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00152232-201010001-00241AbstractSpine: Affiliated Society Meeting AbstractsSpine: Affiliated Society Meeting Abstracts© 2010 Lippincott Williams & Wilkins, Inc.October 2010 p 241P75 NEUROTROPHIN RECEPTOR (P75NTR) MODULATES THE NGF SIGNALING PATHWAY RATHER THAN TROPOMYOSIN-RELATED KINASE A (TRKA) IN RAT DISCOGENIC PAIN MODELSGP99.GENERAL POSTERSOrita, Sumihisa; Nagata, Maiko; Horii, Manato; Yamashita, Masaomi; Yamauchi, Kazuyo; Inoue, Gen; Suzuki, Munetaka; Eguch, Yawara; Kamoda, Hiroto; Arai, Gen; Ishikawa, Tetsuhiro; Miyagi, Masayuki; Suzuki, Miyako; Morinaga, Tatsuo; Ohtori, Seiji; Takahashi, KazuhisaDepartment of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, Chiba, JapanINTRODUCTION: Nerve growth factor (NGF) has been reported to cause discogenic pain by inducing abnormal nerve ingrowth into degenerative discs. NGF has two receptors: a high affinity tropomyosin-related kinase A (TrkA) and a low affinity p75 neurotrophin receptor (p75NTR). The NGF-TrkA complex has been reported to play a primary role in transmitting inflammatory pain. However, their involvement in discogenic pain is unclear. The present study aimed to investigate the role of these receptors in a rat discogenic low back pain model.METHODS: Twenty-eight female Sprague Dawley rats were equally divided into four groups: control, puncture, anti-TrkA, and anti-p75. In the groups except for the control group, the L5–L6 intervertebral disc was exposed and injured by repeated puncture, and then neurotracer Fluoro-Gold (FG) and appropriate agents were applied: sterilized saline for the puncture group, anti-TrkA antibody for the anti-TrkA group, and anti-p75NTR antibody for the anti-p75 group. In the control group only FG was applied into the uninjured disc. Lumbar DRGs were harvested and immunostained for the inflammatory pain marker calcitonin related-gene peptide (CGRP). The expression of CGRP in the DRG neurons was investigated.RESULTS: FG-labeled DRG neurons were observed in all the DRGs with a dominant population in L1 and L2 DRGs. In FG-labeled CGRP-ir DRG neurons innervating discs, CGRP expression was elevated in all the injured-disc groups compared with the control group, while the expression in the two antibody-treated groups was significantly decreased compared with the puncture group (P < 0.05). Furthermore, the expression was significantly lower in the anti-p75NTR group than in the anti-TrkA group (P < 0.05).DISCUSSION: The elevated CGRP expression in the DRGs innervating injured rat discs suggests a pathogenesis for discogenic low back pain. Decreased CGRP expression by p75NTR inhibition suggests the possibility of a more crucial role of p75NTR than TrkA in discogenic pain pathogenesis.<strong xmlns:mrws="http://webservices.ovid.com/mrws/1.0">P75 NEUROTROPHIN RECEPTOR (P75NTR) MODULATES THE NGF SIGNALING PATHWAY RATHER THAN TROPOMYOSIN-RELATED KINASE A (TRKA) IN RAT DISCOGENIC PAIN MODELS</strong>: <strong xmlns:mrws="http://webservices.ovid.com/mrws/1.0">GP99.</strong>Orita Sumihisa; Nagata, Maiko; Horii, Manato; Yamashita, Masaomi; Yamauchi, Kazuyo; Inoue, Gen; Suzuki, Munetaka; Eguch, Yawara; Kamoda, Hiroto; Arai, Gen; Ishikawa, Tetsuhiro; Miyagi, Masayuki; Suzuki, Miyako; Morinaga, Tatsuo; Ohtori, Seiji; Takahashi, KazuhisaGENERAL POSTERSGENERAL POSTERSp 241