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Requirement of NF-kappa B Activation in Different Mice Brain Areas during Long-Term Memory Consolidation in Two Contextual One-Trial Tasks with Opposing Valences

View Article: PubMed Central - PubMed

ABSTRACT

NF-kappa B is a transcription factor whose activation has been shown to be necessary for long-term memory consolidation in several species. NF-kappa B is activated and translocates to the nucleus of cells in a specific temporal window during consolidation. Our work focuses on a one trial learning tasks associated to the inhibitory avoidance (IA) setting. Mice were trained either receiving or not a footshock when entering a dark compartment (aversive vs. appetitive learning). Regardless of training condition (appetitive or aversive), latencies to step-through during testing were significantly different to those measured during training. Additionally, these testing latencies were also different from those of a control group that only received a shock unrelated to context. Moreover, nuclear NF-kappa B DNA-binding activity was augmented in the aversive and the appetitive tasks when compared with control and naïve animals. NF-kappa B inhibition by Sulfasalazine injected either in the Hippocampus, Amygdala or Nucleus accumbens immediately after training was able to impair retention in both training versions. Our results suggest that NF-kappa B is a critical molecular step, in different brain areas on memory consolidation. This was the case for both the IA task and also the modified version of the same task where the footshock was omitted during training. This work aims to further investigate how appetitive and aversive memories are consolidated.

No MeSH data available.


Related in: MedlinePlus

Intra-amygdala injections of sulfasalazine impair aversive and appetitive memory. (A) Mouse atlas sections corresponding to the targeted distance from Bregma are shown. Gray represents the maximum area reached by India ink. Asterisks indicate tip of infusion cannula. Black dots indicate injections in animals that did not reach targeted area and thus were discarded from analysis. (B) Latencies to step-through during testing for groups Si Veh, S Veh and S Sulfa are shown. (C) Latencies to step-through during testing for groups Si Veh, U Veh and U Sulfa are shown. Bars show medians with interquartile ranges. *P < 0.01.
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Figure 4: Intra-amygdala injections of sulfasalazine impair aversive and appetitive memory. (A) Mouse atlas sections corresponding to the targeted distance from Bregma are shown. Gray represents the maximum area reached by India ink. Asterisks indicate tip of infusion cannula. Black dots indicate injections in animals that did not reach targeted area and thus were discarded from analysis. (B) Latencies to step-through during testing for groups Si Veh, S Veh and S Sulfa are shown. (C) Latencies to step-through during testing for groups Si Veh, U Veh and U Sulfa are shown. Bars show medians with interquartile ranges. *P < 0.01.

Mentions: To further study the mechanisms involved in the consolidation of contextual-associative memory we targeted the amygdala. We decided to test the NF-kappa B dependent involvement of this area in both S and U versions of the one trial task. For this, all animals were cannulated bilaterally to reach the amygdala and either 1 μg/amygdala Sulfasalazine or Vehicle was injected immediately post-training (Figure 4A). The Si animals injected with vehicle were used as the behavioral control group. The S Veh animals showed longer latencies to step-through during testing when compared with the Si Veh group (Mann-Whitney U = 0.0; p < 0.01, Median Si Veh = 11, n = 9; Median S Veh = 300, n = 9) and this retention was impaired in the S Sulfa group when compared to S Veh (Mann-Whitney U = 6.0; p < 0.01; Median S Veh = 300, n = 9; Median S Sulfa = 78, n = 7) (Kruskal-Wallis statistic H(2,22) = 20.11, p < 0.01; Figure 4B). The amygdala plays a central role in the consolidation of memory in the IA task, and this role is dependent of the NF-kappa B pathway. For the Un-shocked version of the task Sulfasalazine also affected the latencies to step-through. The U Veh animals show lower latencies to step-through than Si Veh animals (Mann-Whitney U = 10.0; p < 0.01; Median Si Veh = 17, n = 11; Median U Veh = 8, n = 9). As in the Shock version of the task, this memory is also impaired when animals are injected with Sulfasalazine. The U Veh animals show lower latencies to step-through than U Sulfa animals (Mann-Whitney U = 7.5; p < 0.01, Median U Veh = 8, n = 9; Median U Sulfa = 17, n = 9) (Kruskal-Wallis statistic H(2,25) = 35.41, p < 0.01; Figure 4C). When compared to vehicle, Sulfasalazine had no effect on latencies to step-through during testing for the Si group (Supplementary Figure S1A). In mice, the consolidation of both Shocked and Un-shocked memories seems to be dependent of the NF-kappa B pathway of the amygdala. This evidence supports that the amygdala plays a central role in the consolidation of memory regardless of the valence of the stimulus.


Requirement of NF-kappa B Activation in Different Mice Brain Areas during Long-Term Memory Consolidation in Two Contextual One-Trial Tasks with Opposing Valences
Intra-amygdala injections of sulfasalazine impair aversive and appetitive memory. (A) Mouse atlas sections corresponding to the targeted distance from Bregma are shown. Gray represents the maximum area reached by India ink. Asterisks indicate tip of infusion cannula. Black dots indicate injections in animals that did not reach targeted area and thus were discarded from analysis. (B) Latencies to step-through during testing for groups Si Veh, S Veh and S Sulfa are shown. (C) Latencies to step-through during testing for groups Si Veh, U Veh and U Sulfa are shown. Bars show medians with interquartile ranges. *P < 0.01.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC5383659&req=5

Figure 4: Intra-amygdala injections of sulfasalazine impair aversive and appetitive memory. (A) Mouse atlas sections corresponding to the targeted distance from Bregma are shown. Gray represents the maximum area reached by India ink. Asterisks indicate tip of infusion cannula. Black dots indicate injections in animals that did not reach targeted area and thus were discarded from analysis. (B) Latencies to step-through during testing for groups Si Veh, S Veh and S Sulfa are shown. (C) Latencies to step-through during testing for groups Si Veh, U Veh and U Sulfa are shown. Bars show medians with interquartile ranges. *P < 0.01.
Mentions: To further study the mechanisms involved in the consolidation of contextual-associative memory we targeted the amygdala. We decided to test the NF-kappa B dependent involvement of this area in both S and U versions of the one trial task. For this, all animals were cannulated bilaterally to reach the amygdala and either 1 μg/amygdala Sulfasalazine or Vehicle was injected immediately post-training (Figure 4A). The Si animals injected with vehicle were used as the behavioral control group. The S Veh animals showed longer latencies to step-through during testing when compared with the Si Veh group (Mann-Whitney U = 0.0; p < 0.01, Median Si Veh = 11, n = 9; Median S Veh = 300, n = 9) and this retention was impaired in the S Sulfa group when compared to S Veh (Mann-Whitney U = 6.0; p < 0.01; Median S Veh = 300, n = 9; Median S Sulfa = 78, n = 7) (Kruskal-Wallis statistic H(2,22) = 20.11, p < 0.01; Figure 4B). The amygdala plays a central role in the consolidation of memory in the IA task, and this role is dependent of the NF-kappa B pathway. For the Un-shocked version of the task Sulfasalazine also affected the latencies to step-through. The U Veh animals show lower latencies to step-through than Si Veh animals (Mann-Whitney U = 10.0; p < 0.01; Median Si Veh = 17, n = 11; Median U Veh = 8, n = 9). As in the Shock version of the task, this memory is also impaired when animals are injected with Sulfasalazine. The U Veh animals show lower latencies to step-through than U Sulfa animals (Mann-Whitney U = 7.5; p < 0.01, Median U Veh = 8, n = 9; Median U Sulfa = 17, n = 9) (Kruskal-Wallis statistic H(2,25) = 35.41, p < 0.01; Figure 4C). When compared to vehicle, Sulfasalazine had no effect on latencies to step-through during testing for the Si group (Supplementary Figure S1A). In mice, the consolidation of both Shocked and Un-shocked memories seems to be dependent of the NF-kappa B pathway of the amygdala. This evidence supports that the amygdala plays a central role in the consolidation of memory regardless of the valence of the stimulus.

View Article: PubMed Central - PubMed

ABSTRACT

NF-kappa B is a transcription factor whose activation has been shown to be necessary for long-term memory consolidation in several species. NF-kappa B is activated and translocates to the nucleus of cells in a specific temporal window during consolidation. Our work focuses on a one trial learning tasks associated to the inhibitory avoidance (IA) setting. Mice were trained either receiving or not a footshock when entering a dark compartment (aversive vs. appetitive learning). Regardless of training condition (appetitive or aversive), latencies to step-through during testing were significantly different to those measured during training. Additionally, these testing latencies were also different from those of a control group that only received a shock unrelated to context. Moreover, nuclear NF-kappa B DNA-binding activity was augmented in the aversive and the appetitive tasks when compared with control and na&iuml;ve animals. NF-kappa B inhibition by Sulfasalazine injected either in the Hippocampus, Amygdala or Nucleus accumbens immediately after training was able to impair retention in both training versions. Our results suggest that NF-kappa B is a critical molecular step, in different brain areas on memory consolidation. This was the case for both the IA task and also the modified version of the same task where the footshock was omitted during training. This work aims to further investigate how appetitive and aversive memories are consolidated.

No MeSH data available.


Related in: MedlinePlus