Endocannabinoid-mediated metaplasticity in the hippocampus
Endocannabinoid-mediated metaplasticity in the hippocampus
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DOI：
10.1016/j.neuron.2004.08.036
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发表时间：
2004-09-16
期刊：
影响因子：
16.2
通讯作者：
Castillo, PE
中科院分区：
文献类型：
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作者：
Chevaleyre, V;Castillo, PE
在海马中的兴奋性突触处通常诱导长时程增强（LTP）的大麻能纤维的重复激活也通过逆行内源性大麻素信号传导在抑制性突触（I-LTD）处触发长时程抑制。然而，鲜为人知的是，关于I-LTD.here的生理意义，我们表明，突触驱动的内源性大麻素释放是一个高度本地化和有效的过程，强烈抑制大麻素敏感的抑制性输入内的树突状隔室的CA 1锥体细胞。通过去除树突树的受限区域中的突触抑制，内源性大麻素选择性地“引发”附近的兴奋性突触，从而促进随后的LTP诱导。这种局部后可塑性的诱导是一种新的机制，内源性大麻素可以通过这种机制促进大脑中信息的储存。
Repetitive activation of glutamatergic fibers that normally induces long-term potentiation (LTP) at excitatory synapses in the hippocampus also triggers long-term depression at inhibitory synapses (I-LTD) via retrograde endocannabinoid signaling. Little is known, however, about the physiological significance of I-LTD. Here, we show that synaptic-driven release of endo-cannabinoids is a highly localized and efficient process that strongly depresses cannabinoid-sensitive inhibitory inputs within the dendritic compartment of CA1 pyramidal cells. By removing synaptic inhibition in a restricted area of the dendritic tree, endocannabinoids selectively "primed" nearby excitatory synapses, thereby facilitating subsequent induction of LTP. This induction of local metaplasticity is a novel mechanism by which endocannabinoids can contribute to the storage of information in the brain.