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    Synaptic plasticity in spinal lamina I projection neurons that mediate hyperalgesia (2003)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2003-02-22
    Description: Inflammation, trauma, or nerve injury may cause enduring hyperalgesia, an enhanced sensitivity to painful stimuli. Neurons in lamina I of the spinal dorsal horn that express the neurokinin 1 receptor for substance P mediate this abnormal pain sensitivity by an unknown cellular mechanism. We report that in these, but not in other nociceptive lamina I cells, neurokinin 1 receptor-activated signal transduction pathways and activation of low-threshold (T-type) voltage-gated calcium channels synergistically facilitate activity- and calcium-dependent long-term potentiation at synapses from nociceptive nerve fibers. Thereby, memory traces of painful events are retained.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Heinke, Bernhard -- Ruscheweyh, Ruth -- Sandkuhler, Jurgen -- New York, N.Y. -- Science. 2003 Feb 21;299(5610):1237-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology and Pathophysiology, Heidelberg University, D-69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/12595694" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Calcium/metabolism ; Calcium Channels, T-Type/*metabolism ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Ion Channel Gating ; *Long-Term Potentiation ; Membrane Potentials ; Nerve Fibers, Unmyelinated/physiology ; Neurokinin-1 Receptor Antagonists ; Nickel/pharmacology ; Patch-Clamp Techniques ; Posterior Horn Cells/metabolism/*physiology ; Quinuclidines/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Receptors, Neurokinin-1/*metabolism ; Signal Transduction ; Substance P/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Synaptic amplifier of inflammatory pain in the spinal dorsal horn (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-06-17
    Description: Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia), which is in part due to altered sensory processing in the spinal cord. The synaptic hypothesis of hyperalgesia, which postulates that hyperalgesia is induced by the activity-dependent long-term potentiation (LTP) in the spinal cord, has been challenged, because in previous studies of pain pathways, LTP was experimentally induced by nerve stimulation at high frequencies ( approximately 100 hertz). This does not, however, resemble the real low-frequency afferent barrage that occurs during inflammation. We identified a synaptic amplifier at the origin of an ascending pain pathway that is switched-on by low-level activity in nociceptive nerve fibers. This model integrates known signal transduction pathways of hyperalgesia without contradiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ikeda, Hiroshi -- Stark, Johanna -- Fischer, Harald -- Wagner, Matthias -- Drdla, Ruth -- Jager, Tino -- Sandkuhler, Jurgen -- P 18129/Austrian Science Fund FWF/Austria -- New York, N.Y. -- Science. 2006 Jun 16;312(5780):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16778058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Hyperalgesia/*physiopathology ; Inflammation/*physiopathology ; Long-Term Potentiation ; Nerve Fibers, Unmyelinated/*physiology ; Neuronal Plasticity ; Nitric Oxide/physiology ; Pain/*physiopathology ; Patch-Clamp Techniques ; Periaqueductal Gray/physiology ; Posterior Horn Cells/*physiopathology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Spinal Cord/physiopathology ; Synapses/physiology ; *Synaptic Transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
    Location Call Number Expected Availability
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