Consolidation theory proposes that through the synthesis of new proteins recently acquired memories are strengthened over time into a stable long-term memory trace. However, evidence has accumulated suggesting that retrieved memory is susceptible to disruption, seeming to consolidate again (reconsolidate) to be retained in long-term storage. Here we show that intracortical blockade of protein synthesis in the gustatory cortex after retrieval of taste-recognition memory disrupts previously consolidated memory to a restricted degree only if the experience is updated. Our results suggest that retrieved memory can be modified as part of a mechanism for incorporating updated information into previously consolidated memory.The memory consolidation hypothesis has been the major theoretical framework to explain long-term memory storage (McGaugh 1966(McGaugh , 2000. However, it has been reported that memory activated by retrieval becomes susceptible to disruption by the same means that disrupt consolidation (Misanin et al. 1968;Nader et al. 2000). This process, called reconsolidation, suggests that consolidated memory returns to a labile state similar to recently acquired memory each time it is retrieved (Sara 2000; Debiec et al. 2002). However, most of the studies in which reconsolidation process is achieved have used associative learning tasks requiring the association between a conditioned stimulus (CS) and an unconditioned stimulus (US) followed by extinction trials in which the CS is no longer followed by the US. Therefore, during retrieval, when reconsolidation is assessed, there is a competition between the extinction (CS-noUS) and the associative (CS-US) traces, which both require protein synthesis to be retained in long-term memory (Eisenberg et al. 2003;Pedreira and Maldonado 2003). Here we address the post-retrieval consolidation issue on a taste-recognition memory task that allows us to access the formation of memory in the absence of extinction. That is, we used a CS with the same valence during acquisition and retrieval so extinction does not occur and a competition between memories is not established.Animals exposed to novel taste show reduced consumption (neophobic response). This is followed by graded increases in intake after repeated presentations of the same tastant until a plateau is reached. This behavior is called attenuation of neophobia or AN (Domjan 1977;Buresova and Bures 1980; de VosKorthals and van Hof 1984;Dogterom and van Hof 1988;Bermudez-Rattoni 2004). AN is a long-lasting behavior in which animals must remember a taste as having been experienced previously. This kind of memory is referred as taste-recognition memory (Bermudez-Rattoni 2004), and the insular cortex (IC) (the gustatory neocortex) has been proven to be an important site of gustatory memory formation (Rosenblum et al. 1993; Gutierrez et al. 2003a,b;Bermudez-Rattoni 2004). In AN, the animal exposed to a particular taste will drink more of that solution regardless of the time elapsed between two consecutive taste presentatio...

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.

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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