Participation of Rel/NF-κB transcription factors in long-term memory in the crab Chasmagnathus

Freudenthal, Ramiro; Romano, Arturo

doi:10.1016/s0006-8993(99)02358-6

Cited by 111 publications

(80 citation statements)

References 27 publications

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“…Synapse-to-nucleus signals have been shown to exist in the context of synaptic plasticity in invertebrate neurons (37)(38)(39)(40), but demonstration of synapse-to-nucleus signaling in vertebrate neurons has been difficult. These two models of synaptic plasticity differ in many anatomical and physiological respects, and the essential studies have not yet been performed to directly link such signaling to hippocampal LTP.…”

Section: Discussionmentioning

confidence: 99%

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Dudek

Fields

2002

Proc. Natl. Acad. Sci. U.S.A.

104

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A question of critical importance confronting neuroscientists today is how biochemical signals initiated at a synapse are conveyed to the nucleus. This problem is particularly relevant to the generation of the late phases of long-term potentiation (LTP). Here we provide evidence that some signaling pathways previously associated with late-LTP can be activated in hippocampal CA1 neurons without synaptic activity; somatic action potentials, induced by backfiring the cells, were found to be sufficient for phosphorylation of extracellular signal-regulated kinase-1/2 and cAMP response element-binding protein, as well as for induction of zif268. Furthermore, such antidromic stimulation was adequate to rescue ''tagged'' synapses (early-LTP) from decay. These results show that a synapse-to-nucleus signal is not necessary for late-phase LTPassociated signaling cascades in the regulation of gene expression.

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Section: Discussionmentioning

confidence: 99%

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Dudek

Fields

2002

Proc. Natl. Acad. Sci. U.S.A.

104

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“…The first evidence indicating that learning activates NF-B was found in the context-signal learning of the crab Chasmagnathus. In this model, a high correlation between memory formation and NF-B activation was demonstrated (Freudenthal et al 1998;Freudenthal and Romano 2000). In addition, the inhibition of this TF by a specific IKK inhibitor, sulfasalazine, induced amnesia during the two periods in which NF-B was active (Merlo et al 2002).…”

mentioning

confidence: 82%

“…In addition, the inhibition of this TF by a specific IKK inhibitor, sulfasalazine, induced amnesia during the two periods in which NF-B was active (Merlo et al 2002). Moreover, activated NF-B was found in synaptic terminals after LTM induction, giving physiological support for the synapse-to-nucleus signaling role of NF-B (Freudenthal and Romano 2000). More recently, evidence of a role of NF-B in memory in rodents was obtained (Yeh et al 2002(Yeh et al , 2004Meffert et al 2003).…”

mentioning

confidence: 93%

Activation of the transcription factor NF-κB by retrieval is required for long-term memory reconsolidation

Merlo¹,

Freudenthal²,

Maldonado³

et al. 2005

Learn. Mem.

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Several studies support that stored memories undergo a new period of consolidation after retrieval. It is not known whether this process, termed reconsolidation, requires the same transcriptional mechanisms involved in consolidation. Increasing evidence supports the participation of the transcription factor NF-B in memory. This was initially demonstrated in the crab Chasmagnathus model of associative contextual memory, in which re-exposure to the training context induces a well characterized reconsolidation process. Here we studied the role of NF-B in reconsolidation. NF-B was specifically activated in trained animals re-exposed to the training context but not to a different context. NF-B was not activated when animals were re-exposed to the context after a weak training protocol insufficient to induce long-term memory. A specific inhibitor of the NF-B pathway, sulfasalazine, impaired reconsolidation when administered 20 min before re-exposure to the training context but was not effective when a different context was used. These findings indicate for the first time that NF-B is activated specifically by retrieval and that this activation is required for memory reconsolidation, supporting the view that this molecular mechanism is required in both consolidation and reconsolidation.

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“…In fact, recent studies support distinct molecular requirements, such as the participation of protein phosphatases (Genoux et al, 2002) and endocannabinoids (Marsicano et al, 2002;Suzuki et al, 2004) in the consolidation of extinction, but not in the consolidation of the original memory. The transcription factor NF-B plays a key role in long-term memory consolidation (Freudenthal and Romano, 2000;Meffert et al, 2003;Romano et al, 2006) and reconsolidation Boccia et al, 2007), whereas it is inhibited during extinction induction in crabs (Merlo and Romano, 2008). In contrast, little is known about the role of the transcription factor of activated T-cells [nuclear factor of activated T-cells (NFAT)] in the brain, albeit the way of NFAT activation by calcineurin has been deeply studied in other systems (i.e., immunology).…”

Section: Introductionmentioning

confidence: 99%

Reconsolidation or Extinction: Transcription Factor Switch in the Determination of Memory Course after Retrieval

Fuente¹,

Freudenthal²,

Romano³

2011

J. Neurosci.

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In fear conditioning, aversive stimuli are readily associated with contextual features. A brief reexposure to the training context causes fear memory reconsolidation, whereas a prolonged reexposure induces memory extinction. The regulation of hippocampal gene expression plays a key role in contextual memory consolidation and reconsolidation. However, the mechanisms that determine whether memory will reconsolidate or extinguish are not known. Here, we demonstrate opposing roles for two evolutionarily related transcription factors in the mouse hippocampus. We found that nuclear factor-B (NF-B) is required for fear memory reconsolidation. Conversely, calcineurin phosphatase inhibited NF-B and induced nuclear factor of activated T-cells (NFAT) nuclear translocation in the transition between reconsolidation and extinction. Accordingly, the hippocampal inhibition of both calcineurin and NFAT independently impaired memory extinction, whereas inhibition of NF-B enhanced memory extinction. These findings represent the first insight into the molecular mechanisms that determine memory reprocessing after retrieval, supporting a transcriptional switch that directs memory toward reconsolidation or extinction. The precise molecular characterization of postretrieval processes has potential importance to the development of therapeutic strategies for fear memory disorders.

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Participation of Rel/NF-κB transcription factors in long-term memory in the crab Chasmagnathus

Cited by 111 publications

References 27 publications

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Somatic action potentials are sufficient for late-phase LTP-related cell signaling

Activation of the transcription factor NF-κB by retrieval is required for long-term memory reconsolidation

Reconsolidation or Extinction: Transcription Factor Switch in the Determination of Memory Course after Retrieval

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