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突触后内源性大麻素的释放对纹状体的长期抑制至关重要。

Postsynaptic endocannabinoid release is critical to long-term depression in the striatum.

作者信息

Gerdeman G L, Ronesi J, Lovinger D M

机构信息

Department of Molecular Physiology & Biophysics, Vanderbilt University, Nashville, Tennessee 37232-0615, USA.

出版信息

Nat Neurosci. 2002 May;5(5):446-51. doi: 10.1038/nn832.

DOI:10.1038/nn832
PMID:11976704
Abstract

The striatum functions critically in movement control and habit formation. The development and function of cortical input to the striatum are thought to be regulated by activity-dependent plasticity of corticostriatal glutamatergic synapses. Here we show that the induction of a form of striatal synaptic plasticity, long-term depression (LTD), is dependent on activation of the CB1 cannabinoid receptor. LTD was facilitated by blocking cellular endocannabinoid uptake, and postsynaptic loading of anandamide (AEA) produced presynaptic depression. The endocannabinoid necessary for striatal LTD is thus likely to be released postsynaptically as a retrograde messenger. These findings demonstrate a new role for endocannabinoids in the induction of long-term synaptic plasticity in a circuit necessary for habit formation and motor control.

摘要

纹状体在运动控制和习惯形成中起着关键作用。纹状体皮质输入的发育和功能被认为受皮质纹状体谷氨酸能突触的活动依赖性可塑性调节。在这里,我们表明,一种纹状体突触可塑性形式——长时程抑制(LTD)的诱导依赖于CB1大麻素受体的激活。通过阻断细胞内源性大麻素摄取可促进LTD,并且花生四烯酸乙醇胺(AEA)的突触后加载会产生突触前抑制。因此,纹状体LTD所需的内源性大麻素可能作为逆行信使从突触后释放。这些发现证明了内源性大麻素在习惯形成和运动控制所需回路中长时程突触可塑性诱导中的新作用。

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