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首页> 外文期刊>Neuron >Endocannabinoids control the induction of cerebellar LTD.
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Endocannabinoids control the induction of cerebellar LTD.

机译：内源性大麻素控制小脑LTD的诱导。

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摘要

The long-term depression (LTD) of parallel fiber (PF) synapses onto Purkinje cells plays a central role in motor learning. Endocannabinoid release and LTD induction both depend upon activation of the metabotropic glutamate receptor mGluR1, require postsynaptic calcium increases, are synapse specific, and have a similar dependence on the associative activation of PF and climbing fiber synapses. These similarities suggest that endocannabinoid release could account for many features of cerebellar LTD. Here we show that LTD induction is blocked by a cannabinoid receptor (CB1R) antagonist, by inhibiting the synthesis of the endocannabinoid 2-arachidonyl glycerol (2-AG), and is absent in mice lacking the CB1R. Although CB1Rs are prominently expressed presynaptically at PF synapses, LTD is expressed postsynaptically. In contrast, a previously described transient form of inhibition mediated by endocannabinoids is expressed presynaptically. This indicates that Purkinje cells release 2-AG that activates CB1Rs toboth transiently inhibit release and induce a postsynaptic form of LTD.
机译：平行纤维（PF）突触到浦肯野细胞上的长期抑制（LTD）在运动学习中起着核心作用。内源性大麻素的释放和LTD的诱导均取决于促代谢型谷氨酸受体mGluR1的激活，需要突触后钙的增加，突触特异，并且对PF和攀爬纤维突触的相关激活具有类似的依赖性。这些相似性表明，内源性大麻素释放可能解释了小脑LTD的许多特征。在这里，我们显示LTD诱导被大麻素受体（CB1R）拮抗剂阻断，通过抑制内源性大麻素2-花生四烯酸甘油酯（2-AG）的合成而在缺乏CB1R的小鼠中不存在。尽管CB1Rs在PF突触前突触突出表达，LTD在突触后表达。相反，先前描述的由内源性大麻素介导的抑制的瞬时形式被突触地表达。这表明浦肯野细胞释放能激活CB1Rs的2-AG，从而瞬时抑制释放并诱导突触后形式的LTD。

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