<?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>0185-3325</journal-id>
<journal-title><![CDATA[Salud mental]]></journal-title>
<abbrev-journal-title><![CDATA[Salud Ment]]></abbrev-journal-title>
<issn>0185-3325</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Psiquiatría Ramón de la Fuente Muñiz]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0185-33252006000100051</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Neurotransmisores del sistema límbico. Amígdala. Segunda parte]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Castro-Sierra]]></surname>
<given-names><![CDATA[Eduardo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Chico Ponce de León]]></surname>
<given-names><![CDATA[Fernando]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Portugal Rivera]]></surname>
<given-names><![CDATA[Alison]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital Infantil de México Federico Gómez  ]]></institution>
<addr-line><![CDATA[DF ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Hospital Infantil de México Federico Gómez Departamento de Neurocirugía ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Hospital Infantil de México Federico Gómez  ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>02</month>
<year>2006</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>02</month>
<year>2006</year>
</pub-date>
<volume>29</volume>
<numero>1</numero>
<fpage>51</fpage>
<lpage>55</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0185-33252006000100051&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0185-33252006000100051&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0185-33252006000100051&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: Los neurotransmisores de la amígdala en el sistema límbico comprenden, entre otros, a las monoaminas (noradrenalina [NA]), la acetilcolina (ACh), los corticoides y la histamina. Ciertas drogas infundidas a la amígdala podrían modular la consolidación en la memoria de la inhibición del entrenamiento dirigido a evitar situaciones de estrés. La administración de anta gonistas de los receptores de la &#946; NA en la amígdala afecta la retención en la memoria por un lapso de un día cuando se administra inmediatamente después del entrenamiento, pero no surte ningún efecto cuando se administra a las seis horas. Infusiones intraamigdalinas de NA acompañadas de antagonistas de aquellos receptores atenuarán el trastorno mnemónico. De manera importante, se ha podido determinar que la NA produce un incremento de la consolidación de la memoria, que depende tanto del tiempo como de la dosis de aplicación cuando el fármaco se infunde a la amígdala inmediatamente después de la inhibición de este tipo de entrenamiento. La amígdala, la neocorteza y el hipocampo son regiones meta del sistema cerebral frontal basal colinérgico, que se relaciona estrechamente con diversas funciones del aprendizaje y la memo ria. Cualquier neurotransmisor con actividad fosforiladora o desfosforiladora podrá regular el estado de sensibilidad a la ACh, así como las propiedades funcionales de las neuronas amigdalinas. Es posible, entonces, que exista una modulación entre los estados de aprendizaje y de recuerdo de lo aprendido en la amígdala, la neocorteza y el hipocampo que esté regida por receptores muscarínicos acetilcolinérgicos. Por medio de receptores presinápticos de la histamina 3 (H3) y un mecanismo por el momento aún desconocido, la histamina disminuye o aumenta la transmisión sináptica excitadora en el BLA. Tal modulación histaminérgica de la actividad neuronal cumple un papel importante en los procesos fisiológicos y patofisiológicos del miedo, el aprendizaje y la memoria de la emo ción y los trastornos afectivos.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: Neurotransmitters of the amygdala in the limbic system include monoamines (noradrenaline [NA]) acetylcholine (ACh), corticoids and histamine. Drugs infused into the amygdala may modulate consolidation in memory of inhibition of training directed to avoid stressful situations. Administration of antagonists of &#946; NA receptors to the amygdala will affect retention in memory for a whole day when given immediately after training, but will have no effect when given six hours after training a test animal. Intra-amygdalar infusions of NA which may be accompanied by antagonists of those receptors will attenuate the memory disturbance. It is worth mentioning that later studies have been able to show that NA will produce an increment of memory consolidation, which will depend on the time as well as on the dose of application, when the drug is infused to the amygdala shortly after inhibition of training directed to avoid stressful situations. The amygdala, the neocortex and the hippocampus are target regions of the frontal basal cholinergic brain system, which has different effects on cognitive functions, such as memory and learning. Any neurotransmitter with phosphorylating or dephosphorylating activity may regulate the sensitive state of ACh, as well as the functional properties of amygdalar neurons. It is possible, then, that modulation mechanisms may exist between learning and recall states in the amygdala, the neocortex and the hippocampus, which could be controlled by muscarinic acetylcholinergic receptors. Through pre-synaptic receptors of histamine 3 (H3) and a currently unknown mechanism, histamine will decrease or increase excitatory synaptic transmission in BLA. Such histaminergic modulation of neuronal activity will play an important role in fear-related physiological and patho-physiological processes, learning and memory of emotion, and affective disturbances.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Limbic system]]></kwd>
<kwd lng="en"><![CDATA[neurotransmitters]]></kwd>
<kwd lng="en"><![CDATA[noradrenaline]]></kwd>
<kwd lng="en"><![CDATA[acetylcholine]]></kwd>
<kwd lng="en"><![CDATA[corticoids]]></kwd>
<kwd lng="en"><![CDATA[histamine]]></kwd>
<kwd lng="es"><![CDATA[Sistema límbico]]></kwd>
<kwd lng="es"><![CDATA[neurotransmisores]]></kwd>
<kwd lng="es"><![CDATA[noradrenalina]]></kwd>
<kwd lng="es"><![CDATA[acetilcolina]]></kwd>
<kwd lng="es"><![CDATA[corticoides]]></kwd>
<kwd lng="es"><![CDATA[histamina]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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