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本文引用的文献

1
Endocannabinoid signaling controls pyramidal cell specification and long-range axon patterning.内源性大麻素信号传导控制锥体神经元的分化和长距离轴突模式形成。
Proc Natl Acad Sci U S A. 2008 Jun 24;105(25):8760-5. doi: 10.1073/pnas.0803545105. Epub 2008 Jun 18.
2
A diacylglycerol lipase-CB2 cannabinoid pathway regulates adult subventricular zone neurogenesis in an age-dependent manner.二酰基甘油脂肪酶-CB2大麻素途径以年龄依赖性方式调节成年脑室下区神经发生。
Mol Cell Neurosci. 2008 Aug;38(4):526-36. doi: 10.1016/j.mcn.2008.05.001. Epub 2008 May 15.
3
Design logic of a cannabinoid receptor signaling network that triggers neurite outgrowth.触发神经突生长的大麻素受体信号网络的设计逻辑。
Science. 2008 May 16;320(5878):903-9. doi: 10.1126/science.1152662.
4
Integrin clustering enables anandamide-induced Ca2+ signaling in endothelial cells via GPR55 by protection against CB1-receptor-triggered repression.整合素聚集通过保护内皮细胞免受CB1受体触发的抑制作用,从而使内皮细胞中通过GPR55实现花生四烯酸乙醇胺诱导的Ca2+信号传导。
J Cell Sci. 2008 May 15;121(Pt 10):1704-1717. doi: 10.1242/jcs.020958. Epub 2008 Apr 29.
5
Brain-derived neurotrophic factor-mediated retrograde signaling required for the induction of long-term potentiation at inhibitory synapses of visual cortical pyramidal neurons.脑源性神经营养因子介导的逆行信号传导是视觉皮层锥体神经元抑制性突触处长期增强诱导所必需的。
Neurosci Res. 2008 Jun;61(2):192-200. doi: 10.1016/j.neures.2008.02.006. Epub 2008 Mar 2.
6
The endocannabinoid receptor, CB1, is required for normal axonal growth and fasciculation.内源性大麻素受体CB1是正常轴突生长和束状化所必需的。
Mol Cell Neurosci. 2008 May;38(1):89-97. doi: 10.1016/j.mcn.2008.02.001. Epub 2008 Mar 10.
7
GPR55 is a cannabinoid receptor that increases intracellular calcium and inhibits M current.GPR55是一种大麻素受体,可增加细胞内钙并抑制M电流。
Proc Natl Acad Sci U S A. 2008 Feb 19;105(7):2699-704. doi: 10.1073/pnas.0711278105. Epub 2008 Feb 8.
8
Anandamide biosynthesis catalyzed by the phosphodiesterase GDE1 and detection of glycerophospho-N-acyl ethanolamine precursors in mouse brain.磷酸二酯酶GDE1催化的花生四烯乙醇胺生物合成及小鼠脑中甘油磷酸-N-酰基乙醇胺前体的检测。
J Biol Chem. 2008 Apr 4;283(14):9341-9. doi: 10.1074/jbc.M707807200. Epub 2008 Jan 27.
9
Anandamide inhibits metabolism and physiological actions of 2-arachidonoylglycerol in the striatum.花生四烯乙醇胺抑制纹状体内2-花生四烯酸甘油的代谢及生理作用。
Nat Neurosci. 2008 Feb;11(2):152-9. doi: 10.1038/nn2042. Epub 2008 Jan 20.
10
The orphan receptor GPR55 is a novel cannabinoid receptor.孤儿受体GPR55是一种新型大麻素受体。
Br J Pharmacol. 2007 Dec;152(7):1092-101. doi: 10.1038/sj.bjp.0707460. Epub 2007 Sep 17.

神经网络的连接与激活:内源性大麻素成为焦点。

Wiring and firing neuronal networks: endocannabinoids take center stage.

作者信息

Harkany Tibor, Mackie Ken, Doherty Patrick

机构信息

Division of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Scheeles väg 1 :A1, Karolinska Institute, SE-17177 Stockholm, Sweden.

出版信息

Curr Opin Neurobiol. 2008 Jun;18(3):338-45. doi: 10.1016/j.conb.2008.08.007.

DOI:10.1016/j.conb.2008.08.007
PMID:18801434
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3928023/
Abstract

Endocannabinoids (eCBs) function as retrograde messengers at both excitatory and inhibitory synapses, and control various forms of synaptic plasticity in the adult brain. The molecular machinery required for specific eCB functions during synaptic plasticity is well established. However, eCB signaling plays surprisingly fundamental roles in controlling the acquisition of neuronal identity during CNS development. Recent work suggests that selective recruitment of regulatory signaling networks to CB1 cannabinoid receptors dictates neuronal state-change decisions. In addition, the spatial localization and temporal precision of eCB actions emerges as a novel organizer in developing neuronal networks. Current challenges include fitting novel molecular candidates into regulatory eCB signaling pathways, and defining the temporal dynamics of context-dependent signaling mechanisms underpinning particular neuronal specification events.

摘要

内源性大麻素(eCBs)在兴奋性和抑制性突触中均作为逆行信使发挥作用,并控制成人大脑中各种形式的突触可塑性。突触可塑性过程中特定eCB功能所需的分子机制已得到充分确立。然而,eCB信号传导在中枢神经系统发育过程中控制神经元特性的获得方面发挥着令人惊讶的重要作用。最近的研究表明,将调节信号网络选择性招募到CB1大麻素受体决定了神经元状态改变的决策。此外,eCB作用的空间定位和时间精度成为发育中神经网络的一种新型组织者。当前的挑战包括将新的分子候选物纳入调节性eCB信号通路,以及确定支持特定神经元特化事件的上下文依赖性信号机制的时间动态。