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Cited by 569

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Synaptic Plasticity in Spinal Lamina I Projection Neurons That Mediate Hyperalgesia

Ikeda, Hiroshi, Heinke, Bernhard, Ruscheweyh, Ruth, Sandkühler, Jürgen·2003·Science

Abstract

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.

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Crossref · 10.1126/science.1080659

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Metadata

Authors
Ikeda, H., Heinke, B., Ruscheweyh, R., & Sandkühler, J.
Venue
Science
Published
2003-02-21
Volume
299
Issue
5610
Pages
1237-1240
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
OpenAlex
W1979675387
Cited by
569
References
2
FWCI
23.88
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Synaptic Plasticity in Spinal Lamina I Projection Neurons That Mediate Hyperalgesia. https://app.cochat.ai/papers/10.1126/science.1080659
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Ikeda, H., Heinke, B., Ruscheweyh, R., & Sandkühler, J. (2003). Synaptic Plasticity in Spinal Lamina I Projection Neurons That Mediate Hyperalgesia. Science. https://doi.org/10.1126/science.1080659

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.