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http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/66348完整後設資料紀錄
| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 嚴震東 | |
| dc.contributor.author | Yu-Hsin Huang | en |
| dc.contributor.author | 黃郁昕 | zh_TW |
| dc.date.accessioned | 2021-06-17T00:31:24Z | - |
| dc.date.available | 2014-03-19 | |
| dc.date.copyright | 2012-03-19 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-02-10 | |
| dc.identifier.citation | Amir, R., Kocsis, J. D., & Devor, M. (2005). Multiple interacting sites of ectopic spike electrogenesis in primary sensory neurons. J Neurosci, 25(10), 2576-2585.
Apkarian, A. V., Bushnell, M. C., Treede, R. D., & Zubieta, J. K. (2005). Human brain mechanisms of pain perception and regulation in health and disease. Eur J Pain, 9(4), 463-484. Benison, A. M., Chumachenko, S., Harrison, J. A., Maier, S. F., Falci, S. P., Watkins, L. R., et al. (2011). Caudal granular insular cortex is sufficient and necessary for the long-term maintenance of allodynic behavior in the rat attributable to mononeuropathy. J Neurosci, 31(17), 6317-6328. Bingel, U., Quante, M., Knab, R., Bromm, B., Weiller, C., & Buchel, C. (2002). Subcortical structures involved in pain processing: evidence from single-trial fMRI. Pain, 99(1-2), 313-321. Borsody, M. K., & Weiss, J. M. (1996). Influence of corticotropin-releasing hormone on electrophysiological activity of locus coeruleus neurons. Brain Res, 724(2), 149-168. Bostock, H., Campero, M., Serra, J., & Ochoa, J. L. (2005). Temperature-dependent double spikes in C-nociceptors of neuropathic pain patients. Brain, 128(Pt 9), 2154-2163. Bourinet, E., Alloui, A., Monteil, A., Barrere, C., Couette, B., Poirot, O., et al. (2005). Silencing of the Cav3.2 T-type calcium channel gene in sensory neurons demonstrates its major role in nociception. EMBO J, 24(2), 315-324. Bourquin, A. F., Suveges, M., Pertin, M., Gilliard, N., Sardy, S., Davison, A. C., et al. (2006). Assessment and analysis of mechanical allodynia-like behavior induced by spared nerve injury (SNI) in the mouse. Pain, 122(1-2), 14 e11-14. Campbell, J. N., Raja, S. N., Meyer, R. A., & Mackinnon, S. E. (1988). Myelinated afferents signal the hyperalgesia associated with nerve injury. Pain, 32(1), 89-94. Chaplan, S. R., Bach, F. W., Pogrel, J. W., Chung, J. M., & Yaksh, T. L. (1994). Quantitative assessment of tactile allodynia in the rat paw. J Neurosci Methods, 53(1), 55-63. Chen, W. K., Liu, I. Y., Chang, Y. T., Chen, Y. C., Chen, C. C., Yen, C. T., et al. (2010). Ca(v)3.2 T-type Ca2+ channel-dependent activation of ERK in paraventricular thalamus modulates acid-induced chronic muscle pain. J Neurosci, 30(31), 10360-10368. Chen, Y. Y., Shih, Y. Y., Lo, Y. C., Lu, P. L., Tsang, S., Jaw, F. S., et al. (2010). MicroPET imaging of noxious thermal stimuli in the conscious rat brain. Somatosens Mot Res, 27(3), 69-81. Choi, Y., Yoon, Y. W., Na, H. S., Kim, S. H., & Chung, J. M. (1994). Behavioral signs of ongoing pain and cold allodynia in a rat model of neuropathic pain. Pain, 59(3), 369-376. Coffeen, U., Manuel Ortega-Legaspi, J., Lopez-Munoz, F. J., Simon-Arceo, K., Jaimes, O., & Pellicer, F. (2011). Insular cortex lesion diminishes neuropathic and inflammatory pain-like behaviours. Eur J Pain, 15(2), 132-138. Condes-Lara, M., Maie, I. A., & Dickenson, A. H. (2005). Oxytocin actions on afferent evoked spinal cord neuronal activities in neuropathic but not in normal rats. Brain Res, 1045(1-2), 124-133. Cornblath, D. R., & McArthur, J. C. (1988). Predominantly sensory neuropathy in patients with AIDS and AIDS-related complex. Neurology, 38(5), 794-796. Costigan, M., Scholz, J., & Woolf, C. J. (2009). Neuropathic pain: a maladaptive response of the nervous system to damage. Annu Rev Neurosci, 32, 1-32. Courteix, C., Eschalier, A., & Lavarenne, J. (1993). Streptozocin-induced diabetic rats: behavioural evidence for a model of chronic pain. Pain, 53(1), 81-88. Craig, A. D., Jr., & Burton, H. (1981). Spinal and medullary lamina I projection to nucleus submedius in medial thalamus: a possible pain center. J Neurophysiol, 45(3), 443-466. Cruz, F., Lima, D., & Coimbra, A. (1987). Several morphological types of terminal arborizations of primary afferents in laminae I-II of the rat spinal cord, as shown after HRP labeling and Golgi impregnation. J Comp Neurol, 261(2), 221-236. Decosterd, I., & Woolf, C. J. (2000). Spared nerve injury: an animal model of persistent peripheral neuropathic pain. Pain, 87(2), 149-158. Dostrovsky, J. O., & Guilbaud, G. (1990). Nociceptive responses in medial thalamus of the normal and arthritic rat. Pain, 40(1), 93-104. Dowdall, T., Robinson, I., & Meert, T. F. (2005). Comparison of five different rat models of peripheral nerve injury. Pharmacol Biochem Behav, 80(1), 93-108. Fields, H. L., Rowbotham, M., & Baron, R. (1998). Postherpetic neuralgia: irritable nociceptors and deafferentation. Neurobiol Dis, 5(4), 209-227. Fu, Y., Han, J., Ishola, T., Scerbo, M., Adwanikar, H., Ramsey, C., et al. (2008). PKA and ERK, but not PKC, in the amygdala contribute to pain-related synaptic plasticity and behavior. Mol Pain, 4, 26. Geha, P. Y., Baliki, M. N., Chialvo, D. R., Harden, R. N., Paice, J. A., & Apkarian, A. V. (2007). Brain activity for spontaneous pain of postherpetic neuralgia and its modulation by lidocaine patch therapy. Pain, 128(1-2), 88-100. Greenspan, J. D., & Winfield, J. A. (1992). Reversible pain and tactile deficits associated with a cerebral tumor compressing the posterior insula and parietal operculum. Pain, 50(1), 29-39. Gutierrez, V. P., Konno, K., Chacur, M., Sampaio, S. C., Picolo, G., Brigatte, P., et al. (2008). Crotalphine induces potent antinociception in neuropathic pain by acting at peripheral opioid receptors. Eur J Pharmacol, 594(1-3), 84-92. Hains, B. C., & Waxman, S. G. (2007). Sodium channel expression and the molecular pathophysiology of pain after SCI. Prog Brain Res, 161, 195-203. Hargreaves, K., Dubner, R., Brown, F., Flores, C., & Joris, J. (1988). A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia. Pain, 32(1), 77-88. Hoffmann, T., Sauer, S. K., Horch, R. E., & Reeh, P. W. (2008). Sensory transduction in peripheral nerve axons elicits ectopic action potentials. J Neurosci, 28(24), 6281-6284. Huang, S. C. (2000). Anatomy of SUV. Standardized uptake value. Nucl Med Biol, 27(7), 643-646. Iwata, H., Takasusuki, T., Yamaguchi, S., & Hori, Y. (2007). NMDA receptor 2B subunit-mediated synaptic transmission in the superficial dorsal horn of peripheral nerve-injured neuropathic mice. Brain Res, 1135(1), 92-101. Jancso, G., & Kiraly, E. (1980). Distribution of chemosensitive primary sensory afferents in the central nervous system of the rat. J Comp Neurol, 190(4), 781-792. Jones, E. G. (2000). Cortical and subcortical contributions to activity-dependent plasticity in primate somatosensory cortex. Annu Rev Neurosci, 23, 1-37. Keller, A. F., Beggs, S., Salter, M. W., & De Koninck, Y. (2007). Transformation of the output of spinal lamina I neurons after nerve injury and microglia stimulation underlying neuropathic pain. Mol Pain, 3, 27. Khan, G. M., Chen, S. R., & Pan, H. L. (2002). Role of primary afferent nerves in allodynia caused by diabetic neuropathy in rats. Neuroscience, 114(2), 291-299. Kohno, T., Ji, R. R., Ito, N., Allchorne, A. J., Befort, K., Karchewski, L. A., et al. (2005). Peripheral axonal injury results in reduced mu opioid receptor pre- and post-synaptic action in the spinal cord. Pain, 117(1-2), 77-87. Koltzenburg, M., Wall, P. D., & McMahon, S. B. (1999). Does the right side know what the left is doing? Trends Neurosci, 22(3), 122-127. Kupers, R., Lonsdale, M. N., Aasvang, E., & Kehlet, H. (2011). A positron emission tomography study of wind-up pain in chronic postherniotomy pain. Eur J Pain, 15(7), 698 e691-616. Kupers, R. C., Nuytten, D., De Castro-Costa, M., & Gybels, J. M. (1992). A time course analysis of the changes in spontaneous and evoked behaviour in a rat model of neuropathic pain. Pain, 50(1), 101-111. Lee, A. T., Ariffin, M. Z., Zhou, M., Ye, J. Z., Moochhala, S. M., & Khanna, S. (2011). Forebrain medial septum region facilitates nociception in a rat formalin model of inflammatory pain. Pain, 152(11), 2528-2542. Luo, L., Chang, L., Brown, S. M., Ao, H., Lee, D. H., Higuera, E. S., et al. (2007). Role of peripheral hyperpolarization-activated cyclic nucleotide-modulated channel pacemaker channels in acute and chronic pain models in the rat. Neuroscience, 144(4), 1477-1485. Mao, J., Mayer, D. J., & Price, D. D. (1993). Patterns of increased brain activity indicative of pain in a rat model of peripheral mononeuropathy. J Neurosci, 13(6), 2689-2702. Mao, J., Price, D. D., Hayes, R. L., Lu, J., Mayer, D. J., & Frenk, H. (1993). Intrathecal treatment with dextrorphan or ketamine potently reduces pain-related behaviors in a rat model of peripheral mononeuropathy. Brain Res, 605(1), 164-168. McKenna, J. E., & Melzack, R. (2001). Blocking NMDA receptors in the hippocampal dentate gyrus with AP5 produces analgesia in the formalin pain test. Exp Neurol, 172(1), 92-99. Moore, K. A., Kohno, T., Karchewski, L. A., Scholz, J., Baba, H., & Woolf, C. J. (2002). Partial peripheral nerve injury promotes a selective loss of GABAergic inhibition in the superficial dorsal horn of the spinal cord. J Neurosci, 22(15), 6724-6731. Obata, K., Yamanaka, H., Fukuoka, T., Yi, D., Tokunaga, A., Hashimoto, N., et al. (2003). Contribution of injured and uninjured dorsal root ganglion neurons to pain behavior and the changes in gene expression following chronic constriction injury of the sciatic nerve in rats. Pain, 101(1-2), 65-77. Ohashi, K., Ichikawa, K., Chen, L., Callahan, M., Zasadny, K., & Kurebayashi, Y. (2008). MicroPET detection of regional brain activation induced by colonic distention in a rat model of visceral hypersensitivity. J Vet Med Sci, 70(1), 43-49. Okamoto, M., Baba, H., Goldstein, P. A., Higashi, H., Shimoji, K., & Yoshimura, M. (2001). Functional reorganization of sensory pathways in the rat spinal dorsal horn following peripheral nerve injury. J Physiol, 532(Pt 1), 241-250. Olds, J., & Milner, P. (1954). Positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain. J Comp Physiol Psychol, 47(6), 419-427. Paulson, P. E., Minoshima, S., Morrow, T. J., & Casey, K. L. (1998). Gender differences in pain perception and patterns of cerebral activation during noxious heat stimulation in humans. Pain, 76(1-2), 223-229. Pedersen, L. H., Scheel-Kruger, J., & Blackburn-Munro, G. (2007). Amygdala GABA-A receptor involvement in mediating sensory-discriminative and affective-motivational pain responses in a rat model of peripheral nerve injury. Pain, 127(1-2), 17-26. Petrovic, P., Ingvar, M., Stone-Elander, S., Petersson, K. M., & Hansson, P. (1999). A PET activation study of dynamic mechanical allodynia in patients with mononeuropathy. Pain, 83(3), 459-470. Peyron, R., Garcia-Larrea, L., Gregoire, M. C., Convers, P., Lavenne, F., Veyre, L., et al. (1998). Allodynia after lateral-medullary (Wallenberg) infarct. A PET study. Brain, 121 ( Pt 2), 345-356. Peyron, R., Laurent, B., & Garcia-Larrea, L. (2000). Functional imaging of brain responses to pain. A review and meta-analysis (2000). Neurophysiol Clin, 30(5), 263-288. Pinto, V., Derkach, V. A., & Safronov, B. V. (2008). Role of TTX-sensitive and TTX-resistant sodium channels in Adelta- and C-fiber conduction and synaptic transmission. J Neurophysiol, 99(2), 617-628. Rho, J. H., & Swanson, L. W. (1987). Neuroendocrine CRF motoneurons: intrahypothalamic axon terminals shown with a new retrograde-Lucifer-immuno method. Brain Res, 436(1), 143-147. Schmalhofer, W. A., Calhoun, J., Burrows, R., Bailey, T., Kohler, M. G., Weinglass, A. B., et al. (2008). ProTx-II, a selective inhibitor of NaV1.7 sodium channels, blocks action potential propagation in nociceptors. Mol Pharmacol, 74(5), 1476-1484. Schweinhardt, P., Fransson, P., Olson, L., Spenger, C., & Andersson, J. L. (2003). A template for spatial normalisation of MR images of the rat brain. J Neurosci Methods, 129(2), 105-113. Schweinhardt, P., Glynn, C., Brooks, J., McQuay, H., Jack, T., Chessell, I., et al. (2006). An fMRI study of cerebral processing of brush-evoked allodynia in neuropathic pain patients. Neuroimage, 32(1), 256-265. Shih, Y. Y., Chiang, Y. C., Chen, J. C., Huang, C. H., Chen, Y. Y., Liu, R. S., et al. (2008). Brain nociceptive imaging in rats using (18)f-fluorodeoxyglucose small-animal positron emission tomography. Neuroscience, 155(4), 1221-1226. Simpson, D. A., Headley, P. M., & Lumb, B. M. (2008). Selective inhibition from the anterior hypothalamus of C- versus A-fibre mediated spinal nociception. Pain, 136(3), 305-312. Soleimannejad, E., Naghdi, N., Semnanian, S., Fathollahi, Y., & Kazemnejad, A. (2007). Antinociceptive effect of intra-hippocampal CA1 and dentate gyrus injection of MK801 and AP5 in the formalin test in adult male rats. Eur J Pharmacol, 562(1-2), 39-46. Southworth, R., Parry, C. R., Parkes, H. G., Medina, R. A., & Garlick, P. B. (2003). Tissue-specific differences in 2-fluoro-2-deoxyglucose metabolism beyond FDG-6-P: a 19F NMR spectroscopy study in the rat. NMR Biomed, 16(8), 494-502. Thompson, S. W., Woolf, C. J., & Sivilotti, L. G. (1993). Small-caliber afferent inputs produce a heterosynaptic facilitation of the synaptic responses evoked by primary afferent A-fibers in the neonatal rat spinal cord in vitro. J Neurophysiol, 69(6), 2116-2128. Tracey, I. (2005). Nociceptive processing in the human brain. Curr Opin Neurobiol, 15(4), 478-487. Ultenius, C., Linderoth, B., Meyerson, B. A., & Wallin, J. (2006). Spinal NMDA receptor phosphorylation correlates with the presence of neuropathic signs following peripheral nerve injury in the rat. Neurosci Lett, 399(1-2), 85-90. Witting, N., Kupers, R. C., Svensson, P., & Jensen, T. S. (2006). A PET activation study of brush-evoked allodynia in patients with nerve injury pain. Pain, 120(1-2), 145-154. Woolf, C. J., & Salter, M. W. (2000). Neuronal plasticity: increasing the gain in pain. Science, 288(5472), 1765-1769. Xu, H., Wu, L. J., Wang, H., Zhang, X., Vadakkan, K. I., Kim, S. S., et al. (2008). Presynaptic and postsynaptic amplifications of neuropathic pain in the anterior cingulate cortex. J Neurosci, 28(29), 7445-7453. Yu, S. Q., Lundeberg, T., & Yu, L. C. (2003). Involvement of oxytocin in spinal antinociception in rats with inflammation. Brain Res, 983(1-2), 13-22. Yudin, D., Hanz, S., Yoo, S., Iavnilovitch, E., Willis, D., Gradus, T., et al. (2008). Localized regulation of axonal RanGTPase controls retrograde injury signaling in peripheral nerve. Neuron, 59(2), 241-252. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/66348 | - |
| dc.description.abstract | 神經性疼痛是體感覺神經系統的損傷所引發的慢性疼痛，自發性疼痛，觸感異常以及痛覺敏感化是神經性疼痛三大徵狀。近期研究指出在神經性疼痛中脊髓以上的中樞神經活性變化對於疼痛的調控扮演很重要的角色。本實驗結合行為測試和搭配氟 18 去氧葡萄糖 (FDG) 為追蹤劑進行正子斷層掃描，探討大鼠在坐骨神經分支選擇結紮切斷 (SNI) 的神經性疼痛痛模型的大鼠腦中葡萄糖代謝活性之變化。SNI 手術後，大鼠表現出自發性疼痛行為，機械性觸感痛覺和熱痛覺敏感至少持續4個禮拜。在 PET 探討自發性疼痛的結果中，大腦葡萄糖代謝活性在 SNI 手術後相比手術前的控制組於對側後島腦區 (posterior insular cortex, PIC) 顯著增加；相比偽手術後控制組於中膈區 (septum) 和 視丘室旁核 (paraventricular thalamic nucleus, PVA) 顯著增加。PIC 之代謝活性與自發性疼痛程度呈顯著相關。在利用 PET 探討機械性觸發異常觸感的結果中，大腦葡萄糖代謝活性在 SNI 手術後相比手術前組的改變於雙側初級體感覺皮層 (primary somatosensory cortex)，對側次級體感覺皮層 (secondary somatosensory cortex)，對側初級運動皮層 (primary motor cortex)， 同側次級運動皮層 (secondary motor cortex) ，下視丘 (hypothalamus) ，前側島腦 (rostral agranular insular cortex, RAIC)，PIC ，小腦 (cerebellum) 顯著增加。實驗結果顯示在大腦的層次，神經性疼痛症狀中的自發性疼痛及觸感痛均有多個腦區參與，其中島腦可能扮演很重要的角色。 | zh_TW |
| dc.description.abstract | Neuropathic pain is triggered by lesions in the somatosensory nervous system. Pain occurs spontaneously and responses to noxious and innocuous stimuli are pathologically amplified. Neural activity in supraspinal centers play an important role in the modulation of pain behavior in neuropathic pain, but the precise mechanism underlying are not fully understood. In this study, we combined behavioural test with positron emission tomography (PET), using 18- fluorode-oxyglucose (18-FDG) as a tracer, to investigate the change of brain glucose metabolic activity in the spared nerve injury (SNI) model of neuropathic pain of the rat. Two major branches of the sciatic nerve were transected under anesthesia condition. After SNI surgery, the rats displayed spontaneous pain behavior, mechanical allodynia and thermal hyperalgesia behavior lasting at least 4 weeks. In PET study of spontaneous paw lifting, glucose metabolic activity in SNI condition was significantly increased in contralateral posterior insular cortex (PIC) compared to pre-surgery control, and significantly increased in septum and paraventricular thalamic nucleus (PVA) compared to sham control. And the glucose metabolic activity of insular cortex correlated linearly with the magnitude of spontaneous paw lifting. In PET study of allodynia, 6 g vonFrey hair was used to stimulus the paw pad of the affected hindlimb. Glucose metabolic activity change in SNI condition was significantly increased in bilateral primary sensory cortex (S1), contralateral secondary sensory cortex (S2), contralateral primary motor cortex (M1), ipsilateral secondary motor cortex (M2), contralateral rostral agranular insular cortex (RAIC)，posterior insular cortex (PIC), hypothalamus, mediodorsal nucleus (MD) of thalamus and cerebellum compared to pre-surgery control. The data suggest that there are many brain areas involved in neuropathic pain, and insular cortex may play an important role in spontaneous pain condition. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-17T00:31:24Z (GMT). No. of bitstreams: 1 ntu-101-R98b41028-1.pdf: 1500504 bytes, checksum: ace8b5c89aabb93b420fdda3aa6e3a1c (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | 中文摘要 1
英文摘要 2 第一章 前言 1. 疼痛的神經傳遞路徑 4 2. 周邊神經性疼痛的生成機制 4 3. 功能性腦照影與神經性疼痛 7 4. 正子斷層造影 9 5. 實驗目的 11 第二章 材料與方法 12 1. 實驗動物 12 2. Spared nerve injury (SNI) 神經性疼痛動物模式手術 12 行為測試 13 3a. 自發性疼痛行為紀錄 13 3b. 機械性觸感痛覺測試 13 3c. 熱痛覺敏感測試 14 4. 正子斷層造影 14 影像處理 15 5a. Voxel based statistical analysis 15 5b. Region of interesting analysis 17 第三章 實驗結果 19 1. 行為測試結果 19 FDG 分佈同時記錄 spontaneous pain behavioral的結果 20 PET 數據 voxel based analysis 結果 21 3a. 自發性疼痛實驗 21 3b. 機械性觸感痛實驗 21 PET 數據 region of interesting analysis 結果 22 自發性疼痛行為程度和 ROI 活化指數強度之相關性 23 第四章 討論 1. SNI 手術後大鼠疼痛相關行為之改變 25 自發性疼痛相關的的大腦核區 27 機械性觸感痛相關的的大腦核區 29 自發性疼痛行為程度和 contralateral PIC 活化指數之相關性 32 結論 33 參考文獻 34 附錄 44 表一 自發性疼痛實驗組 ROI 分析結果 44 表二 機械性觸感痛實驗組 ROI 分析結果 45 圖一 Spared nerve injury (SNI) 手術示意圖 47 圖二 實驗流程圖 48 圖三 PET 實驗流程 49 圖四 Voxel based analysis 的影像前處理流程 50 圖五 ROI analysis 圈選的範圍 51 圖六 自發性疼痛行為紀錄結果 52 圖七 Mechanical allodynia 行為測試結果 53 圖八 Heat hyperalgesia 行為測試結果 54 圖九 FDG 分佈同時記錄 spontaneous pain behavioral的結果 55 圖十 自發性疼痛實驗 voxel based statistical analysis 結果圖 56 圖十一 機械性觸感痛實驗 voxel based statistical analysis 結果圖 58 圖十二 SNI 手術後相比 SNI 手前及 sham 手術後 voxel based statistical analysis 結果圖 60 圖十三 同一大鼠手術前後 SUV 變化之一例 62 圖十四 自發性疼痛行為和不同腦區的葡萄糖代謝率活化指數 (AI 值) 關係圖 63 | |
| dc.language.iso | zh-TW | |
| dc.subject | 正子斷層掃描 | zh_TW |
| dc.subject | 神經性疼痛 | zh_TW |
| dc.subject | 觸感痛 | zh_TW |
| dc.subject | 自發性疼痛 | zh_TW |
| dc.subject | positron emission tomography | en |
| dc.subject | neuropathic pain | en |
| dc.subject | allodynia | en |
| dc.subject | spontaneous pain | en |
| dc.title | 坐骨神經分支選擇結紮切斷神經性疼痛模式大鼠之腦葡萄糖代謝改變之研究 | zh_TW |
| dc.title | Change of Brain Glucose Metabolic Activity in Spared Nerve Injury Neuropathic Pain Rat | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-1 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 曾凱元,孫維仁,蔡明達,陳建璋 | |
| dc.subject.keyword | 神經性疼痛,正子斷層掃描,自發性疼痛,觸感痛, | zh_TW |
| dc.subject.keyword | neuropathic pain,positron emission tomography,spontaneous pain,allodynia, | en |
| dc.relation.page | 66 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2012-02-13 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 動物學研究所 | zh_TW |
| 顯示於系所單位： | 動物學研究所 | |
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