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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Taste memories are amongst the most important kinds of memories, as adequate identification of safe and toxic edibles will determine the subject's survival. Despite the well-established role that the medial temporal lobe plays in consolidation of memory, specific contributions of the different regions of the temporal lobe to taste memory consolidation remain unknown. In the present report, we assessed the participation of perirhinal cortex (Ph), dorsal hippocampus (Hipp), basolateral (BLA) and central nuclei of the amygdala (CeA) in safe and aversive taste memories by means of local infusions of the protein synthesis inhibitor anisomycin in the rat. The results showed that protein synthesis in the CeA, but not BLA, is required to stabilize taste aversion memory. Surprisingly, the Ph and Hipp seem to be essential to consolidate safe taste memory. These data suggest that different networks within the temporal lobe are recruited to consolidate memory depending on the consequences associated with tastes.

Peritoneal infection with Taenia crassiceps cysticerci of naturally resistant (C57BL/10J and C57BL/6J) and susceptible (BALB/cAnN) mice induces a cellular immune depression. T-cell proliferation in response to concanavalin A (ConA) or anti-CD3 was significantly depressed in infected mice of all strains tested. However, in resistant mice, the diminished response to ConA was transient and animals recovered normal responsiveness at day 40, whereas susceptible mice remained suppressed throughout the 40 days of the experiment. In contrast, the proliferative response to anti-CD3 was lower in infected mice than in noninfected controls regardless of differences in natural susceptibility of the strains. Intraperitoneal injection of mice with a parasite extract also induced a depression of the response to ConA, although not as strong as that produced by the parasite itself. This depression is not due to direct effects by parasite antigens over host lymphocytes, as proliferation is not affected by the presence of cysticercal antigens added in vitro. Diminished interleukin-2 production during the parasitosis accounts at least in part for the diminished responses to ConA. A primary infection favors parasite establishment after a second challenge, pointing to the relevance of the immunodepression in generating a host environment favorable to the parasite.

The relevance of perirhinal cortical cholinergic and glutamatergic neurotransmission for taste recognition memory and learned taste aversion was assessed by microinfusions of muscarinic (scopolamine), NMDA (AP-5), and AMPA (NBQX) receptor antagonists. Infusions of scopolamine, but not AP5 or NBQX, prevented the consolidation of taste recognition memory using attenuation of neophobia as an index. In addition, learned taste aversion in both shortand long-term memory tests was exclusively impaired by scopolamine. These data provide neurochemical support for the theory that cholinergic activity of the perirhinal cortex participates in the formation of the taste memory trace and that it is independent of the NMDA and AMPA receptor activity. These results support the idea that cholinergic neurotransmission in the perirhinal cortex is also essential for acquisition and consolidation of taste recognition memory.

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