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請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/9003
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dc.contributor.advisor閔明源(MIN-YUAN MIN)
dc.contributor.authorHui Chenen
dc.contributor.author陳慧zh_TW
dc.date.accessioned2021-05-20T20:06:17Z-
dc.date.available2011-08-22
dc.date.available2021-05-20T20:06:17Z-
dc.date.copyright2011-08-22
dc.date.issued2011
dc.date.submitted2011-08-15
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dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/9003-
dc.description.abstract杏仁體中央被核(CeAC)可接收經由杏仁體-旁臂核(PBA)路徑傳遞,來自腦幹及脊髓的痛覺訊息,同時也接收直接由脊髓投射上來的痛覺訊息,此核區被稱為「痛覺杏仁核」已將近十年,先前研究指出佛波醇12,13-乙酸酯(PDA)可顯著促進旁臂核到CeAC的神經傳導作用,且與細胞內部的胞外訊息傳遞激脢(ERK)有關,本研究使用全細胞紀錄電生理紀錄以及藥理方式探討ERK在調節CeAC神經細胞興奮性上所扮演的角色,給予短期PDA(蛋白激脢C之活化劑)可提高動作電位發生的頻率,然而給予長期PDA卻會降低其頻率;另外短期PDA也會增加Ih-current,但長期PDA則減緩其強度,此外,給予長期PDA也會延遲動作電位發生的時間,在給予蛋白激脢C(PKC)抑制劑-Chelerythrine與GF109203X之後,短期與長期的PDA反應都不復出現,給予U0126不會影響短期PDA帶來的反應,卻逆轉了長期PDA先前的反應情形,實驗結果顯示:(1)給予PDA會經由PKC—ERK路徑作用,在不同的時間條件下,調節CeAC的神經興奮性;(2)活化ERK加劇動作電位延遲發生的情形(A型鉀離子通道)。zh_TW
dc.description.abstractThe capsular central amygdaloid (CeAC) nucleus acquires nociceptive specific information from the brainstem and spinal cord via the parabrachio-amygdaloid (PBA) pain pathway as well as via direct projections from the spinal cord. It has been termed as “nociceptive amygdala” for almost a decade. Previous study indicated that application of phorbol 12,13-diacetate (PDA) caused marked enhancement of synaptic transmission of parabrachial input onto CeAC nucleus and the elevation of intracellular ERK was involved. In the present study, using patch-clamp technique and pharmacological methods, the role of ERK in regulating neuronal excitability of CeAC was examined. Short-term application of the PKC activator, PDA increased the number of action potentials whereas the long-term application decreased the spike number. Beside, short-term PDA enhanced the size of Ih current but long-term PDA downsized it. In the meanwhile, long-term application of PDA also increased the first spike latency. Protein Kinase C (PKC) inhibitors, Chelerythrine and GF109203X abolished the effect of PDA in both time-scales. Application of U0126 had no effect on short-term PDA however it reversed the effect caused by long term PDA application. The result suggested that (1) PKC—ERK pathway induced by PDA regulated input-output function of neuronal excitability of CeAC in different time-scales; (2) ERK activation enhanced the delay onset of action potential (stongly related to A-type potassium channel).en
dc.description.provenanceMade available in DSpace on 2021-05-20T20:06:17Z (GMT). No. of bitstreams: 1
ntu-100-R97b41036-1.pdf: 2389564 bytes, checksum: 65f03bb48742ce75335329308807f19b (MD5)
Previous issue date: 2011
en
dc.description.tableofcontentsContents
致謝……………………………………………………………………………………I
摘要………………………………………………….………………………………III
ABSTRACT……...…………………………………………………………………..IV
INTRDUCTION
Capsular central amygdaloid nucleus and Nociception………………………………1
Central sensitization…………………………………………………………………...3
Objectives……………………………………………………………………………...6
MATERIALS AND METHODS
Preparation of amygdala slices……………………………………………….……….8
Whole-cell Patch clamp recording…………………………………………………….9
Drug application……………………………………………………………………..10
Data and statistical analyses…………………………………………………………10
RESULTS
Identification of Capsular Central amygdaloid neuron………...……………………12
PDA modulates input-output function of neuronal excitability in different time scales…………………………………………………………………………………13
Effect of Chelerythrine –PDA on capsular central amygdaloid neuron……………..16
Effect of GF109203X –PDA on capsular central amygdaloid neuron……………….18
Effect of U0126–PDA on capsular central amygdaloid neuron……………………...19
DISCUSSION
PKC activation by PDA regulates the neuronal excitability in different time scale....21
ERK activation by PDA decreases neuronal excitability…………………………….23
REFERENCES……………………………………………………………………….27
FIGURES…………………………………………………………………………….35
dc.language.isoen
dc.titleERK在杏仁體中央被核神經元細胞興奮性角色探討zh_TW
dc.titleRole of extracellular signal-regulated kinase in neuronal excitability of capsular central amygdaloid neuronsen
dc.typeThesis
dc.date.schoolyear99-2
dc.description.degree碩士
dc.contributor.oralexamcommittee楊琇雯(XIU-WEN YANG),陳瑞芬(RUI-FEN CHEN)
dc.subject.keyword中樞神經敏感化,神經興奮性,杏仁體,杏仁體中央被核,胞外訊息調節激脢,鉀離子通道,佛波酯,蛋白激脢C,zh_TW
dc.subject.keywordcentral sensitization,neuronal excitability,amygdale,ERK,potassium channel,PDA,PKC,en
dc.relation.page64
dc.rights.note同意授權(全球公開)
dc.date.accepted2011-08-16
dc.contributor.author-college生命科學院zh_TW
dc.contributor.author-dept動物學研究所zh_TW
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