Castro-Sierra E, Chico PLF, Portugal RA

Language: Spanish
References: 13
Page: 27-32
PDF size: 122.39 Kb.

ABSTRACT

Neurotransmitters of the amygdala in the limbic system include, among others, γ-aminobutyric acid (GABA_A,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 pre-synaptic inhibitors of GABA_B 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.

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