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Retrieval does not induce reconsolidation of inhibitory avoidance memory - PubMed

Comparative Study

. 2004 Sep-Oct;11(5):572-8.

doi: 10.1101/lm.76804.

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Comparative Study

Retrieval does not induce reconsolidation of inhibitory avoidance memory

Martín Cammarota et al. Learn Mem. 2004 Sep-Oct.

Abstract

It has been suggested that retrieval during a nonreinforced test induces reconsolidation instead of extinction of the mnemonic trace. Reconsolidation would preserve the original memory from the labilization induced by its nonreinforced recall through a hitherto uncharacterized mechanism requiring protein synthesis. Given the importance that such a process would have in terms of maintaining, as part of the animal behavioral repertoire, a learned response that has been devalued by experience, we analyzed its existence for the memory associated with a one-trial, step-down inhibitory avoidance task (IA), a memory whose consolidation and extinction require protein synthesis in the CA1 region of the dorsal hippocampus (CA1) and involve the participation of the basolateral amygdala (BLA) and entorhinal cortex (ENT). Rats were trained in IA, and 24 h later they were submitted either to a pure reactivation session (retrieval without stepping down), which was unable by itself to initiate extinction of the avoidance response, or to a second training session. Fifteen minutes before or 3 h after either the reactivation or the retraining sessions, animals were infused with the protein synthesis inhibitor anisomycin (ANI) into CA1, BLA, or ENT. Contrary to the prediction of the reconsolidation hypothesis, none of these treatments affected subsequent memory retention. Because reconsolidation is regarded to be a direct consequence of retrieval, one would expect that, when given before a retention test or a pure reactivation session, enhancers of memory expression should permanently improve retention and, therefore, facilitate retrieval both in that and in subsequent sessions. Using two well-known retrieval enhancers, noradrenaline and adrenocorticotropin(1-24), we could not find any evidence suggestive of reconsolidation. Hence, our results indicate that there is no retrieval-induced, protein synthesis-dependent process that would cause reconsolidation of IA memory.

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Figures

Figure 1
Figure 1

Consolidation of IA memory requires protein synthesis in the CA1 region of the dorsal hippocampus. Animals who had cannulas implanted and aimed toward the CA1 region of the dorsal hippocampus were trained in the IA task using a 0.5-mA (A,B) or 0.8-mA (C,D), 2-sec foot-shock. Fifteen minutes before (A,C) or 3 h after (B,D) the training session, the animals received 0.8 μL bilateral infusions of vehicle (VEH) or ANI (80 μg/side). Memory retention was evaluated in a test session carried out 24 h posttraining (TT1). Data represent median ± interquartile range of the step down latency time. *P < 0.005 versus VEH in Mann-Whitney test; n = 10 to 14 per group.

Figure 2
Figure 2

Memory reactivation without stepping down does not induce extinction of the IA response. Animals trained in the IA task (0.5 mA, 2-sec) were randomly assigned to one out of four experimental groups. The control group consisted of trained animals that were not submitted to any other behavioral procedure until they had been tested for IA retention. The reactivation group consisted of trained animals submitted to daily 20-sec pure reactivation sessions for 3 days. These animals were put on the training box platform and allowed to explore it freely. During the 20-sec period, rats avoided stepping down to the grid. The extinction group consisted of trained animals submitted to daily extinction sessions for 3 days. These animals were put on the training box platform and, at the very moment they eventually stepped down from it (no shock delivered), were removed to their home cages. The enhanced extinction group consisted of trained animals submitted to daily enhanced extinction sessions for 3 days. These animals were put on the training box platform and, after stepping down from it (no shock delivered), were allowed to freely explore the training box for 30 sec. Data represent median ± interquartile of the step-down latency time in a retention test session carried out 4 days after training. *P < 0.001 versus control group in Dunn's test after Kruskal-Wallis; n = 18 to 20 per group.

Figure 3
Figure 3

Inhibition of protein synthesis in the CA1 region at the moment of or 3 h after a pure reactivation session does not affect an already consolidated mnemonic trace. Animals implanted with cannulas aimed to the CA1 region of the dorsal hippocampus were trained in the IA task using a 0.5-mA (A) or 0.8-mA (B,C), 2-sec foot-shock and 24 h later were submitted to a 20-sec (A,B) or 40-sec (C) pure reactivation session. Fifteen minutes before or 3 h after that session, the animals received 0.8 μL bilateral infusions of VEH or ANI (80 μg/side). Memory retention was evaluated in a test session carried out 24 h postreactivation (TT2); n = 12 to 15 per group.

Figure 4
Figure 4

Inhibition of protein synthesis in the BLA or the ENT at the moment of or 3 h after a pure reactivation session does not affect an already consolidated mnemonic trace. Animals implanted with cannulas aimed to the BLA (A) or the entorhinal cortex (B) were trained in the IA task using a 0.5-mA, 2-sec foot-shock and, 24 h later, were submitted to a 20-sec pure reactivation session. Fifteen minutes before (-15 min) or 3 h after (+3 h) that session, the animals received 0.8 μL bilateral infusions of VEH or ANI (80 μg/side). Memory retention was evaluated in a test session carried out 24 h postreactivation (TT2); n = 10 to 12 per group.

Figure 5
Figure 5

Inhibition of protein synthesis in the CA1 region does not block the enhancement in memory retention induced by retraining. Animals implanted with cannulas aimed to the CA1 region of the dorsal hippocampus were trained in the IA task using a 0.5-mA, 2-sec foot-shock and, 24 h later, were submitted to a retraining session (TT1). Fifteen minutes before (A) or 3 h after (B) that session, the animals received 0.8 μL bilateral infusions of VEH or ANI (80 μg/side). Memory retention was evaluated in a test session carried out 24 h after retraining (TT2). *P < 0.001 versus TT1 in Mann-Whitney test; n = 10 to 12 per group.

Figure 6
Figure 6

Inhibition of protein synthesis in the BLA or the ENT does not block the enhancement in memory retention induced by retraining. Animals implanted with cannulas aimed to the BLA (A) or the ENT (B) were trained in the IA task using a 0.5-mA, 2-sec foot-shock and, 24 h later, were submitted to a retraining session (TT1). Fifteen minutes before (-15 min) or 3 h after (+3 h) the second training session, animals received 0.8 μL bilateral infusions of VEH or ANI (80 μg/side). Memory retention was evaluated in a test session carried out 24 h after retraining (TT2). *P < 0.001 versus TT1 in Mann-Whitney test; n = 10 to 12 per group.

Figure 7
Figure 7

Retrieval enhancers do not affect memory expression beyond the test session prior to which they were administered. Either animals implanted with cannulas aimed to the CA1 region of the dorsal hippocampus (CA1), the BLA, or the ENT or nonimplanted animals were trained in the IA task using a 0.5-mA, 2-sec foot-shock and, 24 h after training, were submitted to a retention test session (A,C; TT1) or to a 20-sec pure reactivation session (B,D). Fifteen minutes before those sessions, the animals received intra-CA1, intra-BLA, or intra-ENT infusions of noradrenaline (NOR; A,B) or intraperitoneal injections of ACTH (C,D). Memory was evaluated in a test session carried out 24 h later (TT2); that is, 48 h posttraining. *P < 0.001 versus VEH TT1 in Mann-Whitney test; n = 10 to 14 per group.

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