ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Memory-like alterations in Aplysia axons after nerve injury or localized depolarization.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
- Induction of long-term hyperexcitability by memory-related cAMP signaling in isolated nociceptor cell bodies.bioRxiv : the preprint server for biology · 2024Article
- Persistent nociceptor hyperactivity as a painful evolutionary adaptation.Trends in neurosciences · 2023Review
- The mTOR inhibitor rapamycin suppresses trigeminal neuropathic pain and p-MKK4/p-p38 mitogen-activated protein kinase-mediated microglial activation in the trigeminal nucleus caudalis of mice with infraorbital nerve injury.Frontiers in molecular neuroscience · 2023Article
- MNK-eIF4E signalling is a highly conserved mechanism for sensory neuron axonal plasticity: evidence fromPhilosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Evolution of mechanisms and behaviour important for pain.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Article
- Nerve injury drives a heightened state of vigilance and neuropathic sensitization inScience advances · 2019Article
- Nociceptive Biology of Molluscs and Arthropods: Evolutionary Clues About Functions and Mechanisms Potentially Related to Pain.Frontiers in physiology · 2018Review
- Long-lasting increase in axonal excitability after epidurally applied DC.Journal of neurophysiology · 2017Article
- Comparative biology of pain: What invertebrates can tell us about how nociception works.Journal of neurophysiology · 2017Review
- Commonalities between pain and memory mechanisms and their meaning for understanding chronic pain.Progress in molecular biology and translational science · 2015Review
- Activation of the Mammalian Target of Rapamycin in the Rostral Ventromedial Medulla Contributes to the Maintenance of Nerve Injury-Induced Neuropathic Pain in Rat.Neural plasticity · 2015Article
- Trans-spinal direct current stimulation modifies spinal cord excitability through synaptic and axonal mechanisms.Physiological reports · 2014Article
- Local translation and retrograde axonal transport of CREB regulates IL-6-induced nociceptive plasticity.Molecular pain · 2014Article
- Evolution: the advantage of 'maladaptive' pain plasticity.Current biology : CB · 2014Article
- Cellular, molecular, and epigenetic mechanisms in non-associative conditioning: implications for pain and memory.Neurobiology of learning and memory · 2013Review
- Squid have nociceptors that display widespread long-term sensitization and spontaneous activity after bodily injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- 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
- RNA binding proteins accumulate at the postsynaptic density with synaptic activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Nociceptors as chronic drivers of pain and hyperreflexia after spinal cord injury: an adaptive-maladaptive hyperfunctional state hypothesis.Frontiers in physiology · 2012Article
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Authors and funding
3 authors.
Funding
Abstract
Adaptive, long-term alterations of excitability have been reported in dendrites and presynaptic terminals but not along axons. Persistent enhancement of axonal excitability has been described in proximal nerve stumps at sites of nerve section in mammals, but this hyperexcitability is considered a pathological derangement important only as a cause of neuropathic pain. Identified neurons in Aplysia were used to test the hypothesis that either axonal injury or the focal depolarization that accompanies axonal injury can trigger a local decrease in action potential threshold [long-term hyperexcitability (LTH)] having memory-like properties. Nociceptive tail sensory neurons and a giant secretomotor neuron, R2, exhibited localized axonal LTH lasting 24 hr after a crush of the nerve or connective that severed the tested axons. Axons of tail sensory neurons and tail motor neurons, but not R2, displayed similar localized LTH after peripheral depolarization produced by 2 min exposure to elevated extracellular [K(+)]. Neither the induction nor expression of either form of LTH was blocked by saline containing 1% normal [Ca(2+)] during treatment or testing. However, both were prevented by local application of the protein synthesis inhibitors anisomycin or rapamycin. The features of (1) long-lasting alteration by localized depolarization, (2) restriction of alterations to intensely depolarized regions, and (3) dependence of the alterations on local, rapamycin-sensitive protein synthesis are shared with synaptic mechanisms considered important for memory formation. This commonality suggests that relatively simple, accessible axons may offer an opportunity to define fundamental plasticity mechanisms that were important in the evolution of memory.
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