ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Two signaling pathways regulate the expression and secretion of a neuropeptide required for long-term facilitation in Aplysia.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. 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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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- Article
- 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
- 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
- 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
- Synaptic generation of an intracellular retrograde signal requires activation of the tyrosine kinase and mitogen-activated protein kinase signaling cascades in Aplysia.Neurobiology of learning and memory · 2015Article
- Article
- Article
- Activity-dependent inhibitory gating in molecular signaling cascades induces a novel form of intermediate-term synaptic facilitation in Aplysia californica.Learning & memory (Cold Spring Harbor, N.Y.) · 2014Article
- Longevity pathways and memory aging.Frontiers in genetics · 2014Review
- Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: implications for pain and memory.Neurobiology of learning and memory · 2013Review
- MAPK establishes a molecular context that defines effective training patterns for long-term memory formation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Mapping molecular memory: navigating the cellular pathways of learning.Cellular and molecular neurobiology · 2012Review
- Massed training-induced intermediate-term operant memory in aplysia requires protein synthesis and multiple persistent kinase cascades.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The rates of protein synthesis and degradation account for the differential response of neurons to spaced and massed training protocols.PLoS computational biology · 2011Article
- Persistent long-term synaptic plasticity requires activation of a new signaling pathway by additional stimuli.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Small G protein signaling in neuronal plasticity and memory formation: the specific role of ras family proteins.Neuron · 2010Review
- Mechanisms of translational regulation in synaptic plasticity.Current opinion in neurobiology · 2010Review
- Aplysia cell adhesion molecule and a novel protein kinase C activity in the postsynaptic neuron are required for presynaptic growth and initial formation of specific synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Ribosomal protein S6 kinase is a critical downstream effector of the target of rapamycin complex 1 for long-term facilitation in Aplysia.The Journal of biological chemistry · 2010Article
- Common mechanisms of synaptic plasticity in vertebrates and invertebrates.Current biology : CB · 2010Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Activation of several signaling pathways contributes to long-term synaptic plasticity, but how brief stimuli produce coordinated activation of these pathways is not understood. In Aplysia, the long-term facilitation (LTF) of sensory neuron synapses by 5-hydroxytryptamine (serotonin; 5-HT) requires the activation of several kinases, including mitogen-activated protein kinase (MAPK). The 5-HT-enhanced secretion of the sensory neuron-specific neuropeptide sensorin mediates the activation of MAPK. We find that stimulus-induced activation of two signaling pathways, phosphoinositide 3-kinase (PI3K) and type II protein kinase A (PKA), regulate sensorin secretion and responses. Treatment with 5-HT produces a rapid increase in sensorin synthesis, especially at varicosities, which precedes the secretion of sensorin. PI3K inhibitor and rapamycin block LTF and the rapid synthesis of sensorin at varicosities even in the absence of sensory neuron cell bodies. Secretion of the newly synthesized sensorin from the varicosities and activation of the autocrine responses of sensorin to produce LTF require type II PKA interaction with AKAPs (A-kinase anchoring proteins). Thus, long-term synaptic plasticity is produced when multiple signaling pathways that are important for regulating distinct cellular functions are activated in a specific sequence and recruit the secretion of a neuropeptide to activate additional critical pathways.
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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.