【www.zhangdahai.com--卫生防疫公文】
摘要目的：研究大鼠腰椎小关节在炎症状态下的神经支配模式的多元性及其传导机制。方法：通过逆行神经追踪法，将荧光金注入大鼠左侧L5/6小关节内。5天后，分别将50μl生理盐水或弗氏佐剂注入对照组或实验组。第一次术后12天，麻醉后经心脏用0.9％的盐水，紧跟着500ml 4％ 多聚甲醛磷酸缓冲液（0.1M, PH 7.4）灌注。取双侧T13-L6水平的DRGs，冰冻切片后分组行SP和IB4免疫组化，最后用荧光显微镜观察计数F-G标记神经元与SP和IB4阳性神经元，并测量每个神经元的横截面积。结果：支配大鼠L5/6小关节的神经元分布于同侧的L1-L5 DRGs。在所有F-G标记的神经元中，实验组SP阳性神经元的比例为36%±3%（Mean±S.E.）明显高于对照组的21%±2%（P 2.3对照组和实验组的比较
实验组和对照组中F-G标记神经元的总数量分别为622和615，行SP免疫组化的大鼠中F-G标记神经元的总数分别为310和321，两组之间的差异均无显著性意义。但在炎症组中SP阳性F-G标记的神经元所占的比例为36%±3%，明显高于对照组的21%±2%，P0.01，差异有高度显著性意义。两组中均未发现IB4结合神经元。
图2. 各个背根神经节中SP阳性神经元的数目。对照组及实验组中SP阳性神经元在L1和L2中的数目均明显少于L3、L4、L5中的比例，P [3]Eisenstein SM、 Parry CR. The lumbar facet arthrosis syndrome. Clinical presentation and articular surface changes. J. Bone J. Surg. [Br.]. 1987, 69: 3-7.
[4]Bogduk N、 Long DM. The anatomy of the so-called “articular nerves” and their relationship to facet denervation in the treatment of low back pain. J Neurosurg. 1979, 51:172-177.
[5]Suseki K、 Takahashi Y、 Takahashi K, et al. Innervation of the lumbar facet joints. Spine. 1997, 22: 477-485.
[6]Suseki K、 Takahashi Y、 Takahashi K, et al. CGRP-immunoreactive nerve fibers projecting to lumbar facet joints through the paravertebral sympathetic trunk in rats. Neurosci. Lett.. 1996, 221: 41-44.
[7]Averill S、 McMahon SB、 Clary DO, et al. Immunocytochemical localization of trkA receptors in chemically identified subgroups of adult rat sensory neurons. Eur. J. Neurosci.. 1995, 7: 1484-1494.
[8]Silverman JD, Kruger L. Selective neuronal glycoconjugate expression in sensory and autonomic ganglia: relation of lectin reactivity to peptide and enzyme markers. J. Neuroxytol.. 1990, 19: 789-801.
[9]Molliver DC、 Radeke MJ、 Feinstein SCet al. Presence or absence of trkA protein distinguishes subsets of small sensory neurons with unique cytochemical characteristics and dorsal horn projections. J. Comp. Neurol.. 1995, 361: 404-416.
[10]Ohtori S、 Takahashi K、 Chiba T, et al. Substance P and Calcitonin gene-related peptide immunoreactive sensory DRG neurons innervating the lumbar intervertebral discs in rats. Annals of Anatomy. 2002, 184:235-240.
[11]Ohtori S、Takahashi K、 Chiba T, et al. Substance P and Calcitonin gene-related peptide immunoreactive sensory DRG neurons innervating the lumbar facet joints in rats. Autonomic Neuroscience: Basic and clinical. 2000, 86: 13-17.
[12]Ozawa T、Aoki Y、 Ohtori S, et al. The dorsal portion of the lumbar intervertebral disc is innervated primarily by small peptide-containing dorsal root ganglion neurons in rats. Neurosci. Lett.. 2003, 344: 65-67.
[13]Aoki Y、 Ohtori S、 Takahashi K, et al. Innervation of the lumbar intervertebral disc by Nerve Growth Factor-dependent neurons related to inflammatory pain. Spine. 2004, 29:1077-1081.
[14]Bennett DLH、 Dmietrieva N、 Priestley JV. trkA, CGRP and IB4 expression in retrogradely labelled cutaneous and visceral primary sensory neurons in the rat. Neurosci Lett. 1996, 206:33�36.
[15]Bennett DLH、 Michael GJ、 Ramachandran N. A distinct subgroup of small DRG cells express GDNF receptor components and GDNF is protective for these neurons after nerve injury. J. Neurosci.. 1998, 18: 3059-3072.
[16]Ivanavicius SP、 Blake DR、Chessell IP, et al. Isolectin B4 binding neurons are not present in the rat knee joint. Neuroscience. 2004, 128:555-60.
[17]Malmberg AB、 Chen C、 Tonegawa S, et al. Preserved acute pain and reduced neuropathic pain in mice lacking PKCγ. Science. 1997a, 278:279-283.
[18]Malmberg AB、 Brandon EP、Idzerda RL, et al. Diminished inflammation and nociceptive pain with preservation of neuropathic pain in mice with a targeted mutation of the type I regulatory subunit of camp-dependent protein kinase. Science. 1997b, 17:7462-7470.
[19]Ciobanu V、Gheorghiu M、 Stoichita M, et al. Research on the experimental production of polyarthritis. I. Polyarthritis in rats after administration of Freund’s adjuvant. Stud Cercet Med Interna. 1963, 91:671-7.
[20]Knight B、Katz DR、 Isenberg DA, et al. Induction of adjuvant arthritis in mice. Clin Exp Immunol. 1992, 90:459-65.
[21]Amaya F、 Shimosato G、 Nagano M et al. NGF and GDNF differentially regulate TRPV1 expression that contributes to development of inflammatory thermal hyperalgesia. Eur J Neurosci. 2004, 20:2303-10.
[22]Farquhar-Smith WP、 Rice AS. A novel neuroimmune mechanism in cannabinoid-mediated attenuation of nerve growth factor-induced hyperalgesia. Anesthesiology. 2003, 99:1391-401.
[23]Snider WD、McMahon SB. Tackling pain at the source: new ideas about nociceptors. Neuron. 1998, 20:629-632.
[24]H. Jongsma wallin, L. M. E. Pettersson, V. M. K. Verge, et al. Effect of anti-nerve growth factor treatment on pituitary adenylate cyclase activating polypeptide expression in adult sensory neurons exposed to adjuvant induced inflammation. Neuroscience. 2003, 120:325-331.
注：基金项目 浙江省医药卫生科学研究基金（2005B176）
