Neurotrasmisores del sistema endocrino

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Salud Mental
Instituto Nacional de Psiquiatría Ramón de la Fuente
perezrh@imp.edu.mx

ISSN (Versión impresa): 0185-3325
MÉXICO

2005
Eduardo Castro Sierra / Fernando Chico Ponce de León / Alison Portugal Rivera
NEUROTRANSMISORES DEL SISTEMA LÍMBICO. I. AMÍGDALA. PRIMERA PARTE
Salud Mental, diciembre, año/vol. 28, número 006
Instituto Nacional de Psiquiatría Ramón de la Fuente
DistritoFederal, México
pp. 27-32

Red de Revistas Científicas de América Latina y el Caribe, España y Portugal
Universidad Autónoma del Estado de México

NEUROTRANSMISORES DEL SISTEMA LÍMBICO.
I. AMÍGDALA. PRIMERA PARTE
Eduardo Castro-Sierra 1, F ernando Chico Ponce de León 2, Alison Portugal Rivera 3

SUMMARY
Neurotransmitters of the amygdala in the limbic system include,
among others,γ-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, bothof
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 thecortical 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 thisneurotransmitter, 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 filterof 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 appearto 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.
Key words: Limbic system, neurotransmitters, GABA,...
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