https://scholars.lib.ntu.edu.tw/handle/123456789/136152
標題: | 大鼠梨狀皮質之動作電位-時間差引導的突觸可塑特性研究(2/2) Spike-timing-dependent plasticity (STDP) at resting and conditioned lateral perforant path synapses on granule cells in the dentate gyrus: different roles of NMDA and group I metabotropic glutamate receptors. |
作者: | 閔明源 Min, Ming-Yuan |
關鍵字: | DHPG, Long-term Potentiation (LTP);Long-term depression (LTD);Hippocampus;Rats | 公開日期: | 2005 | 出版社: | 臺北市:國立臺灣大學生命科學系 | 摘要: | 本研究中, 我們檢視在大鼠鋸齒腦迴之lateral perforant pathway (LPP)神經路徑與顆粒細胞間 突觸其『電位-時間差引導的突觸可塑特性(Spike-timing-dependent plasticity; STDP)』機制. 我們使用 海馬迴腦薄片為材料, 並放置兩隻刺激電極於齒腦迴之分子層之外1/3 處與顆粒細胞層下緣, 以 分別誘發field EPSPs (fEPSPs) 與antidromic field somatic spikes (afSSs). 藉由連續的fEPSPsafSSs 的配對刺激, 我們可以成功的在LPP 突觸引”發長期增益(long-term potentiation; LTP)”. 倒轉fEPSPs- afSSs 配對刺激的時間次序, 則導致”長期抑制(long-term depression; LTD)”. 投與 NMDA 受器的抑制劑-AP5 能阻斷LTP/ LTD 的引發, 此外抑制calcium-calmodulin kinase II, PKC, 或mitogen-activated / extracellular-signal regulated kinase, 等酵素的活性, 也能阻斷LTP 的引發, 顯示這些酵素訊息系統有參與LTP 誘發的分子機制. 另一方面, 抑制PKC 與 protein phosphatase 2B, 則能阻斷LTP/ LTD 引發. 在經以高頻率刺激以誘發LTP 或以低高頻率刺激以誘發LTD 等經制約後的LPP 突觸, 配對 fEPSP-afSS 無法對經過”增益性制約”後的突觸有任何影響; 而配對afSS-fEPSP 刺激, 則無法對 經過”抑制性制約”後的突觸有任何影響. 然而在經過”抑制性制約”後的突觸施以配對fEPSP-afSS 刺激, 則能反轉”抑制性制約”; 而同樣地, 在經過”增益性制約後”的突觸以配對afSS -fEPSP 刺 激, 則能反轉”增益性制約”. 此種”增益性制約”或”抑制性制約”的反轉與NMDA 受器的活化 無關, 但能被group I metabotropic glutamate receptor (mGluR)的抑制劑MPEP 所阻斷, 顯示此 反轉效應與活化group I mGluR 有關. 綜合本研究結果我們結論: STDP 可同時在休止狀態與 制約後狀態下的LPP 突觸引發, 並且期引發過程中在休止狀態突觸須有NMDA 受器的參與, 而 在制約後狀態下的LPP 突觸則須group I mGluR 受器的參與. We examined the mechanisms underlying STDP induction at resting and conditioned lateral perforant pathway (LPP) synapses in the rat dentate gyrus. Two stimulating electrodes were placed in the outer third of the molecular layer and the granule cells layer to evoke, respectively, field EPSPs (fEPSPs) and antidromic field somatic spikes (afSSs) in hippocampal slices. LTP of LPP synapses was induced by paired stimulation with fEPSP preceding afSS. Reversal of the temporal order of fEPSP and afSS stimulation resulted in LTD. Induction of LTP/LTD was blocked by AP5, showing that both effects are NMDA receptor (NMDA-R)-dependent. Induction of LTP was also blocked by inhibitors of calcium-calmodulin kinase II, PKC, or mitogen-activated / extracellular-signal regulated kinase, suggesting these are downstream effectors after NMDA-R activation, while induction of LTD was blocked by inhibitors of PKC and protein phosphatase 2B. At LPP synapses previously potentiated or depressed by, respectively, high-frequency or low-frequency stimulation, paired fEPSP-afSS stimulation resulted in “de-depression” at depressed LPP synapses, but had no effect on potentiated synapses, while reversing the temporal order of fEPSP-afSS stimulation resulted in “de-potentiation” at potentiated synapses, but had no effect on depressed synapses. Induction of de-depression and de-potentiation was unaffected by AP5, but was blocked by MPEP, a group I metabotropic glutamate receptor (mGluR) blocker, showing that the both are NMDA-R-independent, but group I mGR-dependent. In conclusion, our results show that STDP can occur at both resting and conditioned LPP synapses, its induction in the former case being NMDA-R-dependent and, in the latter, group I mGluR-dependent. |
URI: | http://ntur.lib.ntu.edu.tw//handle/246246/10295 | 其他識別: | 932320B002136 | Rights: | 國立臺灣大學生命科學系 |
顯示於: | 生命科學系 |
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