title: Basolateral amygdala glutamatergic activation enhances taste aversion through NMDA receptor activation in the insular cortex.
abstract: 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.
authors.affiliation: Laboratoire de Comportement Animal, UMR 6175 INRA-CNRS-Université de Tours-Haras Nationaux, 37380 Nouzilly, France. miranda@inb.unam.mx
authors.forename: G
authors.initials: G
authors.lastname: Ferreira
authors.forename: M I
authors.initials: MI
authors.lastname: Miranda
authors.forename: V
authors.initials: V
authors.lastname: De la Cruz
authors.forename: C J
authors.initials: CJ
authors.lastname: Rodríguez-Ortiz
authors.forename: F
authors.initials: F
authors.lastname: Bermúdez-Rattoni
mesh_terms: D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000679:Amygdala / Q000502:physiology*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects*; D002540:Cerebral Cortex / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D007839:Functional Laterality / Q000502:physiology; D005971:Glutamates / Q000008:administration & dosage / Q000494:pharmacology*; D018021:Lithium Chloride / Q000494:pharmacology; D008297:Male; D008568:Memory / Q000502:physiology; D008845:Microinjections; D051381:Rats; D017208:Rats, Wistar; D016194:Receptors, N-Methyl-D-Aspartate / Q000819:agonists*; D013649:Taste / Q000187:drug effects*
chemical_list: D018691:Excitatory Amino Acid Antagonists; D005971:Glutamates; D016194:Receptors, N-Methyl-D-Aspartate; D015763:2-Amino-5-phosphonovalerate; D018021:Lithium Chloride