Sr 2+  has low efficiency in regulating spontaneous release at the Calyx of Held synapses

CORC > 昆明动物研究所 > 昆明动物研究所 > 动物模型与人类重大疾病机理重点实验室

	Sr 2+ has low efficiency in regulating spontaneous release at the Calyx of Held synapses
	chenpeihua@ibp.ac.cn ; xthu@mail.kiz.ac.cn ; jysun@ibp.ac.cn ; Sun JY3; Shen XF 3; Wang XH 1; Chen PH3; Hu XT*2,4; Wang XF 3,5; Zhang SL 2,3,4,5
刊名	Synapse
	2017
卷号	71 期号:X 页码:e21983
关键词	Strontium Calcium Sensor Single Calcium Channel Currents Spontaneous Release
英文摘要	It has been known that Ca2+ plays an essential role in mediating different modes of neurotransmitter release via different sensing mechanisms. Synaptotagmin 1, 2, 9 were found to act as the Ca2+ sensors for synchronous release and synaptotagmin 7 and Doc-2 were proposed as the Ca2+ sensors for asynchronous release. Comparatively, the Ca2+ sensor for spontaneous release remains a mystery. At the Calyx of Held synapse, the Ca2+ sensor for spontaneous release was found not identical to the sensor for synchronous release, synaptotagmin2. As Ca2+ sensors have different sensitivity to Sr2+ and Ca2+ and induce significantly different rate of vesicle release, Sr2+ is traditionally used as a tool to examine the intrinsic properties of different Ca2+ sensors. Here, we employed cell-attached patch recording and pre-/post-synaptic whole-cell recording at the Calyx of Held synapses of synaptotagmin2 knock-out mice to assay the Sr2+ and Ca2+ influx into the nerve terminal at resting potential and observed the effects of Ca2+ and Sr2+ on spontaneous neurotransmitter release. We found that the dwell time of single voltage gated Ca2+ channel opening increased around 3-fold for Sr2+ than Ca2+ with the channel conductance unchanged; the divalent cation sensing machinery in regulating spontaneous release has much lower sensitivity to Sr2+ than Ca2+ . Thus, our study reveals some of the intrinsic properties of Ca2+sensor(s) of spontaneous transmitter release and provided an insight into the underlying mechanisms.
语种	英语
资助机构	This work was supported by the National Science Foundation of China Grants 31571062 (P.C) and 31527802 (J.S), Youth Innovation Promotion Association CAS of China NO.2017130 (P.C), the National Basic Research Program of China 2013CB835100 (J.S), Science and Technology Program of Yunnan Province Grant 2013GA003 (J.S ; This work was supported by the National Science Foundation of China Grants 31571062 (P.C) and 31527802 (J.S), Youth Innovation Promotion Association CAS of China NO.2017130 (P.C), the National Basic Research Program of China 2013CB835100 (J.S), Science and Technology Program of Yunnan Province Grant 2013GA003 (J.S ; This work was supported by the National Science Foundation of China Grants 31571062 (P.C) and 31527802 (J.S), Youth Innovation Promotion Association CAS of China NO.2017130 (P.C), the National Basic Research Program of China 2013CB835100 (J.S), Science and Technology Program of Yunnan Province Grant 2013GA003 (J.S ; This work was supported by the National Science Foundation of China Grants 31571062 (P.C) and 31527802 (J.S), Youth Innovation Promotion Association CAS of China NO.2017130 (P.C), the National Basic Research Program of China 2013CB835100 (J.S), Science and Technology Program of Yunnan Province Grant 2013GA003 (J.S
内容类型	期刊论文
源URL	[http://159.226.149.26:8080/handle/152453/12036]
专题	昆明动物研究所_动物模型与人类重大疾病机理重点实验室昆明动物研究所_神经系统编码
通讯作者	chenpeihua@ibp.ac.cn; xthu@mail.kiz.ac.cn; jysun@ibp.ac.cn
作者单位	1.Department of General surgery, Xuan Wu Hospital, Capital Medical University, Beijing 100053, China 2.Key Laboratory of Animal Models and Human Disease Mechanisms of the Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Chinese Academy of Sciences, Kunming, Yunnan 650223, China 3.State Key Laboratory of Brain and Cognitive Sciences, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China 4.Kunming College of Life Science, University of Chinese Academy of Sciences, Kunming 650204,China 5.University of Chinese Academy of Sciences, Beijing 100049, Chi
推荐引用方式 GB/T 7714	chenpeihua@ibp.ac.cn,xthu@mail.kiz.ac.cn,jysun@ibp.ac.cn,et al. Sr 2+ has low efficiency in regulating spontaneous release at the Calyx of Held synapses[J]. Synapse,2017,71(X):e21983.
APA	chenpeihua@ibp.ac.cn.,xthu@mail.kiz.ac.cn.,jysun@ibp.ac.cn.,Sun JY*.,Shen XF.,...&Zhang SL.(2017).Sr 2+ has low efficiency in regulating spontaneous release at the Calyx of Held synapses.Synapse,71(X),e21983.
MLA	chenpeihua@ibp.ac.cn,et al."Sr 2+ has low efficiency in regulating spontaneous release at the Calyx of Held synapses".Synapse 71.X(2017):e21983.