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| ???org.dspace.app.webui.jsptag.ItemTag.dcfield??? | Value | Language |
|---|---|---|
| dc.contributor.advisor | 李秀香(Hsiu-Hsiang Lee) | |
| dc.contributor.author | Ya-Chen Cheng | en |
| dc.contributor.author | 鄭雅貞 | zh_TW |
| dc.date.accessioned | 2021-06-15T16:21:53Z | - |
| dc.date.available | 2020-09-25 | |
| dc.date.copyright | 2015-09-25 | |
| dc.date.issued | 2015 | |
| dc.date.submitted | 2015-08-15 | |
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| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/52651 | - |
| dc.description.abstract | 在動物中，心臟不須經由意識即可自行跳動，且具備維持正常生理作用的重要功能。許多心臟疾病例如冠狀動脈心臟病或心房顫動等，其發生原因源自於心臟正常跳動的功能受損。另外，人類神經系統會調控心臟跳動速率變動的現象也是廣為人知，但目前此調控機制仍未相當清楚。藉由果蠅剛蛹化 0-1hr APF (After Puparium Formation)，其外皮仍呈半透明且身體已固定不動的特點，不經解剖即可直接觀察心跳。果蠅的心臟靠近背部呈長條管狀，因此稱為心管 (Cardiac Tube) 或背管 (Dorsal Vessel)。綜觀上述特點，果蠅非常適合提供我們用於研究神經種類對心跳速率 (Heart Rate, HR) 之間的調控關係。
為了解析神經系統對心臟跳動的影響，我們聚焦在果蠅剛蛹化APF 0-1hr時期，在25°C和29°C 兩種環境下心跳速率的變異程度。透過GAL4/UAS system將對溫度敏感的蛋白質 (shibirets , dTrpA1) 或對光敏感的離子通道 (ChR2, NpHR) 表現在特定神經種類中，藉此專一地增加或減少此類神經的活性。實驗結果發現利用GAL4/UAS system專一表現dTrpA1在果蠅剛蛹化0-1 hr APF的廣泛神經 (Pan-neuron) 中，會顯著提升心跳速率改變量 (∆HR)。另一方面使用dTrpA1突變型-shibirets (突變後對溫度敏感)，以GAL4/UAS system專一表現shibirets在果蠅剛蛹化APF 0-1hr的廣泛神經中降低其神經活性，會顯著減少心跳速率改變量。增加膽鹼性神經元 (Cholinergic Neurons) 活性對心跳速率改變量無顯著影響，但減少膽鹼性神經元活性明顯降低心跳速率改變量。然而不論降低或增加glutamatergic neurons活性，其心跳速率改變量均不受影響。另外我們也針對心跳規律度 (Heart Rhythm) 各種異常心跳速率，包含心跳弛緩 (Slower HR, Bradycardia)、心跳過速 (Faster HR, Tachycardia)、心跳停止 (Pause) 進行分析。發現降低廣泛神經活性會減少心跳過速但會提高心跳弛緩的個體數，但增加其活性心跳規律度不會受太大影響。減少膽鹼性神經元活性時，心跳過速現象顯著提升，增加此神經活性無任何不影響。減少glutamatergic neurons活性明顯提升pause現象，但增加此神經活性則無影響。 綜觀上述結果，推測在果蠅剛蛹化0-1hr APF時，廣泛神經中存在某類群的神經可調控心跳速率，其中膽鹼性神經元為主要負責維持正常心跳速率以及維持正常心跳規律度的角色，而glutamatergic neurons則能保持心臟持續跳動。 | zh_TW |
| dc.description.abstract | Cardiac automatism is critical for maintaining normal physiological function in animals. Several cardiac diseases, such as palpitations and atrial fibrillation, are caused by impairment of this process. Moreover, it has demonstrated that nervous system regulates cardiac automatism in human. However, the underlying mechanism of this regulation is unclear. The transparent surface of Drosophila at 0-1 hr APF (After Puparium Formation) makes it easy to directly examine the heart beating. The tubular-shaped dorsal vessel represents heart; therefore, it is plausible and suitable for us to identify how neurons regulate cardiac automatism.
To examine the influence of nervous system on heart beating, we focused on the heart rate difference between 25°C and 29°C in Drosophila at 0-1 hr APF. We took advantage of temperature-sensitive (shits, dTrpA1) or light-sensitive (ChR2, NpHR) genetic tools to acutely and specifically activate or inhibit target neurons in Drosophila by GAL4/UAS system. We found that activation of pan-neuron by dTrpA1 at 0-1 hr APF significantly accelerated the heart rate. On the contrary, inhibition of pan-neuron by shibire temperature-sensitive mutant slowed down the heart rate difference. Activating cholinergic neurons did not alter the heart rate difference, but inhibiting cholinergic neurons decreased the alteration of heart rate difference. However, activation or inhibition of glutamatergic neurons did not have effect on heart rate. Also, we focused on the heart rhythm. We found that when inhibiting pan-neuron enhaced the rate of slower HR and decreased the rate of faster HR. Otherwise, we found that when inhibiting cholinergic neurons caused abnormal heart rhythm, but activating cholinergic neurons did not alter heart rhythm. Moreover, inhibition of glutamatergic neurons decreased pause phenomenons, but activation of glutamatergic neurons did not work on heart rhythm. Together, these results suggested some neurons exist in pan-neuron may regulate heart beating rate. And cholinergic neurons may play role in regulating heart rate and regular heart rhythm in Drosophila at 0-1 hr APF. The function of glutamatergic neurons is to maintain the heart beat in Drosophila at 0-1 hr APF 0hr. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-15T16:21:53Z (GMT). No. of bitstreams: 1 ntu-104-R02448011-1.pdf: 2758736 bytes, checksum: b7fcc086a61f389c661a4172472e7338 (MD5) Previous issue date: 2015 | en |
| dc.description.tableofcontents | 口試委員會審定書 II
誌 謝 III 目 錄 V 摘要 IX Abstract X 第一章 簡介 1 第二章 材料與方法 6 2.1 果蠅品系、飼養及交配 6 2.2 心管位置解剖 6 2.3 性別分辨 7 2.4 心跳測量 7 2.4.1 用溫度改變方式 7 2.4.2 用光刺激方式 8 2.5心跳數據分析 8 2.6 TrpA1功能測試 9 2.7 mhc-GAL80對膽鹼性神經元分布位置影響之測試 9 第三章 研究結果 10 3.1 廣泛神經活性對心跳速率改變量之調控 10 3.1.1 降低廣泛神經活性減少心跳速率改變量 10 3.1.2 增加廣泛神經活性提升心跳速率改變量 10 3.1.3 劑量補償效應增強廣泛神經活性影響心跳速率改變量之效果 10 3.2 膽鹼性神經元對心跳速率改變量之調控 11 3.2.1 降低膽鹼性神經元活性減少心跳速率改變量 11 3.2.2 增加膽鹼性神經元活性不影響心跳速率改變量 11 3.2.3 排除TrpA1失活導致心跳速率改變量不受影響 12 3.2.4 排除GAL4滲漏到肌肉而影響心跳速率的可能性 12 3.3 Glutamatergic Neurons對心跳速率改變量之調控 13 3.3.1 降低Glutamatergic Neurons活性不影響心跳速率改變量 13 3.3.2 增加Glutamatergic Neurons活性不影響心跳速率改變量 13 3.4 降低廣泛神經活性對心跳規律度之調控 13 3.4.1降低廣泛神經活性降低Normal HR平均值 14 3.4.2降低廣泛神經活性顯著提升異常心跳速率所占時間比率 14 3.4.3降低廣泛神經活性減少Pause短長度次數但略增平均每次長度 15 3.4.4降低廣泛神經活性顯著地增加Slower HR各長度次數及平均每次長度 15 3.4.5降低廣泛神經活性降低Faster HR長時間長度次數但不影響平均每次長度 15 3.4.6降低廣泛神經活性減少Faster HR及提高Slower HR之個體數發生率 16 3.4.7 w*基因提升Slower HR之個體數發生率 16 3.5增加廣泛神經活性對心跳規律度之調控 16 3.5.1增加廣泛神經活性不改變各異常心跳速率平均值 16 3.5.2增加廣泛神經活性不影響各異常心跳速率所占時間比率 17 3.5.3增加廣泛神經活性不影響Pause各長度次數及平均每次長度 17 3.5.4增加廣泛神經活性不影響Slower HR各長度次數及平均每次長度 17 3.5.5增加廣泛神經活性不影響Faster HR各長度次數及平均每次長度 18 3.5.6增加廣泛神經活性不影響各異常心跳速率個體數機率 18 3.6降低膽鹼性神經元活性對心跳規律度之調控 18 3.6.1降低膽鹼性神經元活性降低Normal及Faster HR心跳速率平均值 19 3.6.2降低膽鹼性神經元活性不影響各異常心跳速率所占時間比率 19 3.6.3降低膽鹼性神經元活性不影響Pause各長度次數及平均每次長度 19 3.6.4降低膽鹼性神經元活性不影響Slower HR各長度次數及平均每次長度 19 3.6.5降低膽鹼性神經元活性提升Faster HR短長度次數但降低平均每次長度 19 3.6.6降低膽鹼性神經元活性降低Faster HR及Pause之個體數機率 20 3.7增加膽鹼性神經元活性對心跳規律度之調控 20 3.7.1增加膽鹼性神經元活性降低Normal HR心跳速率平均值 20 3.7.2增加膽鹼性神經元活性不影響各異常心跳速率所占時間比率 20 3.7.3增加膽鹼性神經元活性不影響Pause各長度次數及平均每次長度 21 3.7.4增加膽鹼性神經元活性不影響Slower HR各長度次數及平均每次長度 21 3.7.5增加膽鹼性神經元活性不影響Faster HR各長度次數及平均每次長度 21 3.7.6增加膽鹼性神經元活性不影響各異常心跳速率個體數機率 21 3.8降低Glutamatergic Neurons活性對心跳規律度之調控 21 3.8.1降低Glutamatergic Neurons活性降低Normal HR與提高Slower HR心跳速率平均值 22 3.8.2降低Glutamatergic Neurons活性降低Faster HR及提高Pause心跳速率所占時間比率 22 3.8.3降低Glutamatergic Neurons活性增加Pause短長度次數及平均每次長度 22 3.8.4降低Glutamatergic Neurons活性不影響Slower HR各長度次數及平均每次長度 23 3.8.5降低Glutamatergic Neurons活性不影響Faster HR各長度次數與平均每次長度 23 3.8.6降低Glutamatergic Neurons活性提升Slower HR及Pause之個體數機率 23 3.9增加Glutamatergic Neurons活性對心跳規律度之調控 23 3.9.1增加Glutamatergic Neurons活性不改變各異常心跳速率平均值 24 3.9.2增加Glutamatergic Neurons活性不影響各異常心跳速率所占時間比率 24 3.9.3增加Glutamatergic Neurons活性不影響Pause各長度次數及平均每次長度 24 3.9.4增加Glutamatergic Neurons活性不影響Slower HR各長度次數及平均每次長度 24 3.9.5增加Glutamatergic Neurons活性不影響Faster HR各長度次數及平均每次長度 25 3.9.6增加Glutamatergic Neurons活性不影響各異常心跳速率個體數機率 25 第四章 討論 26 4.1. 正常生理和病理之心跳變異程度需提高N值才能顯現差異 26 4.2. 廣泛神經和離體心臟節律點對心跳之調控差異 26 4.4. 高頻率的心跳暫停現象，暗示果蠅心管尚未進化完全 27 4.5. 神經與神經傳遞物質兩者對果蠅心跳速率改變量之影響具一致性 28 4.6. 增加或降低神經活性之方法 (optogenetics) 29 4.7. 心跳改變量更進階之分析 29 4.8. 果蠅神經和心跳關聯之研究可供日後深究 29 參考文獻 31 圖 38 表 118 附錄 124 | |
| dc.language.iso | zh-TW | |
| dc.subject | 果蠅 | zh_TW |
| dc.subject | 心管 | zh_TW |
| dc.subject | 神經系統 | zh_TW |
| dc.subject | 心跳速率 | zh_TW |
| dc.subject | 膽鹼性神經元 | zh_TW |
| dc.subject | Heart rate | en |
| dc.subject | Cardiac tube | en |
| dc.subject | Nervous system | en |
| dc.subject | Cholinergic neurons | en |
| dc.subject | Drosophila | en |
| dc.title | 探討果蠅神經系統對心管跳動速率之調控 | zh_TW |
| dc.title | Invastigating on the Regulation of Nervous System to Cardiac Tube Beating Rate in Drosophila | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 103-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.coadvisor | 何奕倫(Yi-Lwun Ho),吳君泰(June-Tai Wu) | |
| dc.subject.keyword | 果蠅,心管,神經系統,心跳速率,膽鹼性神經元, | zh_TW |
| dc.subject.keyword | Drosophila,Cardiac tube,Nervous system,Heart rate,Cholinergic neurons, | en |
| dc.relation.page | 125 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2015-08-17 | |
| dc.contributor.author-college | 醫學院 | zh_TW |
| dc.contributor.author-dept | 分子醫學研究所 | zh_TW |
| Appears in Collections: | 分子醫學研究所 | |
Files in This Item:
| File | Size | Format | |
|---|---|---|---|
| ntu-104-1.pdf Restricted Access | 2.69 MB | Adobe PDF |
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