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Induction of CB1 cannabinoid receptor by inflammation in primary afferent neurons facilitates antihyperalgesic effect of peripheral CB1 agonist.
Pain. 2006 Sep; 124(1-2):175-83.PAIN

Abstract

Cannabinoids act on various regions in the nervous system to modulate neuronal activity including nociception. Here, we investigated CB1 receptor expression in primary afferent neurons in the dorsal root ganglion (DRG) and the efficacy of a local (intraplantar) application of the selective CB1 agonist, 2-arachidonyl-2-chloroethylamide (ACEA), on inflammatory thermal hyperalgesia. In situ hybridization showed normal CB1 mRNA expression in 28% of DRG neurons. Peripheral inflammation by CFA (complete Freund's adjuvant) significantly increased the ratio of CB1 mRNA-positive neurons to 43%, primarily with increase in NF200-negative C-fiber nociceptors. Furthermore, CB1 and TRPV1 (transient potential receptor vanilloid subtype-1) co-localization was increased from 41% before inflammation to 67% two days after inflammation. Inflammation also increased CB1 immunoreactivity in DRG neurons and in nerve fibers of the hindpaw dermis, indicating increased CB1 transport from the cell body to the peripheral nerve. The intraplantar application of ACEA attenuated CFA-induced thermal hyperalgesia. The antinociceptive properties of ACEA became more prominent at 2 days after inflammation, compared with those in non-inflamed and inflamed animals at 8 h. These results suggest that CB1 expression in primary afferent neurons is increased by inflammation and that the subsequent increase in CB1 transport to peripheral axons contributes to the increased antihyperalgesic efficacy of locally administered CB1 agonist.

Authors+Show Affiliations

Department of Anesthesiology, Kyoto Prefectural University of Medicine, Kyoto, Japan. ama@koto.kpu-m.ac.jpNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16709443

Citation

Amaya, Fumimasa, et al. "Induction of CB1 Cannabinoid Receptor By Inflammation in Primary Afferent Neurons Facilitates Antihyperalgesic Effect of Peripheral CB1 Agonist." Pain, vol. 124, no. 1-2, 2006, pp. 175-83.
Amaya F, Shimosato G, Kawasaki Y, et al. Induction of CB1 cannabinoid receptor by inflammation in primary afferent neurons facilitates antihyperalgesic effect of peripheral CB1 agonist. Pain. 2006;124(1-2):175-83.
Amaya, F., Shimosato, G., Kawasaki, Y., Hashimoto, S., Tanaka, Y., Ji, R. R., & Tanaka, M. (2006). Induction of CB1 cannabinoid receptor by inflammation in primary afferent neurons facilitates antihyperalgesic effect of peripheral CB1 agonist. Pain, 124(1-2), 175-83.
Amaya F, et al. Induction of CB1 Cannabinoid Receptor By Inflammation in Primary Afferent Neurons Facilitates Antihyperalgesic Effect of Peripheral CB1 Agonist. Pain. 2006;124(1-2):175-83. PubMed PMID: 16709443.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Induction of CB1 cannabinoid receptor by inflammation in primary afferent neurons facilitates antihyperalgesic effect of peripheral CB1 agonist. AU - Amaya,Fumimasa, AU - Shimosato,Goshun, AU - Kawasaki,Yasuhiko, AU - Hashimoto,Satoru, AU - Tanaka,Yoshifumi, AU - Ji,Ru-Rong, AU - Tanaka,Masaki, Y1 - 2006/05/18/ PY - 2005/05/17/received PY - 2006/01/10/revised PY - 2006/04/04/accepted PY - 2006/5/20/pubmed PY - 2006/9/22/medline PY - 2006/5/20/entrez SP - 175 EP - 83 JF - Pain JO - Pain VL - 124 IS - 1-2 N2 - Cannabinoids act on various regions in the nervous system to modulate neuronal activity including nociception. Here, we investigated CB1 receptor expression in primary afferent neurons in the dorsal root ganglion (DRG) and the efficacy of a local (intraplantar) application of the selective CB1 agonist, 2-arachidonyl-2-chloroethylamide (ACEA), on inflammatory thermal hyperalgesia. In situ hybridization showed normal CB1 mRNA expression in 28% of DRG neurons. Peripheral inflammation by CFA (complete Freund's adjuvant) significantly increased the ratio of CB1 mRNA-positive neurons to 43%, primarily with increase in NF200-negative C-fiber nociceptors. Furthermore, CB1 and TRPV1 (transient potential receptor vanilloid subtype-1) co-localization was increased from 41% before inflammation to 67% two days after inflammation. Inflammation also increased CB1 immunoreactivity in DRG neurons and in nerve fibers of the hindpaw dermis, indicating increased CB1 transport from the cell body to the peripheral nerve. The intraplantar application of ACEA attenuated CFA-induced thermal hyperalgesia. The antinociceptive properties of ACEA became more prominent at 2 days after inflammation, compared with those in non-inflamed and inflamed animals at 8 h. These results suggest that CB1 expression in primary afferent neurons is increased by inflammation and that the subsequent increase in CB1 transport to peripheral axons contributes to the increased antihyperalgesic efficacy of locally administered CB1 agonist. SN - 1872-6623 UR - https://www.unboundmedicine.com/medline/citation/16709443/Induction_of_CB1_cannabinoid_receptor_by_inflammation_in_primary_afferent_neurons_facilitates_antihyperalgesic_effect_of_peripheral_CB1_agonist_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3959(06)00208-9 DB - PRIME DP - Unbound Medicine ER -