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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-nucleus accumbens 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 5: Intra-nucleus accumbens 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: In pursuit of understanding further which areas are involved in the formation of different valence memories we decided to study the nucleus accumbens. Animals were cannulated bilaterally to reach the nucleus accumbens as described in materials and methods and 1 μg/nucleus accumbens of Sulfasalazine or vehicle was injected on each side immediately post-training (Figure 5A). The S Veh animals showed significantly higher latencies to step-through than Si Veh animals (Mann-Whitney U = 0.0; p < 0.01; Median Si Veh = 12.5, n = 10; Median S Veh = 300, n = 10). The S Sulfa animals showed shorter latencies to step-through than S Veh animals (Mann-Whitney U = 9.0; p < 0.01; Median S Veh = 300, n = 10; Median S Sulfa = 68.5, n = 10) (Kruskal-Wallis statistic H(2,27) = 24.36, p < 0.01; Figure 5B). This result implies that the NF-kappa B pathway in the nucleus accumbens is necessary for the consolidation on long-term Shocked memories. On the other hand we showed that the NF-kappa B pathway in the nucleus accumbens is also necessary for long-term consolidation of Un-shocked memories. The U Veh animals showed shorter step-through latencies than Si Veh animals (Mann-Whitney U = 1.0; p < 0.01; Median U Veh = 3, n = 7; Median Si Veh = 12, n = 7) and U Sulfa animals (Mann-Whitney U = 0.0; p < 0.01; Median U Veh = 3, n = 7 Median U Sulfa = 11.5, n = 8) (Kruskal-Wallis statistic H(2,19) = 13.26, p < 0.01; Figure 5C). Sulfasalazine had no effect on latencies to step-through during testing for the Si group when compared to vehicle (Supplementary Figure S1B). Therefore sulfasalazine impairs long-term memory consolidation of both Shocked and Un-shocked memories when injected intra-nucleus accumbens. The NF-kappa B pathway in the nucleus accumbens is involved 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-nucleus accumbens 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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Figure 5: Intra-nucleus accumbens 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: In pursuit of understanding further which areas are involved in the formation of different valence memories we decided to study the nucleus accumbens. Animals were cannulated bilaterally to reach the nucleus accumbens as described in materials and methods and 1 μg/nucleus accumbens of Sulfasalazine or vehicle was injected on each side immediately post-training (Figure 5A). The S Veh animals showed significantly higher latencies to step-through than Si Veh animals (Mann-Whitney U = 0.0; p < 0.01; Median Si Veh = 12.5, n = 10; Median S Veh = 300, n = 10). The S Sulfa animals showed shorter latencies to step-through than S Veh animals (Mann-Whitney U = 9.0; p < 0.01; Median S Veh = 300, n = 10; Median S Sulfa = 68.5, n = 10) (Kruskal-Wallis statistic H(2,27) = 24.36, p < 0.01; Figure 5B). This result implies that the NF-kappa B pathway in the nucleus accumbens is necessary for the consolidation on long-term Shocked memories. On the other hand we showed that the NF-kappa B pathway in the nucleus accumbens is also necessary for long-term consolidation of Un-shocked memories. The U Veh animals showed shorter step-through latencies than Si Veh animals (Mann-Whitney U = 1.0; p < 0.01; Median U Veh = 3, n = 7; Median Si Veh = 12, n = 7) and U Sulfa animals (Mann-Whitney U = 0.0; p < 0.01; Median U Veh = 3, n = 7 Median U Sulfa = 11.5, n = 8) (Kruskal-Wallis statistic H(2,19) = 13.26, p < 0.01; Figure 5C). Sulfasalazine had no effect on latencies to step-through during testing for the Si group when compared to vehicle (Supplementary Figure S1B). Therefore sulfasalazine impairs long-term memory consolidation of both Shocked and Un-shocked memories when injected intra-nucleus accumbens. The NF-kappa B pathway in the nucleus accumbens is involved 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