<?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>S0185-33252005000600027</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Neurotransmisores del sistema límbico. I. Amígdala. Primera 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 Laboratorio de Psicoacústica y Fisiología Auditiva ]]></institution>
<addr-line><![CDATA[ México DF]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Nacional de Psiquiatría Ramón de la Fuente Laboratorio de Neuromorfología ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Hospital Infantil de México Federico Gómez Subdirección de Enseñanza ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>México</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2005</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2005</year>
</pub-date>
<volume>28</volume>
<numero>6</numero>
<fpage>27</fpage>
<lpage>32</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S0185-33252005000600027&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S0185-33252005000600027&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S0185-33252005000600027&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, al ácido &#947;-aminobutírico (GABAA,B,G), el ácido glutámico (GLU) y el N-metil-D-aspartato (NMDA), así como a las monoaminas [dopamina (DA) e hidroxitriptamina (5-HT)]. El GABA es el principal neurotransmisor inhibidor. Su actividad inhibidora se bloquea, por ejemplo, por los efectos ansiolíticos de las benzodiacepinas, tanto en la amígdala como en otros centros del sistema límbico (tálamo, corteza prefrontal, hipocampo, etc.) conectados con esta estructura. Igualmente, la corteza prefrontal cerebral regula los procesos de memoria en los que esté involucrado un componente afectivo a través de conexiones inhibidoras GABAérgicas sobre el núcleo lateral (LA) de la amígdala. Al estimularse las vías córtico-amigdalinas y tálamo-amigdalinas, se produce una excitación seguida de una inhibición mediadas por receptores del GABA en el LA. Una reducción de la inhibición puede obtenerse ya sea al estimular conjuntamente ambas vías, o al estimular primero una y luego la otra vía. Ambos tipos de depresión se regulan por inhibidores presinápticos del GABAB en interneuronas del LA que conectan con el núcleo central (CE) de la amígdala, y que aparentemente llegan por una u otra vía. Este dato apoya la existencia de un ingreso monosináptico convergente de información al LA, ingreso que interviene en la respuesta a diferentes condiciones estresantes y que limita una actividad neuronal excesiva. El GLU es el principal neurotransmisor excitador. Al estimularse la amígdala durante la aversión condicionada contra ciertos sabores por este neurotransmisor, se produce una inhibición de la actividad hipotalámica procedente de vías GABAérgicas amigdalinas que van al hipotálamo. El LA es parte del circuito neural que subyace al condicionamiento pavloviano al miedo. En este circuito, el bloqueo de los receptores de NMDA glutámicos en el LA antes del entrenamiento altera el aprendizaje del condicionamiento al miedo, pero el bloqueo previo a la prueba también altera dicha expresión. Se ha visto que un bloqueo específico causa una disrupción del circuito que interviene en el aprendizaje de este condicionamiento, mas no de la consolidación en la memoria del proceso en un momento posterior al aprendizaje. La estimulación de los colículos inferiores (CI) causa un aumento significativo de los niveles de DA en la corteza prefrontal (PFC). Asimismo, el complejo basolateral de la amígdala (BLA) sirve como filtro de la información con carga negativa que promueve el escape y que asciende a estructuras más elevadas del tallo cerebral. Se ha observado que la desactivación del BLA interfiere con la activación de los egresos dopaminérgicos corticales producidos por una estimulación con carga negativa de los CI. Se ha podido demostrar que la información con carga negativa que asciende desde los CI cursa con una modulación opuesta dada por mecanismos de DA/5-HT que descienden desde la PFC. Estos procesos parecen regularse por filtros localizados en el BLA. Existe la posibilidad de que la DA proveniente del BLA module las respuestas de la DA del nucleus accumbens durante el estrés indirectamente por medio de conexiones de la primera con la corteza prefrontal medial, la cual inhibirá, por medio de la DA, la transmisión dopaminérgica de este núcleo.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Summary Neurotransmitters of the amygdala in the limbic system include, among others, &#947;-aminobutyric acid (GABAA,B.G), glutamic acid (GLU) and N-methyl-D-aspartate (NMDA), as well as the monoamines [dopamine (DA) and 5-hydroxytriptamine (5-HT)]. GABA is the main inhibitory neurotransmitter. Its inhibitory activity will be blocked, for example, by the anxiolytic effects of benzodiazepines both in the amygdala and in other nuclei of the limbic system (thalamus, prefrontal cortex, hippocampus, etc.) connected to this structure. Similarly, the cerebral prefrontal cortex will regulate memory and learning processes in which an affective component may be involved through GABAergic inhibitory connections reaching the lateral nucleus (LA) of the amygdala. On stimulating cortico- and thalamo-amygdalar pathways, an excitation will be produced followed by an inhibition, both of which are mediated by GABA receptors in LA. A reduction of the second inhibition may be obtained either by joint stimulation of both pathways or by stimulation of the first and then the other pathway. Both types of depression can be regulated by presynaptic inhibitors of GABAB in LA interneurons connecting with the central nucleus of the amygdala, and which apparently arrive via either the cortical or the thalamic pathway. These data support the existence of a convergent monosynaptic information input which will be active in response to different stressful conditions, and which will limit excessive neuronal activity. GLU is the main excitatory neurotransmitter. When the amygdala is excited in the course of aversive conditioning against certain flavors by this neurotransmitter, a further inhibition of hypothalamic activity will be produced arriving via GABAergic amygdalar pathways to the hypothalamus. LA is part of the neural circuit underlying pavlovian fear conditioning. In this circuit, blocking glutamate NMDA receptors in LA before training will alter acquisition of fear conditioning, but blocking this nucleus before testing will also alter such expression. Recent research has shown that blocking will cause specific disruption of the circuits participating in fear learning, and not of memory consolidation of this process some time after learning. Stimulation of the inferior colliculi (IC) will cause a significant increment of DA levels in prefrontal cortex (PFC). Likewise, the basolateral complex (BLA) of the amygdala will serve as a filter of aversive information ascending to upper structures of the brainstem. In this regard, it has been observed that deactivation of BLA will interfere with activation of cortical dopaminergic outputs produced by aversive stimulation arriving from the IC. Aversive information ascending from the IC has been shown to be modulated by DA/5-HT mechanisms descending from PFC. These processes appear to be regulated by filters located in BLA. In the same fashion, there is the possibility that DA from the basolateral amygdala may modulate responses of DA from the nucleus accumbens during stress indirectly via connections of the amygdala with the PFC, which will inhibit, again, via DA, dopaminergic transmission of the nucleus accumbens.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Sistema límbico]]></kwd>
<kwd lng="es"><![CDATA[neurotransmisores]]></kwd>
<kwd lng="es"><![CDATA[GABA]]></kwd>
<kwd lng="es"><![CDATA[ácido glutámico]]></kwd>
<kwd lng="es"><![CDATA[NMDA]]></kwd>
<kwd lng="es"><![CDATA[dopamina]]></kwd>
<kwd lng="es"><![CDATA[5-hidroxitriptamina]]></kwd>
<kwd lng="en"><![CDATA[Limbic system]]></kwd>
<kwd lng="en"><![CDATA[neurotransmitters]]></kwd>
<kwd lng="en"><![CDATA[GABA]]></kwd>
<kwd lng="en"><![CDATA[glutamic acid]]></kwd>
<kwd lng="en"><![CDATA[NMDA]]></kwd>
<kwd lng="en"><![CDATA[dopamine]]></kwd>
<kwd lng="en"><![CDATA[5-hydroxytriptamine]]></kwd>
</kwd-group>
</article-meta>
</front><back>
<ref-list>
<ref id="B1">
<label>1</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Ahn]]></surname>
<given-names><![CDATA[S]]></given-names>
</name>
<name>
<surname><![CDATA[Phillips]]></surname>
<given-names><![CDATA[AG]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Independent modulation of basal and feeding-evoked dopamine efflux in the nucleus accumbens and medial prefrontal cortex by the central and basolateral amygdalar nuclei in the rat]]></article-title>
<source><![CDATA[Neurosci]]></source>
<year>2003</year>
<volume>116</volume>
<page-range>293-305</page-range></nlm-citation>
</ref>
<ref id="B2">
<label>2</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Bonno]]></surname>
<given-names><![CDATA[S]]></given-names>
</name>
<name>
<surname><![CDATA[Raschilas]]></surname>
<given-names><![CDATA[F]]></given-names>
</name>
<name>
<surname><![CDATA[Mari]]></surname>
<given-names><![CDATA[I]]></given-names>
</name>
<name>
<surname><![CDATA[Pigne]]></surname>
<given-names><![CDATA[E]]></given-names>
</name>
<name>
<surname><![CDATA[Pouchot]]></surname>
<given-names><![CDATA[J]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Kluver-Bucy syndrome in herpetic meningoencephalitis]]></article-title>
<source><![CDATA[Presse Med]]></source>
<year>2003</year>
<volume>30</volume>
<page-range>115-8</page-range></nlm-citation>
</ref>
<ref id="B3">
<label>3</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Huang]]></surname>
<given-names><![CDATA[YY]]></given-names>
</name>
<name>
<surname><![CDATA[Martin]]></surname>
<given-names><![CDATA[KC]]></given-names>
</name>
<name>
<surname><![CDATA[Kandel]]></surname>
<given-names><![CDATA[ER]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Both protein kinase A and mitogen-activated protein kinase are required in the amygdala for the macromolecular synthesis-dependent late phase of LTP]]></article-title>
<source><![CDATA[J Neurosci]]></source>
<year>2000</year>
<volume>20</volume>
<page-range>6317-25</page-range></nlm-citation>
</ref>
<ref id="B4">
<label>4</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Kling]]></surname>
<given-names><![CDATA[AS]]></given-names>
</name>
<name>
<surname><![CDATA[Tachiki]]></surname>
<given-names><![CDATA[K]]></given-names>
</name>
<name>
<surname><![CDATA[Lloyd]]></surname>
<given-names><![CDATA[R]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Neurochemical correlates of the Kluver-Bucy syndrome by in vivo micro-dialysis in monkey]]></article-title>
<source><![CDATA[Behav Brain Res]]></source>
<year>1993</year>
<volume>56</volume>
<page-range>161-70</page-range></nlm-citation>
</ref>
<ref id="B5">
<label>5</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Liu]]></surname>
<given-names><![CDATA[M]]></given-names>
</name>
<name>
<surname><![CDATA[Glowa]]></surname>
<given-names><![CDATA[JR]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Alterations of GABA receptor and its subunit mRNA levels in rat brain associated with increases in punished responding with acute alprazolam administration. Quantitative studies of autoradiography and in situ hybridization]]></article-title>
<source><![CDATA[Abstr Soc Neurosci]]></source>
<year>1998</year>
<volume>24</volume>
<page-range>100</page-range></nlm-citation>
</ref>
<ref id="B6">
<label>6</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Macedo]]></surname>
<given-names><![CDATA[CE]]></given-names>
</name>
<name>
<surname><![CDATA[Cuadra]]></surname>
<given-names><![CDATA[G]]></given-names>
</name>
<name>
<surname><![CDATA[Molina]]></surname>
<given-names><![CDATA[V]]></given-names>
</name>
<name>
<surname><![CDATA[Brandão]]></surname>
<given-names><![CDATA[ML]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Aversive stimulation of the inferior colliculus changes dopamine and serotonin extracellular levels in the frontal cortex: modulation by the basolateral nucleus of the amygdala]]></article-title>
<source><![CDATA[Synapse]]></source>
<year>2005</year>
<volume>55</volume>
<page-range>58-66</page-range></nlm-citation>
</ref>
<ref id="B7">
<label>7</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Pribram]]></surname>
<given-names><![CDATA[KH]]></given-names>
</name>
<name>
<surname><![CDATA[Kruger]]></surname>
<given-names><![CDATA[L]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Functions of the «olfactory brain»]]></article-title>
<source><![CDATA[Ann NY Ac Sci]]></source>
<year>1954</year>
<volume>58</volume>
<page-range>109-38</page-range></nlm-citation>
</ref>
<ref id="B8">
<label>8</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Rodrigues]]></surname>
<given-names><![CDATA[SM]]></given-names>
</name>
<name>
<surname><![CDATA[Schafe]]></surname>
<given-names><![CDATA[GE]]></given-names>
</name>
<name>
<surname><![CDATA[Ledoux]]></surname>
<given-names><![CDATA[JE]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Intra-amygdala blockade of the NR2B subunit of the NMDA receptor disrupts the acquisition but not the expression of fear conditioning]]></article-title>
<source><![CDATA[J Neurosci]]></source>
<year>2001</year>
<volume>21</volume>
<page-range>6889-96</page-range></nlm-citation>
</ref>
<ref id="B9">
<label>9</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Rosenkranz]]></surname>
<given-names><![CDATA[JA]]></given-names>
</name>
<name>
<surname><![CDATA[Moore]]></surname>
<given-names><![CDATA[H]]></given-names>
</name>
<name>
<surname><![CDATA[Grace]]></surname>
<given-names><![CDATA[AA]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[The prefrontal cortex regulates lateral amygdala neuronal plasticity and responses to previously conditioned stimuli]]></article-title>
<source><![CDATA[J Neurosci]]></source>
<year>2003</year>
<volume>23</volume>
<page-range>11054-64</page-range></nlm-citation>
</ref>
<ref id="B10">
<label>10</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Singewald]]></surname>
<given-names><![CDATA[N]]></given-names>
</name>
<name>
<surname><![CDATA[Kouvelas]]></surname>
<given-names><![CDATA[D]]></given-names>
</name>
<name>
<surname><![CDATA[Mostafa]]></surname>
<given-names><![CDATA[A]]></given-names>
</name>
<name>
<surname><![CDATA[Sinner]]></surname>
<given-names><![CDATA[C]]></given-names>
</name>
<name>
<surname><![CDATA[Philippu]]></surname>
<given-names><![CDATA[A]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[release of glutamate and GABA in the amygdala of conscious rats by acute stress and baroreceptor activation: differences between SHR and WKY rats]]></article-title>
<source><![CDATA[Brain Res]]></source>
<year>2000</year>
<volume>864</volume>
<page-range>138-41</page-range></nlm-citation>
</ref>
<ref id="B11">
<label>11</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Stevenson]]></surname>
<given-names><![CDATA[C]]></given-names>
</name>
<name>
<surname><![CDATA[Sullivan]]></surname>
<given-names><![CDATA[RM]]></given-names>
</name>
<name>
<surname><![CDATA[Pomerleaut]]></surname>
<given-names><![CDATA[F]]></given-names>
</name>
<name>
<surname><![CDATA[Gratton]]></surname>
<given-names><![CDATA[A]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Lateralized attenuation of the prefrontal cortical DA stress response following bilateral amygdalar DA depletion]]></article-title>
<source><![CDATA[Abstr Soc Neurosci]]></source>
<year>2000</year>
<volume>26</volume>
<page-range>2248</page-range></nlm-citation>
</ref>
<ref id="B12">
<label>12</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Szinyei]]></surname>
<given-names><![CDATA[C]]></given-names>
</name>
<name>
<surname><![CDATA[Heinbockel]]></surname>
<given-names><![CDATA[T]]></given-names>
</name>
<name>
<surname><![CDATA[Montagne]]></surname>
<given-names><![CDATA[J]]></given-names>
</name>
<name>
<surname><![CDATA[Pape H-]]></surname>
<given-names><![CDATA[C]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Putative cortical and thalamic inputs elicit convergent excitation in a population of GABAergic interneurons of the lateral amygdala]]></article-title>
<source><![CDATA[J Neurosci]]></source>
<year>2000</year>
<volume>20</volume>
<page-range>8909-15</page-range></nlm-citation>
</ref>
<ref id="B13">
<label>13</label><nlm-citation citation-type="journal">
<person-group person-group-type="author">
<name>
<surname><![CDATA[Tucci]]></surname>
<given-names><![CDATA[S]]></given-names>
</name>
<name>
<surname><![CDATA[Rada]]></surname>
<given-names><![CDATA[P]]></given-names>
</name>
<name>
<surname><![CDATA[Hernandez]]></surname>
<given-names><![CDATA[L]]></given-names>
</name>
</person-group>
<article-title xml:lang=""><![CDATA[Role of glutamate in the amygdala and lateral hypothalamus in conditioned taste aversion]]></article-title>
<source><![CDATA[Abstr Soc Neurosci]]></source>
<year>1998</year>
<volume>24</volume>
<page-range>93</page-range></nlm-citation>
</ref>
</ref-list>
</back>
</article>
