ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Persistent long-term synaptic plasticity requires activation of a new signaling pathway by additional stimuli.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
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- The Right Time for a Synapse to Change: Windows and Mechanisms of Multiday Training Trials.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Long-term dynamic profiles of cognitive kinases induced by different learning protocols.bioRxiv : the preprint server for biology · 2025Article
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- Dynamics and Mechanisms of ERK Activation after Different Protocols that Induce Long-Term Synaptic Facilitation inOxford open neuroscience · 2023Article
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- Proteasome and Autophagy-Mediated Impairment of Late Long-Term Potentiation (l-LTP) after Traumatic Brain Injury in the Somatosensory Cortex of Mice.International journal of molecular sciences · 2019Article
- How can memories last for days, years, or a lifetime? Proposed mechanisms for maintaining synaptic potentiation and memory.Learning & memory (Cold Spring Harbor, N.Y.) · 2019Review
- Memory Synapses Are Defined by Distinct Molecular Complexes: A Proposal.Frontiers in synaptic neuroscience · 2018Review
- Selective Erasure of Distinct Forms of Long-Term Synaptic Plasticity Underlying Different Forms of Memory in the Same Postsynaptic Neuron.Current biology : CB · 2017Article
- Superior long-term synaptic memory induced by combining dual pharmacological activation of PKA and ERK with an enhanced training protocol.Learning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Comparative biology of pain: What invertebrates can tell us about how nociception works.Journal of neurophysiology · 2017Review
- Cell-Specific PKM Isoforms Contribute to the Maintenance of Different Forms of Persistent Long-Term Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Responses of Withdrawal Interneurons to Serotonin Applications in Naïve and Learned Snails Are Different.Frontiers in cellular neuroscience · 2017Article
- Persistent Associative Plasticity at an Identified Synapse Underlying Classical Conditioning Becomes Labile with Short-Term Homosynaptic Activation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Spontaneous and Partial Repair of Ribbon Synapse in Cochlear Inner Hair Cells After Ototoxic Withdrawal.Molecular neurobiology · 2015Article
- Escitalopram Ameliorates Forskolin-Induced Tau Hyperphosphorylation in HEK239/tau441 Cells.Journal of molecular neuroscience : MN · 2015Article
- cJun and CREB2 in the postsynaptic neuron contribute to persistent long-term facilitation at a behaviorally relevant synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Extending injury- and disease-resistant CNS phenotypes by repetitive epigenetic conditioning.Frontiers in neurology · 2015Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Most memories are strengthened by additional stimuli, but it is unclear how additional stimulation or training reinforces long-term memory. To address this we examined whether long-term facilitation (LTF) of Aplysia sensorimotor synapses in cell culture-a cellular correlate of long-term sensitization of defensive withdrawal reflexes in Aplysia californica-can be prolonged by additional stimulation. We found that 1 d treatment with serotonin (5-HT; five brief applications at 20 min intervals) produced LTF lasting ∼3 d, whereas 2 d of such 5-HT treatments induced a persistent LTF lasting >7 d. Incubation with the protein synthesis inhibitor rapamycin during the second set of 5-HT treatments abolished all facilitation, and synapse strength returned prematurely to baseline. Persistent LTF required more persistent elevation in the expression of the neurotrophin-like peptide sensorin and its secretion. Activation of protein kinase C (PKC) during the second day of 5-HT treatments, not required for LTF or changes in sensorin expression during the first set of 5-HT treatments, is critical for persistent LTF and replaces phosphoinositide 3 kinase (PI3K) activity in mediating the increase in sensorin expression. In contrast, activations of PKC during the first day of 5-HT treatments and PI3K during the second day of 5-HT treatments are unnecessary for persistent LTF or the increases in sensorin expression. Thus, additional stimuli make preexisting plasticity labile as they recruit a new signaling cascade to regulate the synthesis of a neurotrophin-like peptide required for persistent alterations in synaptic efficacy.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.