A novel cysteine-rich neurotrophic factor in <i>Aplysia</i> facilitates growth, MAPK activation, and long-term synaptic facilitation

Pu, Lu; Kopec, Ashley M.; Boyle, Heather D.; Carew, Thomas

doi:10.1101/lm.033662.113

Cited by 18 publications

(16 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…One approach to that problem is to examine numerically simpler systems such as the marine mollusk Aplysia californica. Several early studies suggested that, as in mammals, long-term memory and long-term facilitation in Aplysia involve BDNF-like neurotrophins and Trk-like receptors (Purcell et al 2003;Ormond et al 2004;Sharma et al 2006;Pu et al 2014), and more recently true Aplysia orthologs of BDNF and TrkB have been described and shown to be required for long-term facilitation (Kassabov et al 2013). In mammals BDNF transcription is regulated in an activitydependent manner by epigenetic mechanisms including DNA methylation (West et al 2014;Karpova 2014), and BDNF can in turn regulate transcription (Bambah-Mukku et al 2014).…”

mentioning

confidence: 99%

Intermediate-term memory in Aplysia involves neurotrophin signaling, transcription, and DNA methylation

et al. 2018

View full text Add to dashboard Cite

Long-term but not short-term memory and synaptic plasticity in many brain areas require neurotrophin signaling, transcription, and epigenetic mechanisms including DNA methylation. However, it has been difficult to relate these cellular mechanisms directly to behavior because of the immense complexity of the mammalian brain. To address that problem, we and others have examined numerically simpler systems such as the hermaphroditic marine mollusk Aplysia californica. As a further simplification, we have used a semi-intact preparation of the Aplysia siphon withdrawal reflex in which it is possible to relate cellular plasticity directly to behavioral learning. We find that inhibitors of neurotrophin signaling, transcription, and DNA methylation block sensitization and classical conditioning beginning ∼1 h after the start of training, which is in the time range of an intermediate-term stage of plasticity that combines elements of short-and long-term plasticity and may form a bridge between them. Injection of decitabine (an inhibitor of DNA methylation that may have other actions in these experiments) into an LE sensory neuron blocks the neural correlates of conditioning in the same time range. In addition, we found that both DNA and RNA methylation in the abdominal ganglion are correlated with learning in the same preparations. These results begin to suggest the functions and integration of these different molecular mechanisms during behavioral learning.

show abstract

mentioning

confidence: 99%

Intermediate-term memory in Aplysia involves neurotrophin signaling, transcription, and DNA methylation

et al. 2018

View full text Add to dashboard Cite

show abstract

“…3D–E), there appears to be a spatial dissociation of the functional engagement of GF signaling: specifically, TrkB signaling is initiated at the SN-MN synapse, while TGFβr-II signaling is initiated at the SN somata (Fig 3B–C). Previous reports have indicated the localization of neurotrophin-like ligands and Trk-like receptors in both the SN and MN (Kassabov et al, 2013; Ormond et al, 2004; Pu et al, 2014). Taken together, these data suggest that GF signaling via Trk-like receptors may occur both pre- and post-synaptically.…”

Section: Discussionmentioning

confidence: 99%

Distinct Growth Factor Families Are Recruited in Unique Spatiotemporal Domains during Long-Term Memory Formation in Aplysia californica

Kopec

Philips

Carew

2015

Neuron

View full text Add to dashboard Cite

SUMMARY Several growth factors (GFs) have been implicated in long-term memory (LTM), but no single GF can support all the plastic changes that occur during memory formation. Because GFs engage highly convergent signaling cascades that often mediate similar functional outcomes, the relative contribution of any particular GF to LTM is difficult to ascertain. To explore this question, we determined the unique contribution of distinct GF families (signaling via TrkB and TGFβr-II) to LTM formation in Aplysia. We demonstrate that TrkB and TGFβr-II signaling are differentially recruited during Two-Trial training in both time (by Trial 1 or 2, respectively) and space (in distinct subcellular compartments). These GFs independently regulate MAPK activation, and synergistically regulate gene expression. We also show that Trial 1 TrkB and Trial 2 TGFβr-II signaling are required for LTM formation. These data support the view that GFs engaged in LTM formation are interactive components of a complex molecular network.

show abstract

“…Sensorin binds autoreceptors and activates MAPK post 5-HT treatment (Hu et al 2004;Hu et al 2006;Ormond et al 2004;Sharma et al 2003). Another Aplysia neurotrophin, ApCRNF, enhances neurite elongation and facilitates MAPK activation and LTF (Pu et al 2014). More study is needed, however, to determine whether the sensorin and ApCRNF pathways form parts of closed positive feedback loops.…”

Section: Ltp and Excitabilitymentioning

confidence: 99%

How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory

Smolen¹,

Baxter²,

Byrne³

2019

Learn. Mem.

View full text Add to dashboard Cite

With memory encoding reliant on persistent changes in the properties of synapses, a key question is how can memories be maintained from days to months or a lifetime given molecular turnover? It is likely that positive feedback loops are necessary to persistently maintain the strength of synapses that participate in encoding. Such feedback may occur within signal-transduction cascades and/or the regulation of translation, and it may occur within specific subcellular compartments or within neuronal networks. Not surprisingly, numerous positive feedback loops have been proposed. Some posited loops operate at the level of biochemical signal transduction cascades, such as persistent activation of Ca 2+ /calmodulin kinase II (CaMKII) or protein kinase M ζ. Another level consists of feedback loops involving transcriptional, epigenetic and translational pathways, and autocrine actions of growth factors such as BDNF. Finally, at the neuronal network level, recurrent reactivation of cell assemblies encoding memories is likely to be essential for late maintenance of memory. These levels are not isolated, but linked by shared components of feedback loops. Here, we review characteristics of some commonly discussed feedback loops proposed to underlie the maintenance of memory and long-term synaptic plasticity, assess evidence for and against their necessity, and suggest experiments that could further delineate the dynamics of these feedback loops.We also discuss crosstalk between proposed loops, and ways in which such interaction can facilitate the rapidity and robustness of memory formation and storage. Smolen et al. 3

show abstract

A novel cysteine-rich neurotrophic factor in Aplysia facilitates growth, MAPK activation, and long-term synaptic facilitation

Cited by 18 publications

References 42 publications

Intermediate-term memory in Aplysia involves neurotrophin signaling, transcription, and DNA methylation

Intermediate-term memory in Aplysia involves neurotrophin signaling, transcription, and DNA methylation

Distinct Growth Factor Families Are Recruited in Unique Spatiotemporal Domains during Long-Term Memory Formation in Aplysia californica

How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory

Contact Info

Product

Resources

About