Erasure of a Spinal Memory Trace of Pain by a Brief, High-Dose Opioid Administration
Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversib...
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| Published in | Science (American Association for the Advancement of Science) Vol. 335; no. 6065; pp. 235 - 238 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Washington, DC
American Association for the Advancement of Science
13.01.2012
The American Association for the Advancement of Science |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0036-8075 1095-9203 1095-9203 |
| DOI | 10.1126/science.1211726 |
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| Abstract | Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca²⁺ -dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. |
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| AbstractList | Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca²⁺ -dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca2+-dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca(2+)-dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. Opioids are among the most widely used and extensively studied drugs in the world. A continuous application of relatively low opioid doses is thought to be necessary to maintain synaptic depression in pain pathways. Drdla-Schutting et al. (p. 235) found that a single opioid application could produce lasting reversal of synaptic long-term potentiation in pain pathways. Chronic pain is often associated with synaptic potentiation in nociceptive pathways. A brief, high-dose application of opioids depotentiated long-term potentiation in spinal pain pathways. The same dose also reversed hyperalgesia in behaving animals. Thus, opioids not only attenuate pain but also may eradicate a significant cause for chronic pain. Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca2+-dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. [PUBLICATION ABSTRACT] Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca(2+)-dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain.Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca(2+)-dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. Opioids are among the most widely used and extensively studied drugs in the world. A continuous application of relatively low opioid doses is thought to be necessary to maintain synaptic depression in pain pathways. Drdla-Schutting et al. (p. 235 ) found that a single opioid application could produce lasting reversal of synaptic long-term potentiation in pain pathways. Chronic pain is often associated with synaptic potentiation in nociceptive pathways. A brief, high-dose application of opioids depotentiated long-term potentiation in spinal pain pathways. The same dose also reversed hyperalgesia in behaving animals. Thus, opioids not only attenuate pain but also may eradicate a significant cause for chronic pain. Opioid administration turns down a pain amplifier by reversing synaptic long-term potentiation in spinal nociceptive pathways. Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. μ-Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca 2+ -dependent signaling and normalization of the phosphorylation state of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a cellular model for pain amplification (hyperalgesia) and for a memory trace of pain. mu -Opioid receptor agonists exert a powerful but reversible depression at C-fiber synapses that renders the continuous application of low opioid doses the gold standard in pain therapy. We discovered that brief application of a high opioid dose reversed various forms of activity-dependent LTP at C-fiber synapses. Depotentiation involved Ca2+-dependent signaling and normalization of the phosphorylation state of alpha -amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors. This also reversed hyperalgesia in behaving animals. Opioids thus not only temporarily dampen pain but may also erase a spinal memory trace of pain. |
| Author | Benrath, Justus Drdla-Schutting, Ruth Sandkühler, Jürgen Wunderbaldinger, Gabriele |
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| Keywords | Drug Nociception Synapse Pain Treatment Capsaicin Pharmacotherapy Route of administration Nerve fiber C Hyperalgesia |
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| Snippet | Painful stimuli activate nociceptive C fibers and induce synaptic long-term potentiation (LTP) at their spinal terminals. LTP at C-fiber synapses represents a... Opioids are among the most widely used and extensively studied drugs in the world. A continuous application of relatively low opioid doses is thought to be... |
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| SubjectTerms | agonists Analgesics Analgesics, Opioid - administration & dosage Animals Biological and medical sciences Calcium Calcium Signaling Drug dosages Evoked Potentials Fibers Hyperalgesia Hyperalgesia - chemically induced Hyperalgesia - drug therapy Long term depression Long term potentiation Long-Term Potentiation - drug effects Male Medical sciences memory Memory trace Naloxone - administration & dosage Narcotics Nerve Fibers, Unmyelinated - drug effects Nerve Fibers, Unmyelinated - physiology Neurons Neuropharmacology Neuroscience Nociceptive Pain - drug therapy Nociceptive Pain - physiopathology Opioid analgesics Pain Pain management Pharmacology Pharmacology. Drug treatments Phosphorylation Piperidines - administration & dosage Protein Kinase C - antagonists & inhibitors Protein Kinase C - metabolism Protein Phosphatase 1 - antagonists & inhibitors Protein Phosphatase 1 - metabolism Rats Rats, Sprague-Dawley Receptors Receptors, AMPA - metabolism Receptors, Opioid, mu - agonists Receptors, Opioid, mu - metabolism Sciatic Nerve - drug effects Sciatic Nerve - physiology somatosensory disorders Somatostatin - administration & dosage Somatostatin - analogs & derivatives Spinal cord Spinal Cord - physiology synapse Synapses Synapses - drug effects Synapses - physiology therapeutics |
| Title | Erasure of a Spinal Memory Trace of Pain by a Brief, High-Dose Opioid Administration |
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