<?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>0034-7744</journal-id>
<journal-title><![CDATA[Revista de Biología Tropical]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. biol. trop]]></abbrev-journal-title>
<issn>0034-7744</issn>
<publisher>
<publisher-name><![CDATA[Universidad de Costa Rica]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0034-77442021000200545</article-id>
<article-id pub-id-type="doi">10.15517/rbt.v69i2.44539</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Action of heparin and acetylcholine modulators on the neurotoxicity of the toad Rhinella schneideri (Anura: Bufonidae) in Brazil]]></article-title>
<article-title xml:lang="es"><![CDATA[Acción de la heparina y moduladores de acetilcolina en la neurotoxicidad del sapo Rhinella schneideri (Anura: Bufonidae) en Brasil]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rostelato-Ferreira]]></surname>
<given-names><![CDATA[Sandro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Vettorazzo]]></surname>
<given-names><![CDATA[Orlando-B.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Tribuiani]]></surname>
<given-names><![CDATA[Natália]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Leal]]></surname>
<given-names><![CDATA[Allan-P.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Dal-Belo]]></surname>
<given-names><![CDATA[Cháriston-A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rodrigues-Simioni]]></surname>
<given-names><![CDATA[Léa]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Floriano]]></surname>
<given-names><![CDATA[Rafael-S.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Oshima-Franco]]></surname>
<given-names><![CDATA[Yoko]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Paulista University Institute of Health Sciences ]]></institution>
<addr-line><![CDATA[ São Paulo]]></addr-line>
<country>Brazil</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,University of Sorocaba Graduate Program in Pharmaceutical Sciences ]]></institution>
<addr-line><![CDATA[ São Paulo]]></addr-line>
<country>Brazil</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Federal University of Santa Maria Graduate Program in Toxicological Biochemistry ]]></institution>
<addr-line><![CDATA[ Rio Grande do Sul]]></addr-line>
<country>Brazil</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Federal University of Pampa Laboratory of Neurobiology and Toxinology ]]></institution>
<addr-line><![CDATA[ Rio Grande do Sul]]></addr-line>
<country>Brazil</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,State University of Campinas Faculty of Medical Sciences Department of Pharmacology]]></institution>
<addr-line><![CDATA[ São Paulo]]></addr-line>
<country>Brazil</country>
</aff>
<aff id="Af6">
<institution><![CDATA[,University of Western São Paulo Graduate Program in Health Sciences ]]></institution>
<addr-line><![CDATA[ São Paulo]]></addr-line>
<country>Brazil</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>06</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>06</month>
<year>2021</year>
</pub-date>
<volume>69</volume>
<numero>2</numero>
<fpage>545</fpage>
<lpage>556</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_arttext&amp;pid=S0034-77442021000200545&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_abstract&amp;pid=S0034-77442021000200545&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.sa.cr/scielo.php?script=sci_pdf&amp;pid=S0034-77442021000200545&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction: Rhinella schneideri is a toad widely distributed in South America and its poison is characterized by inducing cardiotoxicity and neurotoxicity.  Objective:  In this work, we investigated pharmacological strategies to attenuate the peripheral neurotoxicity induced by R. schneideri poison in avian neuromuscular preparation.  Methods:  The experiments were carried out using isolated chick biventer cervicis preparation subjected to field stimulation for muscle twitches recordings or exposed to acetylcholine and potassium chloride for contracture responses.  Results:  Poison (10 &#956;g/ml) produced complete neuromuscular blockade in chick biventer cervicis preparation within approximately 70 min incubation (times for 50 and 90 % blockade: 15 ± 3 min and 40 ± 2 min, respectively; P &lt; 0.05, N= 5); contracture responses to exogenous acetylcholine and KCl were unaffected by poison indicating no specificity with postsynaptic receptors or myotoxicity, respectively. Poison (10 &#956;g/ml)-induced neuromuscular blockade was not prevented by heparin (5 and 150 IU/ml) under pre- or post-treatment conditions. Incubation at low temperature (23-25 °C) abolished the neuromuscular blockade; after raising the temperature to 37 °C, the complete neuromuscular blockade was slightly slower than that seen in preparations directly incubated at 37 °C (times for 50 and 90 % blockade: 23 ± 2 min and 60 ± 2.5 min, respectively; P &lt; 0.05, N= 4). Neostigmine (3.3 &#956;M) did not reverse the neuromuscular blockade in BC preparation whereas 3,4-diaminopyridine (91.6 &#956;M) produced a partial and sustained reversal of the twitch responses (29 ± 7.8 % of maximal reversal reached in approximately 40 min incubation; P &lt; 0.05, N= 4).  Conclusions: R. schneideri poison induces potent peripheral neurotoxicity in vitro which can be partially reversible by 3,4-diaminopyridine.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción: Rhinella schneideri está ampliamente distribuida en Suramérica y su veneno es caracterizado por inducir cardiotoxicidad y neurotoxicidad.  Objetivo:  En este trabajo, investigamos estrategias farmacológicas para atenuar la neurotoxicidad periférica inducida por el veneno de R. schneideri en preparaciones neuromusculares de aves.  Métodos:  Los experimentos fueron realizados usando preparaciones de biventer cervicis de pollos sometidas a estimulación de campo para el registro de las contracciones musculares o expuestas a la acetilcolina y al cloruro de potasio para la respuesta contractural.  Resultados:  El veneno (10 µg/ml) provocó un bloqueo neuromuscular completo en las preparaciones después de aproximadamente 70 min de incubación (tiempos para 50 y 90 % de bloqueo: 15  ± 3 min y 40  ± 2 min, respectivamente; P &lt; 0.05, N = 5); las contracturas en respuesta a la acetilcolina y el KCl exógenos no fueron afectadas por el veneno, indicando que no hay una interacción especifica con receptores postsinápticos o miotoxicidad respectivamente. El bloqueo neuromuscular causado por el veneno (10 µg/ml) no fue prevenido por la heparina (5 y 150 UI/ml) bajo condiciones pre y post-tratamiento. La incubación a bajas temperaturas (23-25 ºC) abolió el bloqueo neuromuscular; después de aumentar la temperatura a 37 ºC, el bloqueo neuromuscular total fue levemente más lento que el visto en preparaciones directamente incubadas a 37 ºC (tiempos para 50 y 90 % de bloqueo: 23  ± 2 min y 60  ± 2.5 min, respectivamente; P &lt; 0.05, N= 4). Neostigmina (3.3 µM) no revirtió el bloqueo neuromuscular, mientras que 3.4-diaminopiridina (91.6 µM) produjo una reversión parcial y sostenida de las respuestas neuromusculares (29  ± 7.8 % de la reversión máxima alcanzada en aproximadamente 40 min de incubación; P &lt; 0.05, N = 4).  Conclusiones:  El veneno de R. schneideri indujo neurotoxicidad periférica potente in vitro, el cual puede ser revertido por 3.4-diaminopiridina.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[amphibian poison]]></kwd>
<kwd lng="en"><![CDATA[paratoid gland secretion]]></kwd>
<kwd lng="en"><![CDATA[chick biventer cervicis preparation]]></kwd>
<kwd lng="en"><![CDATA[neuromuscular blockade]]></kwd>
<kwd lng="en"><![CDATA[reversal]]></kwd>
<kwd lng="es"><![CDATA[veneno de anfibio]]></kwd>
<kwd lng="es"><![CDATA[secreción de la glándula parótida]]></kwd>
<kwd lng="es"><![CDATA[preparaciones de biventer cervicis de pollos]]></kwd>
<kwd lng="es"><![CDATA[bloqueo neuromuscular]]></kwd>
<kwd lng="es"><![CDATA[reversión]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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