Basolateral amygdala glutamatergic activation enhances taste aversion through NMDA receptor activation in the insular cortex.
European Journal of Neuroscience. 2005-11-01; 22(10): 2596-2604
DOI: 10.1111/j.1460-9568.2005.04440.x
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1. Eur J Neurosci. 2005 Nov;22(10):2596-604.
Basolateral amygdala glutamatergic activation enhances taste aversion through
NMDA receptor activation in the insular cortex.
Ferreira G(1), Miranda MI, De la Cruz V, Rodríguez-Ortiz CJ, Bermúdez-Rattoni F.
Author information:
(1)Laboratoire de Comportement Animal, UMR 6175 INRA-CNRS-Université de
Tours-Haras Nationaux, 37380 Nouzilly, France.
In conditioned taste aversion (CTA), a subject learns to associate a novel taste
with visceral malaise. Brainstem, limbic and neocortical structures have been
implicated in CTA memory formation. Nevertheless, the role of interactions
between forebrain structures during these processes is still unknown. The present
experiment was aimed at investigating the possible interaction between the
basolateral nucleus of the amygdala (BLA) and the insular cortex (IC) during CTA
memory formation. Injection of a low dose of lithium chloride (30 mg/kg, i.p.) 30
min after novel taste consumption (saccharin 0.1%) induces a weak CTA. Unilateral
BLA injection of glutamate (2 microg in 0.5 microL) just before low lithium
induces a stronger CTA. Unilateral injection of an N-methyl-d-aspartate (NMDA)
receptor antagonist (AP5, 5 microg in 0.5 microL) in IC has no effect. However,
AP5 treatment in IC at the same time or 1 h after the ipsilateral BLA injection
reverses the glutamate-induced CTA enhancement. Injection of AP5 in IC 3 h after
BLA injection does not interfere with the glutamate effect. Moreover, the
CTA-enhancing effect of glutamate was also blocked by contralateral IC injection
of AP5 at the same time. These results provide strong evidence that NMDA receptor
activation in the IC is essential to enable CTA enhancement induced by glutamate
infusion in the BLA during a limited time period that extends to 1 but not to 3
hours. These findings indicate that BLA-IC interactions regulate the strength of
CTA. The bilateral nature of these amygdalo-cortical interactions is discussed.
DOI: 10.1111/j.1460-9568.2005.04440.x
PMID: 16307602 [Indexed for MEDLINE]