κ-B like DNA-binding activity is enhanced after spaced training that induces long-term memory in the crab Chasmagnathus

Freudenthal, Ramiro; Locatelli, Fernando; Hermitte, Gabriela; Maldonado, Héctor; Lafourcade, Carlos; Delorenzi, Alejandro; Romano, Arturo

doi:10.1016/s0304-3940(98)00059-7

Cited by 85 publications

(56 citation statements)

References 19 publications

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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).…”

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confidence: 85%

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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confidence: 85%

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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“…Both processes can be induced by electrical or chemical means, high frequency stimulation (HFS) causes LTP and low frequency LTD. LTP results in a long-lasting increase in synaptic transmission, whereas LTD results in a persistent functional decrease in synaptic activity. Emerging data is implicating NF-kB as a key component in LTD (Albensi and Mattson, 2000) and previous work has shown a role for NF-kB in LTP (Meberg et al, 1996;Freudenthal et al, 1998).…”

Section: Introductionmentioning

confidence: 97%

Methods of detection of the transcription factor NF-κB in rat hippocampal slices

Butler

Moynagh

O’Connor

2002

Journal of Neuroscience Methods

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The hippocampus is one of the most studied sites for understanding the cellular and molecular mechanisms underlying long-term potentiation (LTP) and long-term depression (LTD), mechanisms believed to underlie the formation and storage of memories. The early-phases of LTP and LTD have been most intensively studied and have been shown to involve the activation of several kinases and phosphatases, respectively. The factors involved in the later stages have largely yet to be elucidated. We have focused our attention on the transcription factor NF-kB as a possible factor involved in such late-phase processes, and have developed both immunocytochemistry and electrophoretic mobility shift assay (EMSA) to measure the activated forms of this factor. This is important as many of the studies in this area are performed in vitro and to our knowledge quantitative assessment has not previously being deemed feasible in slice work. The pro-inflammatory cytokines TNF-a and IL-1b both led to pronounced nuclear activation of NF-kB in the dentate granule cells as demonstrated by immunostaining and EMSA, respectively. Electrophysiological measurements taken from slices treated with TNF-a showed that it inhibited LTP (field excitatory post-synaptic potentials (fEPSP) 1169/10%, n 0/ 9, 60 min post-tetanus compared to control fEPSP 1859/9%, n 0/ 6; P B/0.001). The neurotransmitter L-glutamate also led to activation of NF-kB and electrophysiology recordings showed a small but sustained increase in synaptic transmission (fEPSP 1069/12%, 30 min post-drug). These methods provide valuable tools to forward our understanding of the role of NF-kB in plasticity as well as in many neurological disorders being mimicked by in vitro studies. #

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“…For example, intermediate-term memory formation and synaptic facilitation in Aplysia (Mauelshagen et al, 1998;Sutton et al, 2002;Sherff and Carew, 2004), habituation in the crab Chasmagnathus (Freudenthal et al, 1998), olfactory memory formation in Drosophila (Isabel et al, 2004), and hippocampal long-term potentiation in rodents (Kauer, 1999;Nguyen et al, 2000;Woo et al, 2000;Scharf et al, 2002) all exhibit distinct pattern sensitivity to the training protocol; intermittent (or spaced) stimuli are more robust than sustained (or massed) stimulation in each case. The mechanistic basis of pattern sensitivity in neuroplasticity is not understood (Brennan and Keverne, 1997;Baker et al, 2001;Scharf et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Okadaic Acid-Sensitive Protein Phosphatases Constrain Phrenic Long-Term Facilitation after Sustained Hypoxia

Wilkerson¹,

Satriotomo²,

Baker-Herman³

et al. 2008

J. Neurosci.

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Phrenic long-term facilitation (pLTF) is a serotonin-dependent form of pattern-sensitive respiratory plasticity induced by intermittent hypoxia (IH), but not sustained hypoxia (SH). The mechanism(s) underlying pLTF pattern sensitivity are unknown. SH and IH may differentially regulate serine/threonine protein phosphatase activity, thereby inhibiting relevant protein phosphatases uniquely during IH and conferring pattern sensitivity to pLTF. We hypothesized that spinal protein phosphatase inhibition would relieve this braking action of protein phosphatases, thereby revealing pLTF after SH. Anesthetized rats received intrathecal (C4) okadaic acid (25 nM) before SH (25 min, 11% O 2 ). Unlike (vehicle) control rats, SH induced a significant pLTF in okadaic acid-treated rats that was indistinguishable from rats exposed to IH (three 5 min episodes, 11% O 2 ). IH and SH with okadaic acid may elicit pLTF by similar, serotonin-dependent mechanisms, because intravenous methysergide blocks pLTF in rats receiving IH or okadaic acid plus SH. Okadaic acid did not alter IH-induced pLTF. In summary, pattern sensitivity in pLTF may reflect differential regulation of okadaic acid-sensitive serine/threonine phosphatases; presumably, these phosphatases are less active during/after IH versus SH. The specific okadaic acid-sensitive phosphatase(s) constraining pLTF and their spatiotemporal dynamics during and/or after IH and SH remain to be determined.

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κ-B like DNA-binding activity is enhanced after spaced training that induces long-term memory in the crab Chasmagnathus

Cited by 85 publications

References 19 publications

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

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

Methods of detection of the transcription factor NF-κB in rat hippocampal slices

Okadaic Acid-Sensitive Protein Phosphatases Constrain Phrenic Long-Term Facilitation after Sustained Hypoxia

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