TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury.

By K. Obata, Hirokazu Katsura, Toshiyuki Mizushima, H. Yamanaka, Kimiko Kobayashi, Yi Dai, T. Fukuoka, A. Tokunaga, M. Tominaga, K. Noguchi. Journal of Clinical Investigation, 2005

629 citations recorded by the source corpus.

Subfields: Physiology, Public Health, Environmental and Occupational Health, Sensory Systems

View Paper: https://www.semanticscholar.org/paper/1a76118e3d3956fa6bb21840a9e09a01c52179bd

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Physiology

1. Clifford J. Woolf
2. Ardem Patapoutian
3. R. Ji
4. Arne May
5. G. Moalem-Taylor
6. P. Austin

In Sensory Systems

1. Ardem Patapoutian
2. Clifford J. Woolf
3. A. Dhaka
4. Taryn J. Earley
5. Jayanti Mathur
6. Matt J. Petrus
7. Veena Viswanath
8. Amber N. Murray

Citations in the corpus

• TRPA1 contributes to cold, mechanical, and chemical nociception but is not essential for hair-cell transduction. (2006, positive): “Thus, TRPA1 was proposed to mediate the sensation of cold pain, an idea supported by reduced cold hyperalgesia with TRPA1 knockdown in vivo (Story et al., 2003; Obata et al., 2005).”
• Mechanisms of sensory transduction in the skin (2007, neutral): “and in rats treated with TRPA1-antisense oligonucleotide”
• Trp ion channels and temperature sensation. (2006, background): “Additionally, TRPM8 does not seem to be required for inflammation-induced cold hyperalgesia (Obata et al. 2005).”
• TRPM8 is required for cold sensation in mice. (2007, positive): “Antisense knock down of TRPA1 in rats has shown a requirement for this ion channel in inflammation-induced and nerve injury-induced cold allodynia (a nociceptive response to an innocuous stimulus) ( Obata et al., 2005 ).”