請用此 Handle URI 來引用此文件:
http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/62629
完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 呂俊宏 | |
dc.contributor.author | Hsin-ying Wang | en |
dc.contributor.author | 王馨瑩 | zh_TW |
dc.date.accessioned | 2021-06-16T16:06:01Z | - |
dc.date.available | 2023-06-19 | |
dc.date.copyright | 2013-09-24 | |
dc.date.issued | 2013 | |
dc.date.submitted | 2013-06-19 | |
dc.identifier.citation | Adams CW, Csejtey J, Hallpike JF, Bayliss OB. 1972. Histochemistry of myelin. XV. Changes in the myelin proteins of the peripheral nerve undergoing Wallerian degeneration--electrophoretic and microdensitometric observations. J Neurochem 19(9):2043-2048.
Aimar P, Pasti L, Carmignoto G, Merighi A. 1998. Nitric oxide-producing islet cells modulate the release of sensory neuropeptides in the rat substantia gelatinosa. J Neurosci 18(24):10375-10388. Aimi Y, Fujimura M, Vincent SR, Kimura H. 1991. Localization of NADPH-diaphorase-containing neurons in sensory ganglia of the rat. J Comp Neurol 306(3):382-392. Bennett GJ, Xie YK. 1988. A peripheral mononeuropathy in rat that produces disorders of pain sensation like those seen in man. Pain 33(1):87-107. Berry JF, Cevallos WH, Wade RR, Jr. 1965. Lipid Class and Fatty Acid Composition of Intact Peripheral Nerve and during Wallerian Degeneration. J Am Oil Chem Soc 42:492-500. Bhangoo S, Ren D, Miller RJ, Henry KJ, Lineswala J, Hamdouchi C, Li B, Monahan PE, Chan DM, Ripsch MS, White FA. 2007. Delayed functional expression of neuronal chemokine receptors following focal nerve demyelination in the rat: a mechanism for the development of chronic sensitization of peripheral nociceptors. Mol Pain 3:38. Black JA, Cummins TR, Plumpton C, Chen YH, Hormuzdiar W, Clare JJ, Waxman SG. 1999. Upregulation of a silent sodium channel after peripheral, but not central, nerve injury in DRG neurons. J Neurophysiol 82(5):2776-2785. Bullitt E. 1990. Expression of c-fos-like protein as a marker for neuronal activity following noxious stimulation in the rat. J Comp Neurol 296(4):517-530. Bullitt E. 1991. Somatotopy of spinal nociceptive processing. J Comp Neurol 312(2):279-290. Chan SH, Chang KF, Ou CC, Chan JY. 2004. Nitric oxide regulates c-fos expression in nucleus tractus solitarii induced by baroreceptor activation via cGMP-dependent protein kinase and cAMP response element-binding protein phosphorylation. Mol Pharmacol 65(2):319-325. Chapman V, Buritova J, Honore P, Besson JM. 1995. 7-Nitro-indazole, a selective inhibitor of neuronal nitric oxide synthase, reduces formalin evoked c-Fos expression in dorsal horn neurons of the rat spinal cord. Brain Res 697(1-2):258-261. Chen JJ, Lue JH, Lin LH, Huang CT, Chiang RP, Chen CL, Tsai YJ. 2010. Effects of pre-emptive drug treatment on astrocyte activation in the cuneate nucleus following rat median nerve injury. Pain 148(1):158-166. Chen SH, Tsai YJ, Lin CT, Wang HY, Li SF, Lue JH. 2012a. Changes in GABA and GABA(B) receptor expressions are involved in neuropathy in the rat cuneate nucleus following median nerve transection. Synapse 66(6):561-572. Chen SH, Tsai YJ, Wang HY, Lin CT, Li SF, Lue JH. 2012b. Decreases of glycine receptor expression induced by median nerve injury in the rat cuneate nucleus contribute to NPY release and c-Fos expression. Life Sci 90(7-8):278-288. Choi Y, Raja SN, Moore LC, Tobin JR. 1996. Neuropathic pain in rats is associated with altered nitric oxide synthase activity in neural tissue. J Neurol Sci 138(1-2):14-20. Choi Y, Yoon YW, Na HS, Kim SH, Chung JM. 1994. Behavioral signs of ongoing pain and cold allodynia in a rat model of neuropathic pain. Pain 59(3):369-376. Chung HT, Pae HO, Choi BM, Billiar TR, Kim YM. 2001. Nitric oxide as a bioregulator of apoptosis. Biochem Biophys Res Commun 282(5):1075-1079. Chung K, Langford LA, Coggeshall RE. 1987. Primary afferent and propriospinal fibers in the rat dorsal and dorsolateral funiculi. J Comp Neurol 263(1):68-75. Cizkova D, Lukacova N, Marsala M, Marsala J. 2002. Neuropathic pain is associated with alterations of nitric oxide synthase immunoreactivity and catalytic activity in dorsal root ganglia and spinal dorsal horn. Brain Res Bull 58(2):161-171. Clementi E, Meldolesi J. 1997. The cross-talk between nitric oxide and Ca2+: a story with a complex past and a promising future. Trends Pharmacol Sci 18(8):266-269. Curran T, Van Beveren C, Verma IM. 1985. Viral and cellular fos proteins are complexed with a 39,000-dalton cellular protein. Mol Cell Biol 5(1):167-172. Day AS, Lue JH, Sun WZ, Shieh JY, Wen CY. 2001. A beta-fiber intensity stimulation of chronically constricted median nerve induces c-fos expression in thalamic projection neurons of the cuneate nucleus in rats with behavioral signs of neuropathic pain. Brain Res 895(1-2):194-203. Dib-Hajj SD, Fjell J, Cummins TR, Zheng Z, Fried K, LaMotte R, Black JA, Waxman SG. 1999. Plasticity of sodium channel expression in DRG neurons in the chronic constriction injury model of neuropathic pain. Pain 83(3):591-600. Elliott K, Kest B, Man A, Kao B, Inturrisi CE. 1995. N-methyl-D-aspartate (NMDA) receptors, mu and kappa opioid tolerance, and perspectives on new analgesic drug development. Neuropsychopharmacology 13(4):347-356. Foster RE, Kocsis JD, Malenka RC, Waxman SG. 1980. Lysophosphatidyl choline-induced focal demyelination in the rabbit corpus callosum. Electron-microscopic observations. J Neurol Sci 48(2):221-231. Friebe A, Koesling D. 2003. Regulation of nitric oxide-sensitive guanylyl cyclase. Circ Res 93(2):96-105. Gallo EF, Iadecola C. 2011. Neuronal nitric oxide contributes to neuroplasticity-associated protein expression through cGMP, protein kinase G, and extracellular signal-regulated kinase. J Neurosci 31(19):6947-6955. Garry MG, Richardson JD, Hargreaves KM. 1994. Sodium nitroprusside evokes the release of immunoreactive calcitonin gene-related peptide and substance P from dorsal horn slices via nitric oxide-dependent and nitric oxide-independent mechanisms. J Neurosci 14(7):4329-4337. Garthwaite G, Goodwin DA, Garthwaite J. 1999. Nitric oxide stimulates cGMP formation in rat optic nerve axons, providing a specific marker of axon viability. Eur J Neurosci 11(12):4367-4372. Garthwaite J. 1991. Glutamate, nitric oxide and cell-cell signalling in the nervous system. Trends Neurosci 14(2):60-67. Garthwaite J, Boulton CL. 1995. Nitric oxide signaling in the central nervous system. Annu Rev Physiol 57:683-706. Gildenberg PL, Hirshberg RM. 1984. Limited myelotomy for the treatment of intractable cancer pain. J Neurol Neurosurg Psychiatry 47(1):94-96. Gogas KR, Presley RW, Levine JD, Basbaum AI. 1991. The antinociceptive action of supraspinal opioids results from an increase in descending inhibitory control: correlation of nociceptive behavior and c-fos expression. Neuroscience 42(3):617-628. Gonzalez-Hernandez T, Rustioni A. 1999. Nitric oxide synthase and growth-associated protein are coexpressed in primary sensory neurons after peripheral injury. J Comp Neurol 404(1):64-74. Gregson NA, Hall SM. 1973. A quantitative analysis of the effects of the intraneural injection of lysophosphatidyl choline. J Cell Sci 13(1):257-277. Guan Y, Yaster M, Raja SN, Tao YX. 2007. Genetic knockout and pharmacologic inhibition of neuronal nitric oxide synthase attenuate nerve injury-induced mechanical hypersensitivity in mice. Mol Pain 3:29. Hall SM. 1972. The effect of injections of lysophosphatidyl choline into white matter of the adult mouse spinal cord. J Cell Sci 10(2):535-546. Hall SM, Gregson NA. 1971. The in vivo and ultrastructural effects of injection of lysophosphatidyl choline into myelinated peripheral nerve fibres of the adult mouse. J Cell Sci 9(3):769-789. Hervera A, Negrete R, Leanez S, Martin-Campos JM, Pol O. 2010. The spinal cord expression of neuronal and inducible nitric oxide synthases and their contribution in the maintenance of neuropathic pain in mice. PLoS One 5(12):e14321. Hunt SP, Pini A, Evan G. 1987. Induction of c-fos-like protein in spinal cord neurons following sensory stimulation. Nature 328(6131):632-634. Inoue M, Xie W, Matsushita Y, Chun J, Aoki J, Ueda H. 2008. Lysophosphatidylcholine induces neuropathic pain through an action of autotaxin to generate lysophosphatidic acid. Neuroscience 152(2):296-298. Kehl LJ, Gogas, K.R., Lichtblau, L., Pollack, C.H., Mayes, M., Basbaum, A.I., Wilcox, G.L. 1991. The NMDA antagonist MK801 reduces noxious stimulus-evoked Fos expression in the spinal cord dorsal horn. In: M.R. Bond JEC, C.J. Woolf editor. Proceedings of the VIth world congress on pain. Amsterdeam: Elsevier. p 307–311. Kim CH, Oh Y, Chung JM, Chung K. 2001. The changes in expression of three subtypes of TTX sensitive sodium channels in sensory neurons after spinal nerve ligation. Brain Res Mol Brain Res 95(1-2):153-161. Kim KH, Kim JI, Han JA, Choe MA, Ahn JH. 2011. Upregulation of neuronal nitric oxide synthase in the periphery promotes pain hypersensitivity after peripheral nerve injury. Neuroscience 190:367-378. Kim SH, Chung JM. 1992. An experimental model for peripheral neuropathy produced by segmental spinal nerve ligation in the rat. Pain 50(3):355-363. Lancaster JR, Jr. 1997. A tutorial on the diffusibility and reactivity of free nitric oxide. Nitric Oxide 1(1):18-30. Lee DH, Singh JP, Lodge D. 2005. Experiments with nitric oxide synthase inhibitors in spinal nerve ligated rats provide no evidence of a role for nitric oxide in neuropathic mechanical allodynia. Neurosci Lett 385(3):179-183. Lee JH, Wilcox GL, Beitz AJ. 1992. Nitric oxide mediates Fos expression in the spinal cord induced by mechanical noxious stimulation. Neuroreport 3(10):841-844. Lin CT, Tsai YJ, Chen SH, Wang HY, Lin LH, Lue JH. 2010. Early expression of injury-induced neuropeptide Y in primary sensory neurons and the cuneate nucleus in diabetic rats with median nerve transection. J Chem Neuroanat 40(2):102-111. Lin CT, Tsai YJ, Wang HY, Chen SH, Lin TY, Lue JH. 2012. Pre-emptive treatment of lidocaine attenuates neuropathic pain and reduces pain-related biochemical markers in the rat cuneate nucleus in median nerve chronic constriction injury model. Anesthesiol Res Pract 2012:921405. Lin CT, Wang HY, Tsai YJ, Huang CT, Chen SH, Lue JH. 2009. Pre-treatment with lidocaine suppresses ectopic discharges and attenuates neuropeptide Y and c-Fos expressions in the rat cuneate nucleus following median nerve transection. J Chem Neuroanat 38(1):47-56. Liu W, Hirata K, Kawabuchi M. 2005. The occurrence of nitric oxide synthase-containing axonal baskets surrounding large neurons in rat dorsal root ganglia after sciatic nerve ligation. Arch Histol Cytol 68(1):29-40. Lue JH, Leong SM, Day AS, Tsai YJ, Shieh JY, Wen CY. 2002. Changes in c-Fos protein expression in the rat cuneate nucleus after electric stimulation of the transected median nerve. J Neurotrauma 19(7):897-907. Lukacova N, Cizkova D, Krizanova O, Pavel J, Marsala M, Marsala J. 2003. Peripheral axotomy affects nicotinamide adenine dinucleotide phosphate diaphorase and nitric oxide synthases in the spinal cord of the rabbit. J Neurosci Res 71(2):300-313. Luo ZD, Chaplan SR, Scott BP, Cizkova D, Calcutt NA, Yaksh TL. 1999. Neuronal nitric oxide synthase mRNA upregulation in rat sensory neurons after spinal nerve ligation: lack of a role in allodynia development. J Neurosci 19(21):9201-9208. Ma S, Cornford ME, Vahabnezhad I, Wei S, Li X. 2000. Responses of nitric oxide synthase expression in the gracile nucleus to sciatic nerve injury in young and aged rats. Brain Res 855(1):124-131. Ma W, Bisby MA. 1997. Differential expression of galanin immunoreactivities in the primary sensory neurons following partial and complete sciatic nerve injuries. Neuroscience 79(4):1183-1195. Ma W, Bisby MA. 1998a. Increase of calcitonin gene-related peptide immunoreactivity in the axonal fibers of the gracile nuclei of adult and aged rats after complete and partial sciatic nerve injuries. Exp Neurol 152(1):137-149. Ma W, Bisby MA. 1998b. Partial and complete sciatic nerve injuries induce similar increases of neuropeptide Y and vasoactive intestinal peptide immunoreactivities in primary sensory neurons and their central projections. Neuroscience 86(4):1217-1234. Ma W, Bisby MA. 1999. Ultrastructural localization of increased neuropeptide immunoreactivity in the axons and cells of the gracile nucleus following chronic constriction injury of the sciatic nerve. Neuroscience 93(1):335-348. Ma W, Bisby MA. 2000. Partial sciatic nerve ligation induced more dramatic increase of neuropeptide Y immunoreactive axonal fibers in the gracile nucleus of middle-aged rats than in young adult rats. J Neurosci Res 60(4):520-530. Meller ST, Pechman PS, Gebhart GF, Maves TJ. 1992. Nitric oxide mediates the thermal hyperalgesia produced in a model of neuropathic pain in the rat. Neuroscience 50(1):7-10. Miclescu A, Gordh T. 2009. Nitric oxide and pain: 'Something old, something new'. Acta Anaesthesiol Scand 53(9):1107-1120. Miki K, Fukuoka T, Tokunaga A, Noguchi K. 1998. Calcitonin gene-related peptide increase in the rat spinal dorsal horn and dorsal column nucleus following peripheral nerve injury: up-regulation in a subpopulation of primary afferent sensory neurons. Neuroscience 82(4):1243-1252. Molander C, Hongpaisan J, Grant G. 1992. Changing pattern of c-FOS expression in spinal cord neurons after electrical stimulation of the chronically injured sciatic nerve in the rat. Neuroscience 50(1):223-236. Molander C, Hongpaisan J, Persson JK. 1994. Distribution of c-fos expressing dorsal horn neurons after electrical stimulation of low threshold sensory fibers in the chronically injured sciatic nerve. Brain Res 644(1):74-82. Morgan JI, Curran T. 1989. Stimulus-transcription coupling in neurons: role of cellular immediate-early genes. Trends Neurosci 12(11):459-462. Morris R, Southam E, Braid DJ, Garthwaite J. 1992. Nitric oxide may act as a messenger between dorsal root ganglion neurones and their satellite cells. Neurosci Lett 137(1):29-32. Naik AK, Tandan SK, Kumar D, Dudhgaonkar SP. 2006. Nitric oxide and its modulators in chronic constriction injury-induced neuropathic pain in rats. Eur J Pharmacol 530(1-2):59-69. Natarajan V, Yao JK, Dyck PJ, Schmid HH. 1982. Early stimulation of phosphatidylcholine biosynthesis during Wallerian degeneration of rat sciatic nerve. J Neurochem 38(5):1419-1428. Nathan PW, Smith MC, Cook AW. 1986. Sensory effects in man of lesions of the posterior columns and of some other afferent pathways. Brain 109 ( Pt 5):1003-1041. Noguchi K, Kawai Y, Fukuoka T, Senba E, Miki K. 1995. Substance P induced by peripheral nerve injury in primary afferent sensory neurons and its effect on dorsal column nucleus neurons. J Neurosci 15(11):7633-7643. Ohara S, Roth KA, Beaudet LN, Schmidt RE. 1994. Transganglionic neuropeptide Y response to sciatic nerve injury in young and aged rats. J Neuropathol Exp Neurol 53(6):646-662. Ossipov MH, Zhang ET, Carvajal C, Gardell L, Quirion R, Dumont Y, Lai J, Porreca F. 2002. Selective mediation of nerve injury-induced tactile hypersensitivity by neuropeptide Y. J Neurosci 22(22):9858-9867. Patterson JT, Coggeshall RE, Lee WT, Chung K. 1990. Long ascending unmyelinated primary afferent axons in the rat dorsal column: immunohistochemical localizations. Neurosci Lett 108(1-2):6-10. Patterson JT, Head PA, McNeill DL, Chung K, Coggeshall RE. 1989. Ascending unmyelinated primary afferent fibers in the dorsal funiculus. J Comp Neurol 290(3):384-390. Presley RW, Menetrey D, Levine JD, Basbaum AI. 1990. Systemic morphine suppresses noxious stimulus-evoked Fos protein-like immunoreactivity in the rat spinal cord. J Neurosci 10(1):323-335. Racz GB, McCarron RF, Talboys P. 1989. Percutaneous dorsal column stimulator for chronic pain control. Spine (Phila Pa 1976) 14(1):1-4. Ramer LM, Borisoff JF, Ramer MS. 2004. Rho-kinase inhibition enhances axonal plasticity and attenuates cold hyperalgesia after dorsal rhizotomy. J Neurosci 24(48):10796-10805. Ramer MS, Bradbury EJ, McMahon SB. 2001. Nerve growth factor induces P2X(3) expression in sensory neurons. J Neurochem 77(3):864-875. Roche AK, Cook M, Wilcox GL, Kajander KC. 1996. A nitric oxide synthesis inhibitor (L-NAME) reduces licking behavior and Fos-labeling in the spinal cord of rats during formalin-induced inflammation. Pain 66(2-3):331-341. Rydh-Rinder M, Holmberg K, Elfvin LG, Wiesenfeld-Hallin Z, Hokfelt T. 1996. Effects of peripheral axotomy on neuropeptides and nitric oxide synthase in dorsal root ganglia and spinal cord of the guinea pig: an immunohistochemical study. Brain Res 707(2):180-188. Sedal L, Ghabriel MN, He F, Allt G, Le Quesne PM, Harrison MJ. 1983. A combined morphological and electrophysiological study of conduction block in peripheral nerve. J Neurol Sci 60(2):293-306. Seltzer Z, Dubner R, Shir Y. 1990. A novel behavioral model of neuropathic pain disorders produced in rats by partial sciatic nerve injury. Pain 43(2):205-218. Shealy CN, Mortimer JT, Hagfors NR. 1970. Dorsal column electroanalgesia. J Neurosurg 32(5):560-564. Shi TJ, Holmberg K, Xu ZQ, Steinbusch H, de Vente J, Hokfelt T. 1998. Effect of peripheral nerve injury on cGMP and nitric oxide synthase levels in rat dorsal root ganglia: time course and coexistence. Pain 78(3):171-180. Smith KJ, Hall SM. 1980. Nerve conduction during peripheral demyelination and remyelination. J Neurol Sci 48(2):201-219. Sorkin LS. 1993. NMDA evokes an L-NAME sensitive spinal release of glutamate and citrulline. Neuroreport 4(5):479-482. Spiegelmann R, Friedman WA. 1991. Spinal cord stimulation: a contemporary series. Neurosurgery 28(1):65-70; discussion 70-61. Tamatani M, Senba E, Tohyama M. 1989. Calcitonin gene-related peptide- and substance P-containing primary afferent fibers in the dorsal column of the rat. Brain Res 495(1):122-130. Tanabe M, Nagatani Y, Saitoh K, Takasu K, Ono H. 2009. Pharmacological assessments of nitric oxide synthase isoforms and downstream diversity of NO signaling in the maintenance of thermal and mechanical hypersensitivity after peripheral nerve injury in mice. Neuropharmacology 56(3):702-708. Tao YX, Johns RA. 2000. Activation of cGMP-dependent protein kinase Ialpha is required for N-methyl-D-aspartate- or nitric oxide-produced spinal thermal hyperalgesia. Eur J Pharmacol 392(3):141-145. Thippeswamy T, Haddley K, Corness JD, Howard MR, McKay JS, Beaucourt SM, Pope MD, Murphy D, Morris R, Hokfelt T, Quinn JP. 2007a. NO-cGMP mediated galanin expression in NGF-deprived or axotomized sensory neurons. J Neurochem 100(3):790-801. Thippeswamy T, Howard MR, Cosgrave AS, Arora DK, McKay JS, Quinn JP. 2007b. Nitric oxide-NGF mediated PPTA/SP, ADNP, and VIP expression in the peripheral nervous system. J Mol Neurosci 33(3):268-277. Thippeswamy T, Jain RK, Mumtaz N, Morris R. 2001a. Inhibition of neuronal nitric oxide synthase results in neurodegenerative changes in the axotomised dorsal root ganglion neurons: evidence for a neuroprotective role of nitric oxide in vivo. Neurosci Res 40(1):37-44. Thippeswamy T, McKay JS, Morris R. 2001b. Bax and caspases are inhibited by endogenous nitric oxide in dorsal root ganglion neurons in vitro. Eur J Neurosci 14(8):1229-1236. Thippeswamy T, Morris R. 1997. Cyclic guanosine 3',5'-monophosphate-mediated neuroprotection by nitric oxide in dissociated cultures of rat dorsal root ganglion neurones. Brain Res 774(1-2):116-122. Tracey DJ, Romm MA, Yao NN. 1995. Peripheral hyperalgesia in experimental neuropathy: exacerbation by neuropeptide Y. Brain Res 669(2):245-254. Tsai YJ, Leong SM, Day AS, Wen CY, Shieh JY, Lue JH. 2004. A time course analysis of the changes in neuropeptide Y immunoreactivity in the rat cuneate nucleus following median nerve transection. Neurosci Res 48(4):369-377. Tsai YJ, Lin CT, Huang CT, Wang HY, Tien LT, Chen SH, Lue JH. 2009. Neuropeptide Y modulates c-Fos protein expression in the cuneate nucleus and contributes to mechanical hypersensitivity following rat median nerve injury. J Neurotrauma 26(9):1609-1621. Tsai YJ, Lin CT, Lue JH. 2007. Characterization of the induced neuropeptide Y-like immunoreactivity in primary sensory neurons following complete median nerve transection. J Neurotrauma 24(12):1878-1888. Ueda H. 2008. Peripheral mechanisms of neuropathic pain - involvement of lysophosphatidic acid receptor-mediated demyelination. Mol Pain 4:11. Valtschanoff JG, Weinberg RJ, Rustioni A, Schmidt HH. 1995. Colocalization of neuronal nitric oxide synthase with GABA in rat cuneate nucleus. J Neurocytol 24(3):237-245. Verge VM, Xu Z, Xu XJ, Wiesenfeld-Hallin Z, Hokfelt T. 1992. Marked increase in nitric oxide synthase mRNA in rat dorsal root ganglia after peripheral axotomy: in situ hybridization and functional studies. Proc Natl Acad Sci U S A 89(23):11617-11621. Wakisaka S, Kajander KC, Bennett GJ. 1991. Increased neuropeptide Y (NPY)-like immunoreactivity in rat sensory neurons following peripheral axotomy. Neurosci Lett 124(2):200-203. Wakisaka S, Kajander KC, Bennett GJ. 1992. Effects of peripheral nerve injuries and tissue inflammation on the levels of neuropeptide Y-like immunoreactivity in rat primary afferent neurons. Brain Res 598(1-2):349-352. Wall PD, Devor M, Inbal R, Scadding JW, Schonfeld D, Seltzer Z, Tomkiewicz MM. 1979. Autotomy following peripheral nerve lesions: experimental anaesthesia dolorosa. Pain 7(2):103-111. Wall PD, Waxman S, Basbaum AI. 1974. Ongoing activity in peripheral nerve: injury discharge. Exp Neurol 45(3):576-589. Wallace VC, Cottrell DF, Brophy PJ, Fleetwood-Walker SM. 2003. Focal lysolecithin-induced demyelination of peripheral afferents results in neuropathic pain behavior that is attenuated by cannabinoids. J Neurosci 23(8):3221-3233. Wang H, Nie H, Zhang RX, Qiao JT. 1999. Peripheral nitric oxide contributes to both formalin- and NMDA-induced activation of nociceptors: An immunocytochemical study in rats. J Neurosci Res 57(6):824-829. Wang TJ, Lue JH, Shieh JY, Wen CY. 2001. The distribution and characterization of NADPH-d/NOS-IR neurons in the rat cuneate nucleus. Brain Res 910(1-2):38-48. Wang TJ, Lue JH, Wu CH, Shieh JY, Wen CY. 2002. Neurogenesis of cuneothalamic neurons and NO-containing neurons in the cuneate nucleus of the rat. Exp Brain Res 142(3):327-334. Waxman SG, Cummins TR, Dib-Hajj S, Fjell J, Black JA. 1999. Sodium channels, excitability of primary sensory neurons, and the molecular basis of pain. Muscle Nerve 22(9):1177-1187. Waxman SG, Kocsis JD, Nitta KC. 1979. Lysophosphatidyl choline-induced focal demyelination in the rabbit corpus callosum. Light-microscopic observations. J Neurol Sci 44(1):45-53. White DM. 1997. Intrathecal neuropeptide Y exacerbates nerve injury-induced mechanical hyperalgesia. Brain Res 750(1-2):141-146. Wood JG, Dawson RM. 1974a. Lipid and protein changes in sciatic nerve during Wallerian degeneration. J Neurochem 22(5):631-635. Wood JG, Dawson RM. 1974b. Some properties of a major structural glycoprotein of sciatic nerve. J Neurochem 22(5):627-630. Wood PL, Emmett MR, Rao TS, Cler J, Mick S, Iyengar S. 1990. Inhibition of nitric oxide synthase blocks N-methyl-D-aspartate-, quisqualate-, kainate-, harmaline-, and pentylenetetrazole-dependent increases in cerebellar cyclic GMP in vivo. J Neurochem 55(1):346-348. Xu L, Mabuchi T, Katano T, Matsumura S, Okuda-Ashitaka E, Sakimura K, Mishina M, Ito S. 2007. Nitric oxide (NO) serves as a retrograde messenger to activate neuronal NO synthase in the spinal cord via NMDA receptors. Nitric Oxide 17(1):18-24. Yeh JH, Lue JH, Wang HY, Huang CT, Tsai YJ. 2008. Synaptic relationships between induced neuropeptide Y-like immunoreactive terminals and cuneothalamic projection neurons in the rat cuneate nucleus following median nerve transection. J Chem Neuroanat 36(1):27-32. Yen DH, Chen LC, Shen YC, Chiu YC, Ho IC, Lou YJ, Chen IC, Yen JC. 2011. Protein kinase A-dependent neuronal nitric oxide synthase activation mediates the enhancement of baroreflex response by adrenomedullin in the nucleus tractus solitarii of rats. J Biomed Sci 18:32. Yoon YW, Sung B, Chung JM. 1998. Nitric oxide mediates behavioral signs of neuropathic pain in an experimental rat model. Neuroreport 9(3):367-372. Zhang X, Meister B, Elde R, Verge VM, Hokfelt T. 1993a. Large calibre primary afferent neurons projecting to the gracile nucleus express neuropeptide Y after sciatic nerve lesions: an immunohistochemical and in situ hybridization study in rats. Eur J Neurosci 5(11):1510-1519. Zhang X, Verge V, Wiesenfeld-Hallin Z, Ju G, Bredt D, Synder SH, Hokfelt T. 1993b. Nitric oxide synthase-like immunoreactivity in lumbar dorsal root ganglia and spinal cord of rat and monkey and effect of peripheral axotomy. J Comp Neurol 335(4):563-575. | |
dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/62629 | - |
dc.description.abstract | 先前雖有報告指出,周邊神經損傷導致具有一氧化氮合成酶的神經元數量增加,其所釋出的一氧化氮則與神經病變疼痛的誘發有密切的關連,但尚未有研究探討一氧化氮與正中神經損傷病變疼痛之間的關係。在本研究中,我們將探討一氧化氮在正中神經損傷後所扮演的角色。首先,我們檢測大白鼠正中神經截斷後不同存活時程,在第六頸髓背根神經節與楔狀神經核內神經性一氧化氮合成酶的數量變化。結果發現正中神經截斷後第三天,即可在背根神經節及楔狀神經核內觀察到神經性一氧化氮合成酶免疫反應神經元的數量,與正常未損傷組別相比較,已有增多的情形,並且持續至神經截斷後四週數量仍然居高不下。若術前以局部麻醉劑lidocaine處理,在正中神經截斷後四週,背根神經節及楔狀神經核內神經性一氧化氮合成酶免疫反應神經元的數量會明顯地下降。此外,電刺激前給予一氧化氮合成酶抑制劑L-NAME及7-NI後,發現它們可以明顯降低楔狀神經核內神經胜肽Y釋放量與c-Fos免疫反應神經元數量;而給予一氧化氮供給劑SNAP雖然可以顯著增加c-Fos免疫反應神經元數量,但對於神經胜肽Y釋放量卻沒有影響。
我們進一步利用溶血磷脂醯膽鹼(lysophosphatidylcholine, LPC)作為神經髓鞘損傷藥物,探討正中神經以LPC處理後,一氧化氮與神經病變疼痛的關係。研究結果發現,正中神經以4% LPC處理後第五天及第七天,實驗動物手術側前肢掌面對於非傷害性機械刺激及傷害性溫熱覺刺激產生的神經病變疼痛行為達到最顯著的程度。此外4% LPC處理後一週,手術側正中神經纖維髓鞘有剝離脫落、甚至於髓鞘完全退化消失的現象;但是在LPC處理後二及四週,軸突外圍則包覆有完整的髓鞘。進一步探討正中神經施以4% LPC後不同存活時程,背根神經節及楔狀神經核內一氧化氮合成酶免疫反應神經元及c-Fos免疫反應神經元的數量變化。LPC處理後一週,在背根神經節及楔狀神經核內可觀察到神經性一氧化氮合成酶免疫反應神經元的數量增加並且達到最高值。當正中神經施以4% LPC一週後並配合電刺激處理後,其楔狀神經核內c-Fos免疫反應神經元數量也達到最高。腹腔注射NOS抑制劑L-NAME及7-NI後,發現它們可以明顯緩解LPC處理所引起神經病變疼痛症狀;而給予SNAP後,也會加重LPC處理所引起的痛覺過敏。電刺激前給予L-NAME及7-NI後,發現它們可以顯著地降低楔狀神經核內c-Fos免疫反應神經元數量;而給予SNAP則可以有效地增加c-Fos免疫反應神經元數量。 綜合以上結果,正中神經損傷導致神經性一氧化氮合成酶增加,可能促進一氧化氮的產生。釋放出的一氧化氮除了可調控初級傳入神經終末NPY的釋放而興奮突觸後楔狀丘腦投射神經元外,也可能直接影響楔狀丘腦投射神經元內c-Fos的產生;並藉此參與神經病變疼痛的訊息傳遞。 | zh_TW |
dc.description.abstract | NO is produced by the increase in the number of nitric oxide (NO)-synthesizing neurons after peripheral nerve injury and mediate the neuropathic pain. However, the direct evidence of NO involvement in the median nerve neuropathic sensation is unavailable. In this study, we investigated the role of NO after median nerve injury. We first examined the temporal changes of neuronal nitric oxide synthase (nNOS) expression in the rat dorsal root ganglion (DRG) and cuneate nucleus (CN) after median nerve transection (MNT). From 3 days to 4 weeks following MNT, the amounts of nNOS like immunoreactive (nNOS-LI) neurons in the DRG and CN significantly increased as compared with those of the normal rats. Four weeks after MNT, the maximums of nNOS-LI neurons in the DRG and CN were attenuated by pre-emptive lidocaine treatment in a dose-dependent manner. After MNT, intraperitoneal administration of L-NAME (Nω-Nitro-L-arginine methyl ester, an inhibitor of NOS) or 7-NI (7-nitroindazole, a specific neuronal NOS inhibitor) suppressed the amount of NPY release from the stimulated terminals and thus attenuated c-Fos expression in the CN; however, SNAP (S-Nitroso-N- acetylpenicillamine; a NO donor) application only increased the number of c-Fos-LI neurons in the CN but not the NPY release level.
Using median nerve demyelination model, we further investigated the role of NO in lysophosphatidylcholine (LPC) induced neuropathy rats followed by the administration of NOS inhibitors and NO donor. We found that at 5 and 7 days after LPC treatment of the median nerve, a maximum effect on the signs of mechanical allodynia and thermal hyperalgesia was induced. One week after 4% LPC treatment, nerve fibers without myelin sheaths were detected in the treated nerve. And the myelin sheath reappeared at the treated nerve 2-4 weeks after 4% LPC treatment. Immunohistochemistry revealed that the amounts of nNOS-LI neurons in both the DRG and CN increased and peaked at 1 week after LPC treatment. Following electrical stimulation of the LPC-treated nerve, the number of c-Fos-LI neurons in the ipsilateral CN also increased by LPC treatment in a dose-dependent manner and peaked at 1 week. Administration of L-NAME or 7-NI 1 week after 4% LPC injection attenuated tactile allodynia and thermal hyperalgesia, but SNAP only exacerbated thermal hyperalgesia. After electrical stimulation of the LPC-treated median nerve, the number of c-Fos-LI neurons in the CN diminished in the L-NAME and 7-NI groups, but increased in the SNAP group. Taken together, our findings revealed that the number of nNOS dramatically increased after median nerve injury. And the advanced NO, made by the increased nNOS after median nerve injury, might be involved in the maintenance of neuropathic sensation. In addition, NO produced via the upregulation of the amount of nNOS in the CN might increase the neuronal activity of CTN directly or modulate the amount of NPY release from primary afferent terminals and subsequently promote the excitability of CTN and thus up-regulate c-Fos protein expression. | en |
dc.description.provenance | Made available in DSpace on 2021-06-16T16:06:01Z (GMT). No. of bitstreams: 1 ntu-102-F93446009-1.pdf: 56346312 bytes, checksum: 9843525100365705e386c2f9c30b2c5d (MD5) Previous issue date: 2013 | en |
dc.description.tableofcontents | 口試委員會審定書 I
致謝 II 中文摘要 III 英文摘要 V 緒論 1 第一章 正中神經截斷後,楔狀神經核及背根神經節中nNOS的變化 10 前言 10 材料與方法 13 結果 18 討論 21 第二章 以溶血磷脂醯膽鹼誘發正中神經髓鞘損傷模式探討一氧化氮與神經病變疼痛的關係 24 前言 24 材料與方法 27 結果 33 討論 40 結論 45 參考文獻 46 圖表與說明 56 | |
dc.language.iso | zh-TW | |
dc.title | 正中神經損傷後一氧化氮參與神經病變疼痛機制之研究 | zh_TW |
dc.title | The Role of Nitric Oxide in the Median Nerve Neuropathic Pain | en |
dc.type | Thesis | |
dc.date.schoolyear | 101-2 | |
dc.description.degree | 博士 | |
dc.contributor.oralexamcommittee | 溫振源,吳慶祥,馮琮涵,蔡怡汝 | |
dc.subject.keyword | 正中神經,楔狀神經核,一氧化氮合成酶,神經病變疼痛,c-Fos, | zh_TW |
dc.subject.keyword | median nerve,cuneate nucleus,nNOS,nuropathic pain,c-Fos, | en |
dc.relation.page | 106 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2013-06-19 | |
dc.contributor.author-college | 醫學院 | zh_TW |
dc.contributor.author-dept | 解剖學暨生物細胞學研究所 | zh_TW |
顯示於系所單位: | 解剖學暨細胞生物學科所 |
文件中的檔案:
檔案 | 大小 | 格式 | |
---|---|---|---|
ntu-102-1.pdf 目前未授權公開取用 | 55.03 MB | Adobe PDF |
系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。