The consolidation of new but not reactivated memory requires hippocampal C/EBPβ

Taubenfeld, Stephen M.; Milekic, Maria H.; Monti, Barbara; Alberini, Cristina M.

doi:10.1038/90520

Cited by 390 publications

(395 citation statements)

References 36 publications

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“…These findings are consistent with those of many prior studies involving injections of protein synthesis inhibitors into the hippocampus (e.g., Bourtchouladze et al 1998;Quevedo et al 1999Quevedo et al , 2004Taubenfeld et al 2001;Barriantos et al 2002;Agnihotri et al 2004;Artinian et al 2007), as well as into other brain areas such as the amygdala (Nader et al 2000;Schafe and LeDoux 2000;Debiec et al 2002;Duvarci et al 2005;Parsons et al 2006;Milekic et al 2007), and prefrontal cortex (Santini et al 2004;Akirav and Maroun 2006;Touzani et al 2007). These reports are part of a large set of papers showing that direct brain injections of protein synthesis inhibitors produce amnesia for many tasks (cf.…”

Section: Discussionsupporting

confidence: 92%

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Qi¹,

Gold²

2009

Learn. Mem.

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Intra-amygdala injections of anisomycin produce large increases in the release of norepinephrine (NE), dopamine (DA), and serotonin in the amygdala. Pretreatment with intra-amygdala injections of the b-adrenergic receptor antagonist propranolol attenuates anisomycin-induced amnesia without reversing the inhibition of protein synthesis, and injections of NE alone produce amnesia. These findings suggest that abnormal neurotransmitter responses may be the basis for amnesia produced by inhibition of protein synthesis. The present experiment extends these findings to the hippocampus and adds acetylcholine (ACh) to the list of neurotransmitters affected by anisomycin. Using in vivo microdialysis at the site of injection, release of NE, DA, and ACh was measured before and after injections of anisomycin into the hippocampus. Anisomycin impaired inhibitory avoidance memory when rats were tested 48 h after training and also produced substantial increases in local release of NE, DA, and ACh. In an additional experiment, pretreatment with intrahippocampal injections of propranolol prior to anisomycin and training significantly attenuated anisomycininduced amnesia. The disruption of neurotransmitter release patterns at the site of injection appears to contribute significantly to the mechanisms underlying amnesia produced by protein synthesis inhibitors, calling into question the dominant interpretation that the amnesia reflects loss of training-initiated protein synthesis necessary for memory formation. Instead, the findings suggest that proteins needed for memory formation are available prior to an experience, and that post-translational modifications of these proteins may be sufficient to enable the formation of new memories.A dominant view of the molecular basis for memory is that the formation of long-term memory for an experience depends on de novo protein synthesis initiated by that experience (Davis and Squire

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Section: Discussionsupporting

confidence: 92%

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Qi¹,

Gold²

2009

Learn. Mem.

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“…In addition to those studies using protein-synthesis inhibitors (Judge and Quartermain 1982;Nader et al 2000;Anokhin et al 2002;Sangha et al 2003; for review, see Alberini 2005) other studies were performed in order to test the memory reconsolidation hypothesis using blockers of transcription factors and/or immediate early gene expression (Taubenfeld et al 2001;Kida et al 2002;Bozon et al 2003;Lee et al 2004;Merlo et al 2005), inhibitors of kinases (Kelly et al 2003;Koh and Bernstein 2003), or new potential learning situations (Gordon and Spear 1974;Walker et al 2003;Boccia et al 2005), and only a few studies found evidence of enhancement of memory with post-retrieval treatments (De Vietti et al 1977;Horne et al 1997, Rodriguez et al 1999. This is an important issue if we want to compare consolidation vs. reconsolidation memory processes.…”

Section: Discussionmentioning

confidence: 99%

Post-retrieval effects of icv infusions of hemicholinium in mice are dependent on the age of the original memory

Boccia¹,

Blake²,

Acosta³

et al. 2006

Learn. Mem.

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CF-1 male mice were trained in an inhibitory avoidance task using a high footshock (1,2 mA, 50 Hz, 1 sec) in order to reduce the influence of extinction on retention performance. At 2, 7, 14, or 30 d after training, the first retention test was performed and hemicholinium (HC-3, 1.0 µg/mice), a specific inhibitor of high-affinity choline uptake in brain cholinergic neurons, was given intracerebroventricularly immediately after. Twenty four hours after treatment, mice were tested in an inhibitory avoidance task during five consecutive days, each 24 h apart. Retention performance was impaired by HC-3 when the first re-exposure took place at 2, 7, or 14 d, but the effect was no longer seen when re-exposure occurred 30 d after training. We did not find spontaneous recovery 21 d after training, when memory was retrieved 2 d after training and HC-3 was given immediately after. Although we cannot definitively discard a retrieval deficit, this lack of spontaneous recovery is in accordance with the storage-deficit interpretation. These results confirm and extend previous ones, suggesting that central cholinergic mechanisms are involved in the hypothetical reconsolidation memory processes of an inhibitory avoidance task in mice and also suggest that this participation depends on the "age" of the original memory trace. This implies that the vulnerability of a reactivated memory to a specific treatment, as the one used in this study, inversely correlates with the age of the original memory, and it is likely to determine memory reconsolidation processes.

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“…Lee et al (49) reported that antisense-mediated disruption of the transcription factor zinc finger (zif268) in the rat hippocampus impairs reconsolidation but not consolidation of contextual fear conditioning, whereas, conversely, antisense-mediated disruption of brain-derived neurotrophin factor impairs consolidation but not reconsolidation, suggesting that the molecular mechanisms required by the hippocampus during either consolidation or reconsolidation are distinct. This line of evidence showed that the disruption of C/EBPβ, known as a fundamental molecular pathway required for memory consolidation, by injection of specific antisense oligodeoxynucleotides (β-ODNs) in the hippocampus, impairs long-term memory of inhibitory avoidance in rats (50). In contrast, when injected immediately after memory reactivation it has no effect on memory retention tested 2 days later.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological effects and behavioral interventions on memory consolidation and reconsolidation

Baratti

Boccia

Blake

2009

Braz J Med Biol Res

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In this article, we will review some behavioral, pharmacological and neurochemical studies from our laboratory on mice, which might contribute to our understanding of the complex processes of memory consolidation and reconsolidation. We discuss the post-training (memory consolidation) and post-reactivation (memory reconsolidation) effects of icv infusions of hemicholinium, a central inhibitor of acetylcholine synthesis, of intraperitoneal administration of L-NAME, a non-specific inhibitor of nitric oxide synthase, of intrahippocampal injections of an inhibitor of the transcription factor NF-κB, and the exposure of mice to a new learning situation on retention performance of an inhibitory avoidance response. All treatments impair long-term memory consolidation and retrieval-induced memory processes different from extinction, probably in accordance with the "reconsolidation hypothesis".

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The consolidation of new but not reactivated memory requires hippocampal C/EBPβ

Cited by 390 publications

References 36 publications

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Intrahippocampal infusions of anisomycin produce amnesia: Contribution of increased release of norepinephrine, dopamine, and acetylcholine

Post-retrieval effects of icv infusions of hemicholinium in mice are dependent on the age of the original memory

Pharmacological effects and behavioral interventions on memory consolidation and reconsolidation

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