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首页> 外文期刊>Neuron >The endocannabinoid 2-arachidonoylglycerol produced by diacylglycerol lipase alpha mediates retrograde suppression of synaptic transmission.
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The endocannabinoid 2-arachidonoylglycerol produced by diacylglycerol lipase alpha mediates retrograde suppression of synaptic transmission.

机译：由二酰基甘油脂肪酶α产生的内源性大麻素2-花生四烯酰基甘油介导突触传递的逆行抑制。

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摘要

Endocannabinoids are released from postsynaptic neurons and cause retrograde suppression of synaptic transmission. Anandamide and 2-arachidonoylglycerol (2-AG) are regarded as two major endocannabinoids. To determine to what extent 2-AG contributes to retrograde signaling, we generated and analyzed mutant mice lacking either of the two 2-AG synthesizing enzymes diacylglycerol lipase alpha (DGLalpha) and beta (DGLbeta). We found that endocannabinoid-mediated retrograde synaptic suppression was totally absent in the cerebellum, hippocampus, and striatum of DGLalpha knockout mice, whereas the retrograde suppression was intact in DGLbeta knockout brains. The basal 2-AG content was markedly reduced and stimulus-induced elevation of 2-AG was absent in DGLalpha knockout brains, whereas the 2-AG content was normal in DGLbeta knockout brains. Morphology of the brain and expression of molecules required for 2-AG production other than DGLs were normal in the two knockout mice. We conclude that 2-AG produced by DGLalpha, but not by DGLbeta, mediates retrograde suppression at central synapses.
机译：内源性大麻素从突触后神经元释放，并导致突触传递的逆行抑制。 Anandamide和2-arachidonoylglycerol（2-AG）被认为是两个主要的内源性大麻素。为了确定2-AG在何种程度上有助于逆行信号传导，我们生成并分析了缺少两种2-AG合成酶二酰基甘油脂肪酶α（DGLalpha）和β（DGLbeta）的突变小鼠。我们发现在DGLalpha敲除小鼠的小脑，海马和纹状体中完全没有内源性大麻素介导的逆行突触抑制，而在DGLbeta敲除大脑中则完全没有逆行抑制。在DGLalpha基因敲除的大脑中，基础2-AG含量显着降低，并且没有刺激引起的2-AG升高，而在DGLbeta基因敲除的大脑中，2-AG含量正常。在两只基因敲除小鼠中，大脑形态和DGLs以外产生2-AG所需的分子表达正常。我们得出结论，由DGLalpha而非DGLbeta产生的2-AG介导中枢突触的逆行抑制。

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