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| ???org.dspace.app.webui.jsptag.ItemTag.dcfield??? | Value | Language |
|---|---|---|
| dc.contributor.advisor | 王致恬 | |
| dc.contributor.author | Ching-Yuan Yang | en |
| dc.contributor.author | 楊清媛 | zh_TW |
| dc.date.accessioned | 2021-05-19T17:52:27Z | - |
| dc.date.available | 2022-07-28 | |
| dc.date.available | 2021-05-19T17:52:27Z | - |
| dc.date.copyright | 2017-07-28 | |
| dc.date.issued | 2017 | |
| dc.date.submitted | 2017-07-27 | |
| dc.identifier.citation | Ackman, J.B., Burbridge, T.J., and Crair, M.C. (2012). Retinal waves coordinate patterned activity throughout the developing visual system. Nature 490, 219-225.
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/7755 | - |
| dc.description.abstract | 視網膜波對於正確的視覺網路發育很重要，第二期視網膜波發生在新生大鼠第一天到第九天，其產生機制是由一群突觸前神經元－星狀無軸突細胞，週期性的釋放神經傳導物質例如：乙醯膽鹼和 γ-氨基丁酸至突觸後神經元－視網膜節細胞。先前的研究發現，突觸後視網膜節細胞可能分泌反向訊息到突觸前星狀無軸突細胞，進而影響視網膜波的頻率。而利用麩胺酸受體拮抗劑藥物，我們發現這個反向的調控訊號可能是視網膜節細胞釋放的麩胺酸。於是我們提出假設，麩胺酸可能從視網膜節細胞釋放，以逆行或自分泌的方式在視網膜內傳遞。為了確定麩胺酸在發育中視網膜的存在，我們使用免疫螢光染色以及細胞型態的麩胺酸光學感測器，發現麩胺酸存在於視網膜節細胞，並且大量釋放於視網膜內。為了確認視網膜波會調控麩胺酸的釋放，以及麩胺酸傳導的的方向，我們建立了麩胺酸的光學感測器技術，加以特異表達在視網膜節細胞或是星狀無軸突細胞。在視網膜節細胞或是星狀無軸突細胞中，麩胺酸的光學感測器的螢光強度皆會因為視網膜波的頻率增加而增強；代表第二期視網膜波會調控麩胺酸的釋放，並且麩胺酸的釋放會透過逆行以及自分泌的方式在視網膜內傳遞。接著，為了確認麩胺酸的傳遞對於第二期視網膜波的影響，我們在鈣離子顯像技術技術中使用不同的藥物。先前研究指出，一種腺苷酸受器促進劑會增加星狀無軸突細胞的胞吐作用，進而增加視網膜波的頻率。然而，此腺苷酸受器的促進劑所造成的視網膜波頻率的增加會被麩胺酸受體拮抗劑所抑制，說明了麩胺酸的傳導作用是星狀無軸突細胞胞吐作用的下游反應。此外，Synaptotagmin I被認為在鈣離子調控的胞吐作用中擔任鈣離子感應者的角色，先前研究指出將Synaptotagmin I鈣離子感應能力降低的突變株專一性大量表現在視網膜節細胞中，與控制組及Synaptotagmin I組別相比，會使視網膜波產生的頻率顯著下降。但是我們發現當周圍麩胺酸濃度為5 nM時，會使此突變株大量表現在視網膜節細胞中所造成的視網膜波頻率下降的現象消失，並且其視網膜波頻率增加後與控制組及Synaptotagmin I組別沒有顯著差異。綜合以上結果，我們提出在大鼠發育時期，第二期視網膜波與麩胺酸的釋放之間彼此存在著交互作用。第二期視網膜波的頻率被5 nM的麩胺酸所調控，且麩胺酸訊息會透過自分泌的方式被視網膜節細胞接收，或是逆行分泌的方式被星狀無軸突細胞接收，進而調控第二期視網膜波的時空特性。 | zh_TW |
| dc.description.abstract | Retinal waves are important for visual circuit development. During the first postnatal week in rats (P0-P9), stage II retinal waves are initiated by presynaptic starburst amacrine cells (SACs) releasing neurotransmitters to neighboring SACs and retinal ganglion cells (RGCs). Surprisingly, we previously found that postsynaptic RGCs may send a “retrograde” signal to presynaptic SACs, thus regulating wave frequency. Since the ionotropic glutamate receptor (iGluR) antagonists can significantly reduce the RGC-mediated increase in wave frequency, we thus hypothesized that glutamate signal from RGCs may function in a retrograde or autocrine manner. To determine the presence of glutamate in developing retina, we first performed immunofluorescence staining for the neurotransmitter glutamate and cell-based glutamate optical sensor. We found that glutamate was present in RGCs and volume released throughout the entire retina. To determine whether stage II retinal waves modulate glutamate transmission that may act in an autocrine or retrograde manner, we established the glutamate sensor specifically expressed in RGCs or SACs. The fluorescence intensity of both RGC-expressing and SAC-expressing glutamate sensors was significantly increased by enhancing wave frequency. The results suggest that the glutamate release is up-regulated by enhancing stage II waves, and the glutamate may transmit in an autocrine manner and a retrograde manner. To further determine the role of glutamate transmission in modulating stage II retinal waves, we applied various pharmacological reagents during Ca2+ imaging of retinal waves. The selective A2AR agonist (CGS) was previously found to increase the SAC exocytosis, thus increasing wave frequency. By contrast, the CGS-mediated increase in wave frequency was abolished by the iGluR antagonists, suggesting that glutamate transmission was downstream of the presynaptic effects on retinal waves. Moreover,
Synaptotagmin I (Syt I), a Ca2+ sensor protein, can regulate retinal waves via Ca2+ binding to its Ca2+-binding domains. Overexpressing the weakened Ca2+ -binding mutant of Syt I, Syt I-D230S (Syt I-C2A*), in RGCs decreased wave frequency compared to Ctrl and Syt I. Bath-applying the ambient glutamate (5 nM) occludes the Syt I-C2A*-decreased effects on wave frequency via RGCs. Taken together, we conclude that the interaction exists between stage II retinal waves and RGCs-releasing glutamate in developing rat retinas. The frequency of stage II retinal waves can be modulated by 5 nM glutamate during the stage II period, and glutamate may serve as an autocrine signal to RGCs and a retrograde signal to SACs, further regulating spatiotemporal properties of stage II retinal waves. | en |
| dc.description.provenance | Made available in DSpace on 2021-05-19T17:52:27Z (GMT). No. of bitstreams: 1 ntu-106-R04b43003-1.pdf: 29372441 bytes, checksum: ccd6a62a7e7f130ab09e81e2752d3770 (MD5) Previous issue date: 2017 | en |
| dc.description.tableofcontents | 國立臺灣大學碩士學位論文口試委員會審定書 I
致謝 II 中文摘要 IV ABSTRACT VI ABBREVIATIONS VIII CHAPTER I 1 Introduction 1 1.1 Patterned spontaneous activity in the developing neural circuits 1 1.2 The visual system 2 1.3 Patterned spontaneous activity during retinal development 4 1.4 Stage II retinal waves 5 1.5 Ca2+-dependent exocytosis in presynaptic neurons 6 1.6 Stage II Retinal waves are mediated by exocytotic proteins 8 1.7 The retrograde signaling in the developing retina 9 1.8 Glutamate sensor－The intensity-based glutamate-sensing fluorescent reporter 11 1.9 Objectives of the study 12 CHAPTER II 15 Materials and Methods 15 2.1 Plasmid information 15 2.2 Animals 16 2.3 Retinal dissection and retinal explant culture 16 2.4 Exo vivo transfection 17 2.5 Immunofluorescence staining 18 2.6 Live Ca2+ imaging and data analysis 20 2.7 Live glutamate imaging and data analysis 23 2.8 Cell culture and transfection 24 2.9 Pharmacology 25 2.10 Statistical analysis 26 CHAPTER III 27 Results 27 3.1 Glutamate was present in developing RGCs and distributed diffusely throughout the entire retinas 27 3.2 The cell-based optical sensor detected glutamate volume release from GCL 28 3.3 The CMV promoter can target the glutamate sensor expression to RGCs, while the mGluR2 promoter can target gene expression specifically to SACs 30 3.4 The glutamate sensor in RGCs received the released glutamate in an autocrine manner 31 3.5 The glutamate sensor in SACs detected glutamate release from RGCs in a retrograde manner 33 3.6 The glutamate sensor in retinas overexpressing Syt I and its mutant detected glutamate release during live glutamate imaging 34 3.7 Glutamate transmission was acting downstream of SAC release 35 3.8 Bath application of 5 nM glutamate occludes the effect of SyT I-mediated RGC’s exocytosis on wave frequency 38 CHAPTER IV 41 Discussion 41 4.1 Glutamate transmission from RGCs in stage II retinal waves 42 4.2 The volume release of glutamate in neonatal rat retinas 43 4.3 The autocrine signal and retrograde signal from RGCs during stage II waves 44 4.4 The ambient glutamate concentration during stage II retinal waves 45 4.5 The pharmacological treatment during imaging 46 4.6 The future work of enzyme based microelectrode array 47 References 49 Figure 1. The structure of the retina. 53 Figure 2. The spatial properties of retinal waves and the mechanisms of initiation. 54 Figure 3. SNARE complex and the characterization of Synaptotagmin I. 56 Figure 4. Ca2+ transient frequency is increased by overexpressing Syt I in RGCs, and the iGluR antagonists can abolish the Syt I-mediated increase in wave frequency via RGCs. 59 Figure 5. The Working hypothesis: Glutamate signal from RGCs may function in a retrograde or autocrine manner. 61 Figure 6. Glutamate sensor characterization and glutamate imaging. 62 Figure 7. The acquisition and data analysis for the fluorescence intensity changes of the glutamate sensor. 65 Figure 8. Localization of L-Glutamate in the retinal cross-sections of the developing rat retinas. 67 Figure 9. The cell-based optical sensor can detect glutamate volume release. 68 Figure 10. The CMV promoter drives the glutamate sensor expressed mostly in RGCs, while the mGluR2 promoter expresses the sensor specifically in SACs. 70 Figure 11. Glutamate can be detected in RGCs by enhancing wave frequency. 72 Figure 14. Glutamate can be detected in SACs by enhancing the wave frequency. 74 Figure 13. The glutamate sensor in RGCs can detect glutamate release during CGS application. 75 Figure 14. The glutamate sensor in SACs can detect glutamate release during CGS application. 77 Figure 15. The frequency and amplitude of spontaneous Ca2+ transients are increased during application of CGS. 79 Figure 16. The frequency of spontaneous Ca2+ transients is decreased during application of iGluR antagonists. 81 Figure 17. The CGS-mediated increase of wave frequency was abolished by iGluR antagonists. 84 Figure 18. The wave duration and amplitude were not changed during pharmacological treatments. 85 Figure 19. The spike time tiling coefficient (STTC) was not altered during pharmacological treatments. 87 Figure 20. Application of 5 µM glutamate during Ca2+ imaging. 88 Figure 21. Application of 5 nM glutamate increases the wave frequency in the Syt I-C2A*-expressing retinas. 90 Figure 22. The ambient glutamate (5 nM) occludes the decreased effects of Syt I-C2A* in RGCs on wave frequency. 91 Figure 23. Scheme of stage II retinal waves modulated by glutamate transmission. 92 Supporting Information 93 Figure S1. The 10 mM KCl application increased wave amplitude. 94 Figure S2. Bath application of 100 µM and 10 µM glutamate during Ca2+ imaging. 96 Appendix 97 Appendix 1. The 2016 annual meeting of the Society for Neuroscience 98 Appendix 2. 2017 Institute of Molecular and Cellular Biology Poster Contest 102 | |
| dc.language.iso | en | |
| dc.title | 發育大鼠的視網膜中第二期視網膜波與麩胺酸釋放的交互影響 | zh_TW |
| dc.title | Interaction between Stage II Retinal Waves and Glutamate Release in Developing Rat Retinas | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 105-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 徐立中,陳示國,焦傳金,盧主欽 | |
| dc.subject.keyword | 視網膜波,星狀無軸突細胞,視網膜節細胞,麩胺酸傳遞,Synaptotagmin I, | zh_TW |
| dc.subject.keyword | retinal waves,starburst amacrine cells,retinal ganglion cells,glutamate transmission,Synaptotagmin I, | en |
| dc.relation.page | 103 | |
| dc.identifier.doi | 10.6342/NTU201702122 | |
| dc.rights.note | 同意授權(全球公開) | |
| dc.date.accepted | 2017-07-27 | |
| dc.contributor.author-college | 生命科學院 | zh_TW |
| dc.contributor.author-dept | 分子與細胞生物學研究所 | zh_TW |
| Appears in Collections: | 分子與細胞生物學研究所 | |
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