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Bermúdez-Rattoni F, editor. Neural Plasticity and Memory: From Genes to Brain Imaging. Boca Raton (FL): CRC Press/Taylor & Francis; 2007.

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Neural Plasticity and Memory: From Genes to Brain Imaging.

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Chapter 11Memory Reconsolidation or Updating Consolidation?

and .


For a long time, consolidation was seen as a process achieved only on newly acquired memories aimed to store them for the long term. However, pioneer and recent studies have demonstrated that after retrieval, long-term memories may once more undergo a consolidation-like process referred to as reconsolidation. Mainly, reconsolidation is sustained by the now widely reported observation that after a memory trace is activated by means of retrieval and is susceptible to disruption by the same treatments that disrupt memory during consolidation. However, the functional purpose of this process is still a matter of debate.

Recent evidence indicates that reconsolidation is indeed a process by which updated information is integrated through the synthesis of proteins to a memory trace. Hence, the so-called reconsolidation seems more like an updating consolidation intended to modify retrieved memory by a process that integrates updated experience into long-term memory. Through this process, previously consolidated memory is partially destabilized. By the infusion of disrupting agents, it appears as if the process is intended to consolidate memory again. In this chapter, we discuss this issue and propose that updating consolidation is a more descriptive term for this process.


The classification of memories according to their duration was initiated by Hermann Ebbinghauss in his work titled “Uber das Gadachtnis” (About Memory) and formalized later by William James. From these works it appears that memory has, on the basis of its time course, at least two forms, namely short- and long-term memories. Although no fixed time span segregates these two memory forms, it is clear that information stored in long-term memory (LTM) undergoes a consolidation process that strengthens it over time into a stable memory trace.

This process does not take place for short-term memory (STM), which decays much sooner. The term consolidation is acknowledged to Müller and Pilzecker on their study reported in 1900. In one set of experiments, they trained subjects to memorize a list of paired syllables. On the test day, cue syllables (each one was a single syllable of a pair) were presented and the number of complementary recalled syllables was used as a measure of memory retention. A reduction in the number of retrieved syllables from the first list was observed if a second (distracting) list of syllables was presented shortly after training. Furthermore, the longer the interval between the two lists, the less the performance was affected. The researchers concluded that the second list interfered in a time-dependent manner on a physiological process that accounts for the strengthening of memories. They named this process “consolidirung.”1

These observations were mostly ignored until Duncan reported almost 50 years later that he proved that an electroconvulsive shock (ECS) applied after training disrupted memory. Moreover, he showed that memory disruption correlated with the interval between training and ECS application. Since ECS was longer spaced in time from training, memory impairment was reduced. Since then, several other researchers have shown that interfering treatments — from ECS to intracerebral microinjections of protein synthesis inhibitors — applied after acquisition prevent LTM storage. Consistently, LTM is not affected if the intrusive treatment is applied outside the vulnerability window. This, along with the consolidation hypothesis, led to the idea that memory undergoes this time-dependent stabilization process only once. Reliability among a huge amount of related studies sustained the prominent place that this idea occupies in the current model of consolidation.2,3

An important transition in memory research took place after Hebb’s dual-trace proposal suggesting that memory is at first in a labile state maintained by a reverberating neural ensemble. LTM arises from cellular changes in this ensemble allowing memory stabilization.4 Although it is still matter of intense debate whether STM and LTM are serial or parallel processes, dual-trace theory stressed the weight that cellular entities have in memory processing, turning research to the cellular events underlying memory. At the cellular level, STM undergoes activation of transduction* cascades (mainly kinase pathways) after neuronal stimulation. It is proposed that STM remains as long as these cascades are active but for LTM, transduction signals are carried to the nucleus where transcription* is achieved. Afterward, RNA translation will ultimately lead to protein synthesis. These proteins account for cellular plastic changes that are considered the cellular correlations of stable LTM traces, i.e., they are considered the cellular counterparts of consolidation. Hence, memory consolidation requires protein synthesis. It has been extensively reported that protein synthesis inhibition disrupts LTM without affecting STM.3,7–9


As noted earlier, consolidation was seen as a process achieved only on newly acquired memories with the intent of long-term storage. However, pioneer studies indicated that consolidated memories may undergo a consolidation-like process more than once under certain conditions. In 1968, Misanin et al.10 habituated rats to lick from a drinking bottle in a conditioning chamber, after which they were trained in a fear conditioning task in which a tone (conditioned stimulus, CS) was paired to a footshock (unconditioned stimulus, US). As a result, a conditioned response was obtained and used as a measure of memory, in this case, a reduced licking rate from the water bottle after the tone onset. They reported that an ECS applied immediately after conditioning disrupted memory consolidation (Figure 11.1b, Group 2). The interesting point arose from Group 3. Those animals were trained but without delivery of an ECS. A day later, the consolidated fear memory was reactivated by presenting the tone again. Immediately after this memory reactivation, an ECS was applied with the surprising result that memory was impaired when tested 24 hours later (Figure 11.1b, Group 3). Notably, ECS was unable to disrupt memory if the tone cue was not presented (Figure 11.1b, Group 4) and the phenomenon was referred as cue-dependent amnesia.10

FIGURE 11.1. Data from first report on retrograde amnesia induced after memory reactivation.


Data from first report on retrograde amnesia induced after memory reactivation. (a) Schematic representation of protocol used by Misanin et al. (b) Group 1 shows fear conditioning behavior displayed under this protocol, measured as reduced licking from (more...)

Even though these results were at first not replicated,11 they encouraged further (mainly unnoticed) work on the possibility that consolidated memories enter into an active stage upon retrieval. For example, Gordon showed that as occurs with newly acquired memories, retrieved memories are susceptible to disruption in a time-dependent manner.12 Cue-dependent amnesia was further studied in the active–inactive memory model proposed by Lewis.13 who claimed that memories become active under two conditions: when newly acquired and when reactivated by means of retrieval. Any other memory is in an inactive stable state. Recently, cue-dependent amnesia was taken up again and is now referred as reconsolidation.

Reconsolidation proposes that after a memory trace is activated by means of retrieval, it is susceptible to disruption by the same treatments that disrupt memory during consolidation.14,15 In 1992, Bucherelli and Tassoni16 reported that inactivation of the parabrachial nuclei by infusions of tetrodotoxin disrupted previously consolidated memories when reactivated. Similarly, Susan Sara’s group reported that infusions of either NMDA or β-adrenergic antagonists (which disrupted LTM when applied after training) disrupted a clearly established memory trace upon retrieval.17–19 Since then, memory reconsolidation has actively been studied.

The most acknowledged study is the one carried out by Nader and coworkers in 2000.20 This work brought general attention to the reconsolidation phenomenon because of the clean data reported and because of the use of a translational inhibitor that interfered with protein synthesis, considered to be the main cellular substrate for memory consolidation. The experiments were performed in the widely studied fear conditioning task and showed that the same treatment applied under circumstances that disrupt consolidation also impairs memory after retrieval. Similar to the report by Misanin and coworkers, Nader et al. conditioned rats in a tone-foot-shock association but memory was assessed by the percentage of the time that rats were immobile (except for movements required for breathing) to the total time the tone was presented (freezing). The day after conditioning, the protein synthesis inhibitor anisomycin was injected in the amygdala after the tone presentation.

When the subjects were tested 24 hours later, they performed poorly compared to the rats that were not anisomycin-injected (Figure 11.2b). The same treatment was unable to disrupt memory if a retrieval session was not performed (Figure 11.2b, Group 3). The researchers also showed that the effects of anisomycin were time-dependent. When injected 6 hours after memory reactivation, it is unable to disrupt memory. In the years following the Nader study, a wide variety of reports have shown that reconsolidation is indeed a general process achieved in different species and different kinds of memories.21–30

FIGURE 11.2. Intraamygdalar infusion of a protein-synthesis blocker disrupts consolidated fear memory.


Intraamygdalar infusion of a protein-synthesis blocker disrupts consolidated fear memory. (a) Schematic representation of protocol used by Nader et al. (b) Group 1 shows fear conditioning behavior displayed under this protocol, measured as high percentage (more...)


Despite the huge body of experiments supporting reconsolidation, some did not uncover consolidated memory susceptibility to disruption after retrieval.31–34 However, some recent reports have helped explain to an extent why a reconsolidation process is not revealed under certain protocols.26,35,36 To address this issue, we must first look to what is called extinction and again take up the conditioning protocol on which a great number of memory tasks rely. On conditioning, a CS, like a tone, is associated to an US, like a foot shock. As a result, the CS elicits a response that is used as a measure of memory, like freezing.

However, CS presentation in the absence of US eventually leads to a response decrement; in our example, animals stopped freezing. This is extinction. On extinction, the CS is now associated to no-US. Like any other learning, extinction undergoes consolidation. To assess reconsolidation, the CS is commonly presented as a retrieval cue that may lead to extinction. During testing, treatments applied on retrieval may reflect effects over the CS-US association in which case disruption of the conditioned response is observed (reconsolidation is uncovered).

On the other hand, treatments may impair consolidation of extinction, in which case the CS-US association seems unaltered. On this latter scenario, results may be interpreted as lack of a reconsolidation process. Hence, studies like Vianna et al.32 and Berman and Dudai31 reported that protein synthesis inhibition disrupted extinction, leaving CS-US association unimpaired or even strengthened, and pointing at the impression that reconsolidation does not occur under these protocols.

Pedreira and Maldonado35 offered evidence to move forward using a contextual memory task in crabs. When crabs are placed in a particular context and an object is passed overhead, they escape from the moving object, but when this stimulus is repeated several times, the crabs freeze upon presentation of the passing object. However, when the context is changed, freezing of the crabs does not take place. Thus, the context is associated to the passing object and freezing is used as a measure of memory. To induce extinction, the animals were exposed to the context in the absence of the passing object. Pedreira and Maldonado placed conditioned crabs in the training context for either 5 or 60 min as a retrieval session. During the session, they systemically applied the protein synthesis inhibitor cycloheximide and tested 24 hours later. Crabs exposed for 5 min did not undergo a clear extinction and when tested, effects over reconsolidation were found. Conversely, crabs exposed for 60 min extinguished the conditioned response and when tested, extinction was impaired.

These findings have been replicated by many others.26,36 Eisenberg et al.26 trained rats in a taste aversion task. Task acquisition was achieved by pairing a taste with an intraperitoneal injection of a visceral malaise-inducing agent (LiCl). Taste–malaise association produced a long-term aversive memory observed by a reduced intake of that taste in a second presentation compared to its consumption on acquisition. However, on the third presentation, intake was increased, showing that the aversive memory was extinguished. Protein synthesis inhibition disrupted extinction when applied on the second taste presentation leaving CS-US pairing unaltered, i.e., a failing to detect a reconsolidation process.

However, when rats were subjected to the taste–malaise association for two consecutive sessions, extinction was not observed on the subsequent presentations. Under these conditions, protein synthesis inhibition on the presentation following the association sessions showed aversion impairment when the animals were tested, i.e., reconsolidation was revealed. In the same study, medaka fishes were trained in a fear conditioning task. Consistent with the results obtained from rats, protein synthesis inhibition impairs consolidation on the session that led to extinction affected and, in the absence of extinction, protein synthesis inhibition impaired CS-US reconsolidation. Thus, when consolidation of extinction memory was initiated on the retrieval session, reconsolidation of the CS-US association was not observed.

Other authors have found that pharmacological treatments disrupted LTM of recently consolidated but not older consolidated memories.37,38 That is, when the retrieval session takes place on the days following acquisition, memory is susceptible to consolidation blockers. However, as the retrieval session is spaced in time from training, memory becomes less sensitive to these blockers. These results point to the idea that reconsolidation is a process achieved only by recently consolidated memories upon retrieval. However, Suzuki and co-workers36 reported that stronger and older memories are susceptible to disruption upon retrieval too. They showed that stronger and older memories need of a longer retrieval trial to be disrupted by the blockade of protein synthesis than weaker and younger memories. Consistent with the reports of Pedreira and Maldonado35 and Eisenberg et al.,26 these effects were found as long as the retrieval trial did not lead to extinction. Therefore, it seems that the strength of the reminder is related to memory susceptibility to disruption after retrieval.


Probably the most important question regarding the reconsolidation process is: why and under what circumstances is reconsolidation attained? At first glance, it seems counterintuitive to carry out an already achieved process again, i.e., to consolidate once more an already consolidated memory, as is implied by the reconsolidation term. It has been reported that some of the molecular mechanisms involved in consolidation are also required for reconsolidation of the same memory trace and in the same brain region.20,23,24,26,39–43 For example, particular transcription factors have been proven necessary for both consolidation and reconsolidation processes in different memory tasks. Kida and colleagues40 showed CREB involvement in contextual fear conditioning* memory in mice. Also in mice, Bozon and co-workers41 reported a zif268 requirement in object recognition memory and finally, Merlo et al.42 showed NF-B participation in contextual memory using the crab model described above. In rats, Duvarci, Nader, and LeDoux43 showed that the extracellular signal-regulated kinase (ERK) pathway must be activated in the amygdala for both consolidation and reconsolidation of fear conditioning. Furthermore Sangha et al.24 reported that for the Lymnaea stagnalis snail, consolidation and reconsolidation occurred in the same cell. These data indicate that reconsolidation may be a remaking of the consolidation process.15

However, several other studies suggest that consolidation and reconsolidation are different processes. Taubenfeld and colleagues44 reported that the transcription factor C/EBPβ is needed for consolidation but not for consolidation of a context-dependent task in the dorsal hippocampus. Tronel and Sara45 described differential activation of several brain regions after retrieval compared to consolidation of an odor-reward task learning analyzed by c/Fos immunohistochemistry. In the same regard, Kelly and co-workers28 demonstrated an increase in phosphorylation of ERK kinases in the dentate gyrus and the entorhinal cortex after training in an object recognition task along with increased phosphorylation in the hippocampal CA1 region and the entorhinal cortex after memory retrieval. On taste memory, it was reported that muscarinic receptor activity in the gustatory cortex is required for safe memory consolidation but not for postretrieval consolidation.46 Similarly, protein synthesis in the central amygdala is required for consolidation but not for reconsolidation of conditioned taste aversion.47 Finally, Lee et al.48 reported that the growth factor BDNF is required for consolidation but not for reconsolidation, and transcription factor zif268 is needed for reconsolidation but not consolidation in the same brain region and memory task. All this evidence discards the possibility that reconsolidation is a recapitulation of consolidation but does not solve the problem. The question remains: what is the physiological purpose of reconsolidation?


Early and recent reviews suggest that reconsolidation may be a state for incoming information to modify established memories but experimental support is almost completely absent.13,14,49,50 However, our group recently reported that newly acquired and retrieved taste recognition memory is susceptible to disruption by the protein synthesis inhibitor anisomycin when applied in the insular cortex (IC), a proven site for taste memory consolidation. In that work, the attenuation of neophobia (AN) task was used. Animals showed graded increases in intake after repeated presentations of the same tastant until a plateau was reached (Figure 11.3a).51,52

FIGURE 11.3. Attenuation of neophobia (AN) behavior and protein synthesis inhibition effect (a) Mean ± S.


Attenuation of neophobia (AN) behavior and protein synthesis inhibition effect (a) Mean ± S.E.M. intake (in mL) of 0.3% saccharin solution on unoperated rats. Taste presentations were daily for 15 min. (b) and (c) Anisomycin infusion in insular (more...)

Importantly, anisomycin injections produced a partial disruption of previously consolidated memory and the observed impairment became less noticeable as a response plateau was reached (Figure 11.3b and c). On asymptotic performance, anisomycin affects no longer consolidated memory (Figure 11.3d). These results led to the proposal that a protein-synthesis-dependent process is achieved as long as updated experience capable of affecting behavior is acquired. This process is aimed to integrate updated relevant information to LTM. Consistently, part of the older consolidated memory is dependent on protein synthesis. Partial susceptibility to disruption of a previously consolidated memory trace may be the physiological substrate that allows incoming material to integrate to memory.

Furthermore, when there is no more relevant information to be learned, i.e., after asymptotic task performance is reached, memory is no longer vulnerable to protein synthesis inhibition. Moreover, when the AN plateau has been reached and information of a different quality is provided, like aversive information, the protein-synthesis-dependent process is achieved once more (Figure 11.3e).53

These results were partially replicated in a widely studied hippocampus-dependent memory task, the Morris water maze (WM). In this task, animals escape from cool water by finding a hidden platform underwater. To do so, animals learn spatial cues around the room to locate the platform.54 Rats were trained for either 3 or 5 consecutive days in the WM task. Seven days later on the memory reactivation session, rats swam for 60 sec without the platform and memory was assessed by counting the number of crossings to the platform location during training.

Clearly, the animals trained for 5 days performed much better than those trained only for 3 days. Thus, 3-day trained rats were designated middle-trained and 5-day trained rats were referred to as well-trained. When tested 7 days after the reactivation session, middle-trained subjects infused with a consolidation blocker in the dorsal hippocampus on reactivation performed poorly compared to the corresponding vehicle group. However, the same treatment did not affect consolidated memory in well-trained animals, presumably because no further updating was attained.55 Similarly, Morris et al.56 reported that asymptotic WM task performance was not affected by protein synthesis inhibition in the dorsal hippocampus.

Conversely, task performance was disrupted by the same treatment when updating information was continuously acquired. They trained rats for 6 days in the WM task with the platform in a constant position. On day 7, retrieval was accounted by a single trial and anisomycin was immediately injected locally. Under these conditions memory was unimpaired. Interestingly, when the platform location was changed daily during training, anisomycin injection after retrieval on day 7 disrupted previously consolidated memory. The authors concluded that acquisition of new information is required to observe consolidated memory susceptibility to protein synthesis inhibition.

Thus, the so-called reconsolidation seems more like an updating consolidation intended to modify retrieved memory by a process that integrates updated experience into long-term memory. Previously consolidated memory is partially destabilized and by the infusion of disrupting agents it appears as if the process is intended to consolidate memory again. Two important features must be stressed about the updating consolidation process: it is time- and protein-synthesis-dependent. These features again bring attention to the cellular changes that account for LTM, i.e., the stabilization of neural ensembles.4

Updating consolidation may be the process by means of which neural ensembles are modified and stabilized into updated memory traces. This proposal is based on the analysis of behavior, and even though it is clear that behavior is not merely a reflection of memory; we think it is possible to outline some of the changes that the updating consolidation process may produce in the memory traces based on the behavioral observations depicted above (for more on the behavior–memory dichotomy see Chapter 1). In a simple scenario, two types of information can modify behavior.

Reinforcement of previous learning

As with a learning curve, previous learning is strengthened on each trial because information of the same quality is acquired. Keeping in mind that a neuronal ensemble underlies a particular memory, reinforcing information may modify the existing consolidated trace by two means: by making the synaptic weights of the already existing ensemble stronger or by addition of cellular entities to the previously consolidated ensemble. In both cases, modifications of the synaptic weights involved in the ensemble are required.

Using artificial neural network simulation, it has been proposed that in order to preserve old memories while learning sequential new patterns, an active maintenance process is required. Otherwise, old memory is lost with incoming information. In this model, new learning is incorporated to old patterns by partially rehearsing the old ones. Importantly, modifications in synaptic weights are needed if the ensemble is to retain previously stored material while learning new information.57

Updating consolidation is the proposed mechanism that permits modifications of the ensemble. By protein synthesis inhibition, updating consolidation is unveiled in the limited disruption of previously acquired information that is less noticeable as plateau performance is reached. Consistently, lack of memory disruption by protein synthesis inhibitors correlates with the asymptotical level in task performance. In this regard, positive modulation of a retrieved memory was reported in crabs.58 The study showed that through retrieval, a weak memory is strengthened by an endogenous brain mechanism mediated by angiotensin II. Although, positive modulation of retrieved memories has been reported,14,59 this study was done to shed light upon the functional value of reconsolidation. In accordance with the updating consolidation proposal, the researchers concluded that reconsolidation is a state for modifying memory strength.

A last piece of evidence comes from memory studies in chicks. Summers et al.60 reported that a weak memory is strengthened by means of retrieval. They suggested that memory retrieval initiates a mechanism that allows incorporation of information acquired in the retrieval session to LTM. However, memory retrieval was found to modify memory as long as consolidation was not accomplished. Thus, this mechanism in chicks seems limited to the time before memory is stored.60,61 This is not the case in rats, where memory can be modified after consolidation is attained and even more, as noted above, limited disruption of previously consolidated memory is observed.

Shift of previous learning

Divergent information is integrated to previously consolidated memory. For example, taste aversion can be learned from a taste already tagged as a safe stimulus.53,62 Under these conditions, taste aversion requires a protein synthesis-dependent process to be stored in the long term. One possibility for this integration to occur is that the ensemble suffers greater modifications than when strengthening information is acquired. On the other hand, a different but overlapping trace would be created for this divergent information, in which case modifications in the synaptic weights involved in the first ensemble would take place as well. Overlapping between the ensembles is supposed because they represent divergent associations between overlapping stimuli. In our taste memory example, this overlapping is uncovered on the aversion level that animals show to a taste previously tagged as safe (Figure 11.3e). Less aversion is observed when compared to the aversion shown to the same taste when novel. Reinforcement of aversive learning is required to reach similar aversion levels when the taste was previously learned as safe.

Another example has been reported in the Manduca sexta moth. Daly and colleagues63 found progressive neural recruitment and changes on network activity over the course of olfactory conditioning. Their results point to the idea that olfactory memory traces are modified upon experience. Hence, memories are not separate entities; rather they overlap to some extent. Overlapping of the traces is determined by the similarities of the involved information. This idea is in line with previous theories regarding incorporation of recent experiences into long-term knowledge background.64–66

Extinction is another possibility in which a memory trace can be updated by divergent information. Ample evidence indicates that extinction is not forgetting nor erasing of conditioning learning, but a related learning that elicits a behavioral shift upon CS presentation.67 This evidence is congruent with the proposed model of updating consolidation. Updating does not imply erasing of previous learning but incorporation of a related learning that takes over behavior.53

Eisenberg and Dudai38 consistently reported that disrupted memory upon retrieval is recovered by presentation of an unpaired reinforcer. Similarly, contextual conditioning memory disrupted after retrieval was shown to recover spontaneously after 21 days.68 Power et al.69 found contextual-conditioning memory recovery 6 days after acquisition and, moreover; using the same memory task, Prado-Alcalá et al.70 reported that repeated retrieval sessions are sufficient to fully recover memory previously affected on retrieval by tetrodotoxin injections.

These results suggest that disruption of the reconsolidation process does not abolish consolidated memory; instead, the observed memory destabilization known as reconsolidation may be related to interference with the proposed updating process aimed at the integration of related learning. The result of this process will be stable overlapping traces. The relationships of these converging (trace reinforcement) or diverging (trace shift) overlapping traces will determine behavior.

Recently, it was reported that reconsolidation and integration of new information to memory are dissociable processes. Animals were conditioned using a light and a context as CSs, and footshocks as USs. On retrieval, a new context and the same light were presented without the US. As a consequence, an association was established between the first conditioning, i.e, the first CS-US association, and the new context. When tested, animals elicited the conditioned response (freezing) when placed in the second context, that is, a new CS.

The association between a CS and a previously acquired CS-US association is called second order conditioning. Inhibition of the transcription factor C/EBPβ in the hippocampus disrupted LTM of the second conditioning. Conversely, if retrieval is assessed presenting the same stimuli as in acquisition C/EBPβ is required in the amygdala for memory to remain. Thus, it was concluded that linking new of information occurs without destabilizing the retrieved memory.71

Contrary to this, we found in two different memory tasks and regions that partial disruption of consolidated memory is observed by consolidation blockers upon memory updating. Moreover, protein synthesis is still required in the same region even though updated information is of different quality. It is important to note that the differences in molecular mechanisms found by Tronel et al.71 indeed support the view that linking new information is not the same as reinforcement of previous learning (as reconsolidation is not a bona fide copy of consolidation), but do not support that reconsolidation is not intended to update memory.

The important issue is that reinforcement of previous learning is not synonymous with reconsolidation and that linking new information is different from a reconsolidation process. On their retrieval protocol, Tronel et al. used either the same (which they called reconsolidation) or different information (another context they called linking new information) compared to acquisition. Integration of information of one kind does not necessarily imply that integration of another kind requires the same mechanisms. All in all, we consider that evidence is accumulating for the hypothesis that reconsolidation is indeed an updating consolidation. In this time- and protein-synthesis-dependent process, retrieved memory seems to be modified by the integration of updated relevant experience.


We thank Oreste Carbajal for technical assistance. Part of the work described in this chapter was supported by CONACYT-México 42657/A-1 and DGAPA.-UNAM IN-220706-3.


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Process by which a cell converts an extracellular signal into a response.5


Synthesis of RNA on DNA template.6

Synthesis of protein on mRNA template.6


In this protocol, a context (CS) like a particular chamber is associated with a footshock (US). As with fear conditioning, the response used as a measure of memory is freezing (in this case, a reaction to the chamber, not to a tone).

This kind of memory reflects the judgment of previous experience with particular stimuli. The tasks commonly rely on the natural tendency of rodents to explore new stimuli. In the first phase, animals are habituated to a novel stimulus like a light bulb. After a delay, the second phase involves presentation of a copy of the bulb along with some other stimulus like a glass jar. During this phase, the animals explore the jar over the bulb, indicating that the jar is a new stimulus and the bulb a familiar one, that is, the bulb is recognized as a familiar stimulus.

Copyright © 2007, Taylor & Francis Group, LLC.
Bookshelf ID: NBK3905PMID: 21204424


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