"><![CDATA[M-current]]></kwd>
<kwd lng="en"><![CDATA[Pilocarpine]]></kwd>
<kwd lng="en"><![CDATA[Status epilepticus]]></kwd>
<kwd lng="en"><![CDATA[Epileptogenesis]]></kwd>
<kwd lng="es"><![CDATA[Hipocampo]]></kwd>
<kwd lng="es"><![CDATA[Corriente M]]></kwd>
<kwd lng="es"><![CDATA[Pilocarpina]]></kwd>
<kwd lng="es"><![CDATA[Estado epiléptico]]></kwd>
<kwd lng="es"><![CDATA[Epileptogénesis]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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