<?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>S2954-41222025000400181</article-id>
<article-id pub-id-type="doi">10.24875/anc.m25000035</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Posible participación del receptor acoplado a proteínas G 55 (GPR55) del hipocampo dorsal en la preferencia de lugar condicionada inducida por nicotina]]></article-title>
<article-title xml:lang="en"><![CDATA[Possible involvement of dorsal hippocampal G-protein coupled receptor 55 (GPR55) in nicotine-induced conditioned place preference in rats]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Colis-Arenas]]></surname>
<given-names><![CDATA[Oliver A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Muñoz-Pelayo]]></surname>
<given-names><![CDATA[Angélica]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[López-Lariz]]></surname>
<given-names><![CDATA[Carlos H.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Chávez-Reyes]]></surname>
<given-names><![CDATA[Jesús]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Marichal-Cancino]]></surname>
<given-names><![CDATA[Bruno A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Centro de Ciencias de la Salud Departamento de Medicina ]]></institution>
<addr-line><![CDATA[Aguascalientes ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad Autónoma de Aguascalientes Centro de Ciencias Básicas Departamento de Fisiología y Farmacología]]></institution>
<addr-line><![CDATA[Aguascalientes ]]></addr-line>
<country>México</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>30</volume>
<numero>4</numero>
<fpage>181</fpage>
<lpage>188</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S2954-41222025000400181&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S2954-41222025000400181&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S2954-41222025000400181&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Antecedentes: El receptor acoplado a proteínas G 55 (GPR55) puede interactuar con cannabinoides y lisofosfolípidos. Se expresa en diversos tejidos en los mamíferos, incluyendo el sistema nervioso central (SNC). Sus acciones en el SNC se conocen parcialmente e incluyen efectos en ansiedad, memoria espacial, recompensa y dolor. Un estudio reciente reportó que la administración sistémica de O-1602 (agonista GPR55) inhibe la preferencia de lugar condicionada (CPP) inducida por nicotina, pero el silenciamiento del GPR55 en el núcleo accumbens no modifica las acciones del O-1602, por lo que su sitio de acción se desconoce. El GPR55 se expresa significativamente en el hipocampo dorsal, una estructura involucrada en la asociación contextual de la recompensa por drogas.  Objetivo: Analizar de manera preliminar la participación potencial del GPR55 en la CPP inducida por nicotina.  Método: Ratas Wistar macho fueron canuladas en el hipocampo dorsal para recibirla con (a) vehículo (DMSO10%); (b) ML184 (0.48 nmol; GPR55 antagonista), o (c) CID16020046 (1.16 nmol; GPR55 antagonist) durante la fase de condicionamiento en el CPP mediado por nicotina.  Resultados Los animales a los cuales se les administró con vehículo pasaron más tiempo en la cámara emparejada con nicotina en comparación con la línea base (p &lt; 0.05). Por el contrario, ML184 y CID16020046 previnieron la CPP inducida por la nicotina (p &gt; 0.05).  Conclusión Bajo nuestras condiciones experimentales, la manipulación farmacológica del GPR55 en el hipocampo dorsal previno la CPP inducida por nicotina por mecanismos aún no identificados.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Background: The G-protein coupled receptor 55 (GPR55) is a cannabinoid/lysophospholipid target expressed in several tissues in mammals, including the central nervous system (CNS). Its actions in CNS are only partially known and include anxiety, spatial memory, reward, and pain. A recent study reported that systemic O-1602 (a GPR55 agonist) blocked the nicotine- induced conditioned place preference (CPP), but the knockdown of GPR55 in the nucleus accumbens did not modify the actions of O-1602, so its site of action remains obscure. GPR55 is expressed significantly in the dorsal hippocampus, a structure involved in the context-association to drugs-reward.  Objective: To preliminary analyze the potential participation of dorsal- hippocampal GPR55 in the nicotine-induced CPP.  Method: Male Wistar rats were implanted in dorsal hippocampus to receive: (i) vehicle (dimethyl sulfoxide 10%); (ii) ML184 (0.48 nmol; GPR55 agonist); or (iii) CID16020046 (1.16 nmol; GPR55 antagonist) during the conditioning phase in the nicotine-mediated CPP paradigm.  Results: Animals from the vehicle group exhibited an increased time in the nicotine-paired chamber compared with its baseline (p &lt; 0.05). In contrast, both ML184 and CIDl6020046 prevented the nicotine-induced CPP (p &gt; 0.05).  Conclusion: Under our experimental conditions, pharmacological manipulation of GPR55 in the dorsal hippocampus prevented the nicotine-induced CPP due to mechanisms that remain to be identified.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[GPR55]]></kwd>
<kwd lng="es"><![CDATA[Preferencia de lugar condicionado]]></kwd>
<kwd lng="es"><![CDATA[Nicotina]]></kwd>
<kwd lng="es"><![CDATA[Hipocampo dorsal]]></kwd>
<kwd lng="es"><![CDATA[Recompensa del cerebro]]></kwd>
<kwd lng="en"><![CDATA[G-protein coupled receptor 55]]></kwd>
<kwd lng="en"><![CDATA[Conditioned place preference]]></kwd>
<kwd lng="en"><![CDATA[Nicotine]]></kwd>
<kwd lng="en"><![CDATA[Dorsal hippocampus]]></kwd>
<kwd lng="en"><![CDATA[Brain reward]]></kwd>
</kwd-group>
</article-meta>
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