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Synaptic Amplifier of Inflammatory Pain in the Spinal Dorsal Horn
Hiroshi Ikeda,*
Johanna Stark,
Harald Fischer,
Matthias Wagner,
Ruth Drdla,
Tino Jäger,
Jürgen Sandkühler
Abstract:
Inflammation and trauma lead to enhanced pain sensitivity (hyperalgesia),which is in part due to altered sensory processing in the spinalcord. The synaptic hypothesis of hyperalgesia, which postulatesthat hyperalgesia is induced by the activity-dependent long-termpotentiation (LTP) in the spinal cord, has been challenged,because in previous studies of pain pathways, LTP was experimentallyinduced by nerve stimulation at high frequencies (100 hertz).This does not, however, resemble the real low-frequency afferentbarrage that occurs during inflammation. We identified a synapticamplifier at the origin of an ascending pain pathway that isswitched-on by low-level activity in nociceptive nerve fibers.This model integrates known signal transduction pathways ofhyperalgesia without contradiction.
Department of Neurophysiology, Center for Brain Research, Medical University of Vienna, Vienna, Austria.
* Present address: Department of Human and Artificial IntelligenceSystems, University of Fukui, 3-9-1 Bunkyo, Fukui 910-8507,Japan.
To whom correspondence should be addressed. E-mail: juergen.sandkuehler{at}meduniwien.ac.at
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