P
Peter W. Reeh
Researcher at University of Erlangen-Nuremberg
Publications - 187
Citations - 13190
Peter W. Reeh is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Calcitonin gene-related peptide & TRPV1. The author has an hindex of 61, co-authored 180 publications receiving 12118 citations. Previous affiliations of Peter W. Reeh include Heidelberg University & University of Pécs.
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Sensory Transduction in Peripheral Nerve Axons Elicits Ectopic Action Potentials
TL;DR: In this article, the authors used propagated action potentials as an index of axonal activation and found that axons exhibit sensory transduction capacities similar to their nociceptive terminals in the skin with respect to noxious heat.
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Soluble epoxide hydrolase limits mechanical hyperalgesia during inflammation.
Christian Brenneis,Christian Brenneis,Marco Sisignano,Ovidiu Coste,Kai Altenrath,Michael Fischer,Carlo Angioni,Ingrid Fleming,Ralf P. Brandes,Peter W. Reeh,Clifford J. Woolf,Gerd Geisslinger,Klaus Scholich +12 more
TL;DR: The results show that the sEH can regulate mechanical hyperalgesia during inflammation by inactivating 8,9-EET, which sensitizes TRPA1-expressing nociceptors, and influencing the CYP450 pathway, which is actually highly considered to treat cardiovascular diseases, may cause pain side effects.
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Sensitization to heat through G-protein-coupled receptor pathways in the isolated sciatic mouse nerve
Michael Fischer,Peter W. Reeh +1 more
TL;DR: Evidence is presented that in isolated mouse sciatic nerve axons the intracellular protein kinase A (PKA)‐ and C (PKC)‐dependent transduction pathways modulate heat‐induced CGRP release and no sensitization to heat was observed using a combined stimulation by prostaglandin E2 and bradykinin.
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Conditioning of histamine by bradykinin alters responses of rat nociceptor and human itch sensation.
TL;DR: The data support a hypothesis according to which itching is mediated by a sub-population of polymodal nociceptor units, and pain is induced whenever a larger nocICEptor population is recruited, and that itch processing is either occluded by pain processing, or suppressed by inhibitory processes.
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The pH response of rat cutaneous nociceptors correlates with extracellular [Na+] and is increased under amiloride.
TL;DR: These findings indicate functional expression of amiloride‐sensitive Na+/H+‐antiporters, which enable the nociceptive nerve endings to extrude invading H+.