Tags

Type your tag names separated by a space and hit enter

TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury.
J Clin Invest. 2005 Sep; 115(9):2393-401.JCI

Abstract

Cold hyperalgesia is a well-documented symptom of inflammatory and neuropathic pain; however, the underlying mechanisms of this enhanced sensitivity to cold are poorly understood. A subset of transient receptor potential (TRP) channels mediates thermosensation and is expressed in sensory tissues, such as nociceptors and skin. Here we report that the pharmacological blockade of TRPA1 in primary sensory neurons reversed cold hyperalgesia caused by inflammation and nerve injury. Inflammation and nerve injury increased TRPA1, but not TRPM8, expression in tyrosine kinase A-expressing dorsal root ganglion (DRG) neurons. Intrathecal administration of anti-nerve growth factor (anti-NGF), p38 MAPK inhibitor, or TRPA1 antisense oligodeoxynucleotide decreased the induction of TRPA1 and suppressed inflammation- and nerve injury-induced cold hyperalgesia. Conversely, intrathecal injection of NGF, but not glial cell line-derived neurotrophic factor, increased TRPA1 in DRG neurons through the p38 MAPK pathway. Together, these results demonstrate that an NGF-induced TRPA1 increase in sensory neurons via p38 activation is necessary for cold hyperalgesia. Thus, blocking TRPA1 in sensory neurons might provide a fruitful strategy for treating cold hyperalgesia caused by inflammation and nerve damage.

Authors+Show Affiliations

Department of Anatomy and Neuroscience, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16110328

Citation

Obata, Koichi, et al. "TRPA1 Induced in Sensory Neurons Contributes to Cold Hyperalgesia After Inflammation and Nerve Injury." The Journal of Clinical Investigation, vol. 115, no. 9, 2005, pp. 2393-401.
Obata K, Katsura H, Mizushima T, et al. TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury. J Clin Invest. 2005;115(9):2393-401.
Obata, K., Katsura, H., Mizushima, T., Yamanaka, H., Kobayashi, K., Dai, Y., Fukuoka, T., Tokunaga, A., Tominaga, M., & Noguchi, K. (2005). TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury. The Journal of Clinical Investigation, 115(9), 2393-401.
Obata K, et al. TRPA1 Induced in Sensory Neurons Contributes to Cold Hyperalgesia After Inflammation and Nerve Injury. J Clin Invest. 2005;115(9):2393-401. PubMed PMID: 16110328.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - TRPA1 induced in sensory neurons contributes to cold hyperalgesia after inflammation and nerve injury. AU - Obata,Koichi, AU - Katsura,Hirokazu, AU - Mizushima,Toshiyuki, AU - Yamanaka,Hiroki, AU - Kobayashi,Kimiko, AU - Dai,Yi, AU - Fukuoka,Tetsuo, AU - Tokunaga,Atsushi, AU - Tominaga,Makoto, AU - Noguchi,Koichi, Y1 - 2005/08/18/ PY - 2005/04/22/received PY - 2005/06/07/accepted PY - 2005/8/20/pubmed PY - 2005/12/15/medline PY - 2005/8/20/entrez SP - 2393 EP - 401 JF - The Journal of clinical investigation JO - J Clin Invest VL - 115 IS - 9 N2 - Cold hyperalgesia is a well-documented symptom of inflammatory and neuropathic pain; however, the underlying mechanisms of this enhanced sensitivity to cold are poorly understood. A subset of transient receptor potential (TRP) channels mediates thermosensation and is expressed in sensory tissues, such as nociceptors and skin. Here we report that the pharmacological blockade of TRPA1 in primary sensory neurons reversed cold hyperalgesia caused by inflammation and nerve injury. Inflammation and nerve injury increased TRPA1, but not TRPM8, expression in tyrosine kinase A-expressing dorsal root ganglion (DRG) neurons. Intrathecal administration of anti-nerve growth factor (anti-NGF), p38 MAPK inhibitor, or TRPA1 antisense oligodeoxynucleotide decreased the induction of TRPA1 and suppressed inflammation- and nerve injury-induced cold hyperalgesia. Conversely, intrathecal injection of NGF, but not glial cell line-derived neurotrophic factor, increased TRPA1 in DRG neurons through the p38 MAPK pathway. Together, these results demonstrate that an NGF-induced TRPA1 increase in sensory neurons via p38 activation is necessary for cold hyperalgesia. Thus, blocking TRPA1 in sensory neurons might provide a fruitful strategy for treating cold hyperalgesia caused by inflammation and nerve damage. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/16110328/TRPA1_induced_in_sensory_neurons_contributes_to_cold_hyperalgesia_after_inflammation_and_nerve_injury_ DB - PRIME DP - Unbound Medicine ER -