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Cited by 277

The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.

Role of Neurotransmitters in Sensitization of Pain Responses

Willis, William D.·2001·Annals of the New York Academy of Sciences

Abstract

A bstract:Injection of capsaicin into the skin results in pain, primary heat and mechanical hyperalgesia, and secondary mechanical allodynia and hyperalgesia. Sensory receptors in the area of secondary mechanical allodynia and hyperalgesia are unaffected, and so the sensory changes must be due to central actions of the initial intense nociceptive discharge that follows the capsaicin injection. Central sensitization of the responses of spinothalamic tract neurons lasts several hours, but can be prevented by spinal cord administration of non‐NMDA and NMDA glutamate receptor antagonists or NK1 substance P receptor antagonists. The long‐lasting increase in excitability of spinothalamic tract cells depends on the activation of several second messenger cascades (PKC, PKA, and NO/PKG signal transduction pathways). The excitability change also depends on activation of calcium/calmodulin‐dependent kinase II, which is consistent with the proposal that this central sensitization response is a form of long‐term potentiation.

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Crossref · 10.1111/j.1749-6632.2001.tb05821.x

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Metadata

Authors
Willis, W. D.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2001-03
Volume
933
Issue
1
Pages
142-156
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
OpenAlex
W1969730957
Cited by
277
References
38
FWCI
11.05
Type
journal article
Language
en
Open access
closed

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CoChat. (2026). Citation check: Role of Neurotransmitters in Sensitization of Pain Responses. https://app.cochat.ai/papers/10.1111/j.1749-6632.2001.tb05821.x
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Willis, W. D. (2001). Role of Neurotransmitters in Sensitization of Pain Responses. Annals of the New York Academy of Sciences. https://doi.org/10.1111/j.1749-6632.2001.tb05821.x

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

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