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P2X3 receptor mediates heat hyperalgesia in a rat model of trigeminal neuropathic pain.
J Pain 2007; 8(7):588-97JP

Abstract

The present study was undertaken to determine the role of P2X3 receptor (P2X3R) on heat hyperalgesia in a newly developed rat model of trigeminal neuropathic pain. The unilateral infraorbital nerve (IoN) was partially ligated by 6-0 silk. To assess heat sensitivity, a vibrissal pad (VP) was placed on a hot plate and the latency until the rats withdrew their head was measured. Mechanical sensitivity of VP was also assessed by the use of von Frey filament. Both heat and mechanical hyperalgesia were observed at the VP ipsilateral to the IoN ligation. The latency to heat stimuli was prolonged after subcutaneous administration of pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, P2X1,2,3,5,7,1/5,2/3R antagonist) and 2',3'-O-(2,4,6-trinitrophenyl) adenosine 5'-triphosphate (TNP-ATP, P2X1,3,2/3,1/5R antagonist). The latency was shortened after administration of alpha,beta-methylene ATP (alpha,beta-meATP, P2X1,3,2/3R agonist), although no changes appeared after administration of beta,gamma-methylene-L-ATP (beta,gamma-me-L-ATP, P2X1R agonist). The protein gene product-9.5 and calcitonin gene-related peptide immunoreactive nerve fibers significantly decreased in the VP skin of ipsilateral to the IoN ligation. In the ipsilateral trigeminal ganglion, the number of P2X3-immunoreactive neurons significantly increased in the small cell group. In this study, we developed an experimental model of trigeminal neuropathic pain by partial ligation of IoN, which produced heat and mechanical hyperalgesia in the VP. Pharmacological and immunohistochemical studies revealed that the P2X3R plays an important role in the heat hyperalgesia observed in this model.

PERSPECTIVE

The study describes the development of a novel model of trigeminal neuropathic pain. Heat hyperalgesia in this model was inhibited by peripheral injection of P2XR antagonists. The results suggest that P2X3R is a potential target for development of a novel therapy for trigeminal neuropathic pain.

Authors+Show Affiliations

Department of Functional Anatomy and Neuroscience, Nagoya University Graduate School of Medicine, Nagoya, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17481957

Citation

Shinoda, Masamichi, et al. "P2X3 Receptor Mediates Heat Hyperalgesia in a Rat Model of Trigeminal Neuropathic Pain." The Journal of Pain : Official Journal of the American Pain Society, vol. 8, no. 7, 2007, pp. 588-97.
Shinoda M, Kawashima K, Ozaki N, et al. P2X3 receptor mediates heat hyperalgesia in a rat model of trigeminal neuropathic pain. J Pain. 2007;8(7):588-97.
Shinoda, M., Kawashima, K., Ozaki, N., Asai, H., Nagamine, K., & Sugiura, Y. (2007). P2X3 receptor mediates heat hyperalgesia in a rat model of trigeminal neuropathic pain. The Journal of Pain : Official Journal of the American Pain Society, 8(7), pp. 588-97.
Shinoda M, et al. P2X3 Receptor Mediates Heat Hyperalgesia in a Rat Model of Trigeminal Neuropathic Pain. J Pain. 2007;8(7):588-97. PubMed PMID: 17481957.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - P2X3 receptor mediates heat hyperalgesia in a rat model of trigeminal neuropathic pain. AU - Shinoda,Masamichi, AU - Kawashima,Kiyohito, AU - Ozaki,Noriyuki, AU - Asai,Hideaki, AU - Nagamine,Kenjiro, AU - Sugiura,Yasuo, Y1 - 2007/05/03/ PY - 2006/05/26/received PY - 2007/02/06/revised PY - 2007/03/11/accepted PY - 2007/5/8/pubmed PY - 2007/9/1/medline PY - 2007/5/8/entrez SP - 588 EP - 97 JF - The journal of pain : official journal of the American Pain Society JO - J Pain VL - 8 IS - 7 N2 - UNLABELLED: The present study was undertaken to determine the role of P2X3 receptor (P2X3R) on heat hyperalgesia in a newly developed rat model of trigeminal neuropathic pain. The unilateral infraorbital nerve (IoN) was partially ligated by 6-0 silk. To assess heat sensitivity, a vibrissal pad (VP) was placed on a hot plate and the latency until the rats withdrew their head was measured. Mechanical sensitivity of VP was also assessed by the use of von Frey filament. Both heat and mechanical hyperalgesia were observed at the VP ipsilateral to the IoN ligation. The latency to heat stimuli was prolonged after subcutaneous administration of pyridoxal-phosphate-6-azophenyl-2',4'-disulfonic acid (PPADS, P2X1,2,3,5,7,1/5,2/3R antagonist) and 2',3'-O-(2,4,6-trinitrophenyl) adenosine 5'-triphosphate (TNP-ATP, P2X1,3,2/3,1/5R antagonist). The latency was shortened after administration of alpha,beta-methylene ATP (alpha,beta-meATP, P2X1,3,2/3R agonist), although no changes appeared after administration of beta,gamma-methylene-L-ATP (beta,gamma-me-L-ATP, P2X1R agonist). The protein gene product-9.5 and calcitonin gene-related peptide immunoreactive nerve fibers significantly decreased in the VP skin of ipsilateral to the IoN ligation. In the ipsilateral trigeminal ganglion, the number of P2X3-immunoreactive neurons significantly increased in the small cell group. In this study, we developed an experimental model of trigeminal neuropathic pain by partial ligation of IoN, which produced heat and mechanical hyperalgesia in the VP. Pharmacological and immunohistochemical studies revealed that the P2X3R plays an important role in the heat hyperalgesia observed in this model. PERSPECTIVE: The study describes the development of a novel model of trigeminal neuropathic pain. Heat hyperalgesia in this model was inhibited by peripheral injection of P2XR antagonists. The results suggest that P2X3R is a potential target for development of a novel therapy for trigeminal neuropathic pain. SN - 1526-5900 UR - https://www.unboundmedicine.com/medline/citation/17481957/P2X3_receptor_mediates_heat_hyperalgesia_in_a_rat_model_of_trigeminal_neuropathic_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1526-5900(07)00599-8 DB - PRIME DP - Unbound Medicine ER -