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Differential involvement of cortical muscarinic and NMDA receptors in short- and long-term taste aversion memory

Authors

  • G. Ferreira,

    1. Department of Neurosciences, Institute of Cellular Physiology, Universidad Nacional Autónoma de México, Apartado Postal 70–253, 04510 México D.F., México
    2. Laboratory of Animal Behaviour, UMR 6073 CNRS-INRA-Université de Tours, 37380 Nouzilly, France
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  • R. Gutiérrez,

    1. Department of Neurosciences, Institute of Cellular Physiology, Universidad Nacional Autónoma de México, Apartado Postal 70–253, 04510 México D.F., México
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  • V. De la Cruz,

    1. Department of Neurosciences, Institute of Cellular Physiology, Universidad Nacional Autónoma de México, Apartado Postal 70–253, 04510 México D.F., México
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  • F. Bermúdez-Rattoni

    1. Department of Neurosciences, Institute of Cellular Physiology, Universidad Nacional Autónoma de México, Apartado Postal 70–253, 04510 México D.F., México
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: F. Bermúdez-Rattoni, 1Department of Neurosciences.
E-mail: fbermude@ifisiol.unam.mx

Abstract

In conditioned taste aversion, an animal avoids a taste previously associated with toxic effects, and this aversive memory formation requires an intact insular cortex. In this paper, we investigated the possible differential involvement of cholinergic and glutamatergic receptors in the insular cortex in short-term memory (STM) and long-term memory (LTM) of taste aversion in rats. Taste aversion was induced by intraperitoneal administration of lithium chloride (a malaise-inducing drug) 15 min after experience with an unfamiliar taste. In order to test STM and LTM of taste aversion, taste stimulus was again presented 4 h and 72 h after lithium injection, respectively. During the acquisition, microinjection of the muscarinic antagonist, scopolamine, in the insular cortex before, but not after, the presentation of the new taste, abolished STM as well as LTM. Blockade of the NMDA receptor, in the insular cortex, by AP5 before, but not after, the presentation of the taste stimulus, impaired LTM but left STM intact. Moreover, when injected 1 h after malaise induction (i.e., during taste–illness association), AP5 disrupted both STM and LTM. These results suggest that activation of muscarinic receptors in the insular cortex is involved in the acquisition of taste memory, whereas NMDA receptors participate in taste memory consolidation. These data demonstrate that different neurochemical mechanisms subserve different memory phases. NMDA receptors are also probably involved in processing the visceral input, thus allowing subsequent taste–illness association. This indicates that in the same cortical area the same neurotransmitter system can be involved in distinct processes: taste memory consolidation vs. taste–illness association.

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