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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 張芳嘉 | |
| dc.contributor.author | Chiung-Hsiang Cheng | en |
| dc.contributor.author | 鄭穹翔 | zh_TW |
| dc.date.accessioned | 2021-05-17T09:21:33Z | - |
| dc.date.available | 2014-03-19 | |
| dc.date.available | 2021-05-17T09:21:33Z | - |
| dc.date.copyright | 2012-03-19 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-02-10 | |
| dc.identifier.citation | 1. Cheng RSS, Pomeranz B. Electroacupuncturte analgesia could be mediated by at least two pain-relieving mechanisms: endorphin and nonendorphin system. Life Sci 1979;25:1957–62.
2. Cheng G. Treatment of 55 cases of insomnia by acupuncture. Chin Acupunct Moxibustion 1985;5:26. 3. Cheng LG. Observation of the therapeutic effect on treatment of 2485 cases of insomnia by needling Shenmen point. Chin Acupunct Moxibustion 1986;6:18–19. 4. Cheng XN. Traditional Chinese Acupuncture and Moxibustion. Beijing: People’s Hygiene Press, 1986, 513–16. 5. Lu JS, He SH, Geng SH. Selection of Treatment Experience by Single Acupoint Needling. Beijing: People’s Hygiene Press, 1993. 6. Melzack R, Wall PD. Pain mechanism: a new theory. Science 1965;150:971–9. 7. Son YS, Park HJ, Kwon OB, Jung SC, Shin HC, Lim S. Antipyretic effects of acupuncture on the lipopolysaccharide-induced fever and expression of interleukin-6 and interleukin-1 beta mRNAs in the hypothalamus of rats. Neurosci Lett 2002;319:45–8. 8. Ceccherelli F, Gagliardi G, Visentin R, Sandona F, Casale R, Giron G. The effects of parachlorophenylalanine and naloxone on acupuncture and electroacupuncture modulation of capsaicininduced neurogenic edema in the rat hind paw. A controlled blind study. Clin Exp Rheumatol 1999;17:655–62. 9. Wang JD, Kuo TB, Yang CC. An alternative method to enhance vagal activities and suppress sympathetic activities in humans. Auton Neurosci 2002;100:90–5. 10. Noguchi E, Hayashi H. Increases in gastric acidity in response to electroacupuncture stimulation of the hindlimb of anesthetized rats. Jpn J Physiol 1996;46:53–8. 11. Cottle MK. Degeneration studies of primary afferents of IXth and Xth cranial nerves in the cats. J Comp Neurol 1964;122:329–45. 12. Norgren R. Projections from the nucleus of the solitary tract in the rat. Neuroscience 1978;3:207–18. 13. Ryan LJ. Cholinergic regulation of neocortical spindling in DBA/2 mice. Exp Neurol 1985;89:372–81. 14. Magnes J, Moruzzi G, Pompeiano O. Synchronization of the EEG produced by low-frequency electrical stimulation of the region of the solitary tract. Arch Ital Biol 1961;99:33–41. 15. Bonvallet M, Allen MBJ. Prolonged spontaneous and evoked reticular activation following discrete bulbar lesions. Electroencephalogr Clin Neurophysiol 1963;15:969–88. 16. Reinoso-Barbero F, de Andres I. Effects of opioid microinjections in the nucleus of the solitary tract on the sleep-wakefulness cycle states in cats. Anesthesiology 1995;82:144–52. 17. Yi PL, Tsai CH, Lin JG, Liu HJ, Chang FC. Effects of electroacupuncture at ‘Anmian (extra)’ acupoints on sleep activities in rats: the implication of the caudal nucleus tractus solitarius. J Biomed Sci 2004;11:579–90. 18. Bronstein DM, Day NC, Gutstein HB, Trujillo KA, Akil H. Pre- and posttranslational regulation of beta-endorphin biosynthesis in the CNS: effects of chronic naltrexone treatment. J Neurochem 1993;60:40–9. 19. Saper CB, Scammell TE, Lu J. Hypothalamic regulation of sleep and circadian rhythms. Nature 437: 1257-1263, 2005. 20. Lu BC, Li H, Chen T, Huo FQ, Zhang T, Li YQ. Endomorphin 1- and endomorphin 2-containing neurons in nucleus tractus solitarii send axons to the parabrachial nuclei in the rat. Anat Rec 292: 488-497, 2009. 21. Han JS. Acupuncture and endorphins. Neurosci Lett 2004;361: 258–61 22. F.-C. Chang and M. R. Opp, “Corticotropin-releasing hormone (CRH) as a regulator of waking,” Neuroscience & Biobehavioral Reviews, vol. 25, no. 5, pp. 445-453, 2001. 23. N. Tsujino and T. Sakurai, “Orexin/hypocretin: A neuropeptide at the interface of sleep, energy homeostasis, and reward system,” Pharmacological Reviews, vol. 61, no. 2, pp. 162-176, 2009. 24. D. J. Mayer, D. D. Price, and A. Rafii, “Antagonism of acupuncture analgesia in man by the narcotic antagonist naloxone,” Brain Research, vol. 121, no. 2, pp. 368-372, 1977. 25. B. Pomeranz and D. Chiu, “Naloxone blocks acupuncture analgesia and causes hyperalgesia: endorphin is implicated,” Life Science, vol. 19, no. 11, pp. 1757-1762, 1976. 26. R. Chang and B. Pomeranz, “Electroacupuncture analgesia could be mediated by at least twopain-relieving mechanisms: endorphin and non-endorphin systems,” Life Science, vol. 25, no.23, pp. 1957-1962, 1979. 27. J.-S. Han, X. Z. Ding and S. G. Fan, “The frequency as the cardinal determinant for electroacupuncture analgesia to be reversed by opioid antagonists,” Acta Physiologica Sinica, vol. 38, pp. 475–482, 1986. 28. X. H. Chen and J.-S. Han, “Analgesia induced by electroacupuncture of different frequencies is mediated by different types of opioid receptors: another cross-tolerance study,” Behavioural Brain Research, vol. 47, no. 2, pp. 143-149, 1992. 29. H. Fei, G. X. Xie, and J.-S. Han, “Low and high frequency electroacupuncture stimulation release [Met5]enkephalin and dynorphin A in rat spinal cord,” Science Bulletin China, vol. 32, pp. 1496-1501. 30. C.-H. Cheng, P.-L. Yi, J.-G. Lin, and F.-C. Chang, “Endogenous opiates in the nucleus tractus solitarius mediate electroacupuncture-induced sleep activities in rats,” Evidence-Based Complementary and Alternative Medicine, vol. 2011, article ID 159209, 2011. 31. Chang FC, Opp MR. Blockade of corticotropin-releasing hormone receptors reduces spontaneous waking in the rat. Am J Physiol 1998;275:R793–802. 32. Paxinos G, Watson C. The Rat Brain in Stereotaxic Coordinates, 4th edn. San Diego: Academic Press, 1998. 33. Deboer T, Franken P, Tobler I. Sleep and cortical temperature in the Djungarian hamster under baseline conditions and after sleep deprivation. J Comp Physiol A 1994;174:145–55. 34. Franken P, Tobler I, Borbely AA. Cortical temperature and EEG slow-wave activity in the rat: analysis of vigilance state related changes. Pflugers Arch 1992;420:500–7. 35. Partinen M. Epidemiology of sleep disorders. In: Kryger MH, Roth T, Dement WC (eds). Principles and Practice of Sleep Medicine. Philadelphia: WB Saunders, 1994, 437–52. 36. Van Someren EJW. Circadian and sleep disturbances in the elderly. Exp Gerontol 2000;35:1229–37. 37. Anis NA, Berry SC, Burton NR, Lodge D. The dissociative anesthetics, ketamine and phencyclidine, selectively reduce excitation of central mammalian neurons by N-methyl-aspartate. Br J Pharmacol 1983;79:565–75. 38. Feinberg I, Campbell IG. Ketamine administration during waking increase delta EEG intensity in rat sleep. Neuropsychopharmacology 1993;9:41–8. 39. Feinberg I, Campbell IG. Stimulation of NREM delta EEG by ketamine administration during waking: demonstration of dosedependence. Neuropsychopharmacology 1995;12:89–90. 40. Campbell IG, Feinberg I. Comparison of MK-801 and sleep deprivation effects on NREM, REM, and waking spectra in the rat. Sleep 1999;22:423–32. 41. Lin JH, Shih CH, Kaphle K, Wu LS, Tseng WY, Chiu JH, et al. Acupuncture effects on cardiac functions measured by cardiac magnetic resonance imaging in a feline model. eCAM Advance Access published January 23, 2008, doi:10.1093/ecam/nem187. 42. Lin JG, Chen WL. Acupuncture analgesia: a review of its mechanisms of actions. Am J Chin Med 2008;36:635–45. 43. Han JS. Acupuncture: neuropeptide release produced by electrical stimulation of different frequencies. Trends Neurosci 2003;26:17–22. 44. Ni H, Jing LX, Shen S. The role of medial medulla in the depressive responses in pulmonary and carotid arteries to injection of acetylcholine at fourth ventricle. Sheng Li Hsueh Pao-Acta Physiologica Sinica 1989;41:291–8. 45. Castle M, Comoli E, Loewy AD. Autonomic brainstem nuclei are linked to the hippocampus. Neuroscience 2005;134:657–69. 46. Maley BE. Immunohistochemical localization of neuropeptides and neurotransmitters in the nucleus solitarius. Chem Senses 1996;21:367–76. 47. Beckstead RM, Morse JR, Norgren R. The nucleus of the solitary tractin the monkey: projections to the thalamus and brain stem nuclei. J Comp Neurol 190: 259-282, 1980. 48. Ter Horst GJ, de Boer P, Lutten PGM, van Willigen JD. Ascending projections from the solitary tract nucleus to the hypothalamus. A phaseolus vulgaris lectin tracing study in the rat. Neuroscience 31: 785-797, 1989. 49. Granata AR, Kitai ST. Intracellular study of nucleus parabrachialis and nucleus tractus solitarii interconnections. Brain Res 492: 281-292, 1989. 50. Granata AR. Ascending and descending convergent inputs to neurons in the nucleus parabrachialis of the rat: an intracellular study. Brain Res 600: 315-321, 1993. 51. Jhamandas JH, Harris KH. Excitatory amino acids may mediate nucleus tractus solitarius input to rat parabrachial neurons. Am J Physiol 263: R324-R330, 1992. 52. Rutecki P. Anatomical, physiological, and theorectical basis for the antiepileptic effect of vagus nerve stimulation. Epilepsia 31 (suppl 2): S1-S6, 1990. 53. Berman AL. The brainstem of the cat: a cytoarchitectonic atlas with stereotaxic coordinates, University of Wisconsin Press, Wisconsin, 1968. 54. Norgren R. Taste pathways to hypothalamus and amygdala. J Comp Neurol 166: 17-33, 1976. 55. Coote JH, Hilton SM, Sbrozoyna AW. The pontomedullary area integrating the defense reaction in the cat and its influence on muscle blood flow. J Physiol (Lond) 229: 257-274, 1973. 56. Saito H, Sakai K, Jouvet M. Discharge patterns of the nucleus parabrachialis lateralis neurons of the cat during sleep and waking. Brain Res 134: 59-72, 1977. 57. Berntson GG. Attack grooming and threat elicited by stimulation of the pontine tegmentum in cats. Physiol Behav 11: 81-87, 1973. 58. Pierce TL, Wessendorf MW. Immunocytochemical mapping of endomorphin- 2-immunoreactivity in rat brain. J Chem Neuroanat 18: 181-207, 2000. 59. Tononi G, Cirelli C. Sleep function and synaptic homeostasis. Sleep Med Rev 10: 49-62, 2006. 60. P.-L. Yi, C.-H. Tsai, J.-G. Lin, C.-C. Lee, and F.-C. Chang, “Kindling stimuli delivered at different times in the sleep-wake cycle,” Sleep, vol. 27, no. 2, pp. 203-212, 2004. 61. J. E. Zadina, L. Hackler, L. J. Ge, and A. J. Kastin, “A potent and selective endogenous agonist for the μ-opiate receptor,” Nature, vol. 386, no. 6642, pp. 499-501, 1997. 62. C. Chavkin, L. F. James, and A. Goldstein, “Dynorphin is a specific endogenous legend for the κ-opioid receptor,” Science, vol. 215, no. 4531, pp. 413-415, 1982. 63. M. Waldhoer, S. Bartlett, and J. Whistler, “Opioid receptors,” Annual Review of Biochemistry,vol. 73, pp. 953-990, 2004. 64. H. S. Lee and A. I. Basbaum, “Immunoactive pro-enkephalin and pro-dynorphin products are differentially distributed within the nucleus of the solitary tract of the rat,” Journal of Comparative Neurology, vol. 230, no. 4, pp. 614-619, 1984. 65. A. Mansour, H. Khachaturian, M. E. Lewis, H. Akil, and S. J. Watson, “Anatomy of CNS opioid receptors,” Trends in Neurosciences, vol. 11, no. 7, pp. 308-314, 1988. | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/6932 | - |
| dc.description.abstract | 電針刺激可以有許多治療功用,例如止痛、消炎、治療睡眠障礙。電針刺激改善睡眠的機制目前還不明瞭。在中醫理論裡:安眠穴,是一個可以改善失眠的穴道。之前發現10Hz電針刺激安眠穴可以使孤獨徑核 (nucleus tractus solitaries, NTS) 的乙醯膽鹼性神經活化,造成大鼠在暗期的非快速動眼睡眠(non-rapid eye movement sleep; NREM sleep) 上升。我們假設除了乙醯膽鹼類神經外,內生性嗎啡也可能是影響電針在睡眠的作用。本研究結果顯示,10Hz電刺激安眠穴增加了暗期的非快速動眼睡眠但是不影響快速動眼睡眠 (rapid eye movement sleep; REM sleep),且這些增加的NREM可以被注射到NTS的naloxone (opioid receptor antagonist) 和naloxonazine (μ-opioid receptor antagonist拮抗) 抑制。而注射natrindole (σ-opioid receptor) 和 nor-binaltrophimine (κ-opioid receptor) 則沒有作用。除此之外β-endorphin的表現量在10Hz電針刺激後於腦幹和海馬迴都有上升且會被注射到NTS的muscarinic antagonist: scopolamine拮抗。我們的結果顯示10Hz電刺激安眠穴增加的非快速動眼可能是藉由乙醯膽鹼活化後使opiodergic 神經分泌β-endorphin增高,作用在μ-opioid receptor。
解剖上,從 NTS 來的神經投射到 parabrachial nuclei (PBN),再投射到視丘的腹內側神經核 (ventromedial nucleus of the thalamus; VM);或直接由 NTS 投射到視丘的腹內側神經核。清醒時腦中皮質的神經突觸活性較強,但在睡眠時的神經活動基本上會減少這些突觸的活性。從 NTS 到 PBN 以及 VM 的嗎啡類神經藉由嗎啡類受體過極化了PBN 以及 VM 中的神經。因此我們假設 10 Hz 電針刺激增加 NTS 的突觸活性,造成PBN 以及 VM 的過極化,導致增加睡眠的現象。我們接著研究10 Hz 電針刺激安眠穴後,NTS 和 VM 的突觸密度和長度的改變。我們發現 10 Hz 電針刺激安眠穴後 NTS 和 VM 的突觸密度都有增加,但是突觸總長度只有在 NTS 部位有顯著改變。這實驗結果可能代表了電針刺激會增加興奮性突觸的長度以及密度來增強 NTS 的突觸強度,並且在 VM 增加抑制性突觸的密度來減低 VM 的突觸強度,並藉此達到電針安眠穴增加睡眠的作用。 有報告指出不同頻率的電針刺激可以增加不同種的內源性嗎啡,且作用在不同的類嗎啡受體上。因此我們接著使用100 Hz的電針刺激安眠穴發現也增加非快速動眼睡眠,但不會影響快速動眼睡眠。100Hz電刺激增加的非快速動眼睡眠會因為注射naloxone (opioid receptor antagonist)和nor-binaltrophimine (κ-opioid receptor)到NTS而抑制,但注射naloxonazine (μ-opioid receptor antagonist拮抗) 和natrindole (σ-opioid receptor) 不會影響非快速動眼睡眠。我們的結果顯示高頻率100 Hz的電針刺激可能會藉由NTS的κ-opioid receptor增加非快速動眼睡眠。這些結果顯示低頻率 (10Hz) 以及高頻率 (100Hz) 電刺激安眠穴均會增加非快速動眼睡眠,其機轉和電針止痛在脊髓的機制類似,低頻刺激增加β-endorphin在NTS釋放,作用在μ-receptor;而高頻刺激則是藉由κ-receptor。 | zh_TW |
| dc.description.abstract | Electroacupuncture (EA) possesses various therapeutic effects, including alleviation of pain, reduction of inflammation and improvement of sleep disturbance. The mechanisms of EA on sleep improvement, however, remain to be determined. It has been stated in ancient Chinese literature that the Anmian (EX17) acupoint is one of the trigger points that alleviates insomnia. We previously demonstrated that EA stimulation of Anmian acupoints in rats during the dark period enhanced non-rapid eye movement (NREM) sleep, which involves the induction of cholinergic activity in the nucleus tractus solitarius (NTS). In addition to cholinergic activation of the NTS, activation of the endogenous opioidergic system may also be a mechanism by which acupuncture affects sleep. Therefore, this study was designed to investigate the involvement of the NTS opioidergic system in EA-induced alterations in sleep. Our present results indicate that EA of Anmian acupoints increased NREM sleep, but not rapid eye movement (REM) sleep, during the dark period in rats. This enhancement in NREM sleep was dose-dependently blocked by microinjection of opioid receptor antagonist, naloxone, and the μ-opioid receptor antagonist, naloxonazine, into the NTS; administrations of δ-receptor antagonist, natrindole, and the κ-receptor antagonist, nor-binaltrophimine, however, did not affect EA-induced alterations in sleep. Furthermore, β-endorphin was significantly increased in both the brainstem and hippocampus after the EA stimuli, an effect blocked by administration of the muscarinic antagonist scopolamine into the NTS. Our findings suggest that mechanisms of EA-induced NREM sleep enhancement may be mediated, in part, by cholinergic activation, stimulation of the opiodergic neurons to increase the concentrations of β-endorphin and the involvement of the μ-opioid receptors.
One ascending projection is from NTS to the ventromedial nucleus (VM) of the thalamus (the NTS-VM pathway). Wakefulness is accompanied by synaptic potentiation in the cortical circuits, whereas slow wave activity (SWA) during slow wave sleep (SWS) promotes a generalized depression or downscaling of synaptic strength. The VM receives opioidergic inputs from NTS and the activation of opioid receptors hyperpolarize neurons of VM. Accordingly, 10 Hz EA may increase synaptic activity of NTS and subsequently hyperpolarize and downscale the synaptic strength in the VM of thalamus by inhibitory afferents, which lead to the enhancement of SWS. Enhancement of excitatory synapses in NTS and inhibitory synapses in VM may respectively contribute to the up-regulation of synaptic strength in NTS and downscaling of synaptic strength in the VM after 10 Hz EA. Our results demonstrated that the synaptic density was increased in both NTS and VM after rats received 10 Hz EA stimuli, while the enhanced synaptic length was only observed in the NTS, suggesting that 10 Hz EA altered excitatory synaptic strength of NTS and inhibitory synaptic strength of VM by changing the synaptic morphology. Studies have shown that different kinds of endogenous opiate peptides and receptors may mediate the consequences of EA with different frequencies. Herein we further elucidated that high frequency (100 Hz) EA of Anmian enhanced NREM sleep during the dark period, but exhibited no direct effect on REM sleep. High frequency EA-induced NREM sleep enhancement was dose-dependently blocked by microinjection of naloxone or κ-receptor antagonist (nor-binaltrophimine) into the caudal NTS, but was affected neither by μ-(naloxonazine) nor δ-receptor antagonists (natrindole), suggesting the role of NTS κ-receptors in the enhancement of high frequency EA-induced NREM sleep. Current and previous results have combined to depict the opioid mechanisms of EA-induced sleep. | en |
| dc.description.provenance | Made available in DSpace on 2021-05-17T09:21:33Z (GMT). No. of bitstreams: 1 ntu-101-D95629010-1.pdf: 3374536 bytes, checksum: b54b9fec71638c2afe963057671909cc (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | Certificate i
Acknowledgement ii List of Abbreviations iii Abstract in Chinese iv Abstract vi Chapter 1. General Introduction 1 Chapter 2. Endogenous Opiates in the Nucleus Tractus Solitarius Mediate Electroacupuncture-induced Sleep Activities in Rats 8 2-1 Abstract 8 2-2 Introduction 9 2-3 Methods 12 2-3-1 Pharmacological agents 12 2-3-2 Animals 12 2-3-3 Experimental Protocol 13 2-3-4 Apparatus and Recording 17 2-3-5 ELISA for β-endorphin 18 2-3-6 Statistical Analyses for Experiment Protocol 18 2-4 Results 19 2-4-1 Naloxone and Naloxonazine Blocked the EA-induced Alterations in Sleep 19 2-4-2 Naltrindole and Nor-binaltorphimine did not Affect EA-induced Alterations in Sleep 21 2-4-3 Scopolamine Suppressed EA-induced Expression of Endogenous β-endorphin 22 2-5 Discussion 34 2-6 Conclusion 38 Chapter 3. Morphology Alterations of Synapses in the Ventromedial Nucleus (VM) of Thalamus and Caudal Nucleus Tractus Solitarius (NTS) after 10 Hz Electroacupuncture in Rats 40 3-1 Abstract 40 3-2 Introduction 41 3-3 Materials and Methods 44 3-3-1 Animals 44 3-3-2 Experimental protocol 44 3-3-3 Transmission electron microscopy (TEM) 46 3-3-4 Statistical analyses for experiment protocol 46 3-4 Results 47 3-5 Discussion 54 3-6 Conclusion 57 Chapter 4. Kappa-opioid Receptors in the Caudal Nucleus Tractus Solitarius (NTS) Mediate 100 Hz Electroacupuncture-induced Sleep Activities in Rats 58 4-1 Abstract 58 4-2 Introduction 58 4-3 Materials and Methods 61 4-3-1 Pharmacological agents 61 4-3-2 Animals 62 4-3-3 Experimental protocol 63 4-3-4 Apparatus and recording 66 4-3-5 Statistical analyses for experiment protocol 67 4-4 Results 68 4-4-1 The effect of naloxone on the 100 Hz EA-induced alterations in sleep 68 4-4-2 The effect of naloxonazine on the 100 Hz EA-induced alterations in sleep 69 4-4-3 The effect of naltrindole on the 100 Hz EA-induced alterations in sleep 70 4-4-4 The effect of nor-binaltorphimine on the 100 Hz EA-induced alterations in sleep 70 4-5 Discussion 82 4-6 Conclusion 86 Chapter 5. Conclusions 87 References 89 Appendix:Publication list (2006~2011) 98 | |
| dc.language.iso | en | |
| dc.title | Caudal Nucleus Tractus Solitarius (NTS)在針灸改變睡眠所扮演的角色 | zh_TW |
| dc.title | The Role of Caudal Nucleus Tractus Solitarius (NTS) In Electroacupuncture-induced Sleep Activities | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-1 | |
| dc.description.degree | 博士 | |
| dc.contributor.oralexamcommittee | 林昭庚,詹東榮,林中天,蔡孟利 | |
| dc.subject.keyword | 電針刺激(electroacupuncture, EA),孤獨徑核(nucleus tractus solitaries,NTS),β-endorphin,μ-opioid receptor,κ-opioid receptor,睡眠,突觸形態,視丘的腹內側神經核 (ventromedial nucleus of the thalamus,VM), | zh_TW |
| dc.subject.keyword | electroacupuncture (EA),nucleus tractus solitaries (NTS),β-endorphin,μ-opioid receptor,κ-opioid receptor,sleep,synaptic morphology,ventromedial nucleus of the thalamus (VM), | en |
| dc.relation.page | 101 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2012-02-10 | |
| dc.contributor.author-college | 獸醫專業學院 | zh_TW |
| dc.contributor.author-dept | 獸醫學研究所 | zh_TW |
| 顯示於系所單位: | 獸醫學系 | |
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