非典型内源性大麻素信号在皮质传入到海马的部位引发了一种新形式的与记忆相关的可塑性。
Atypical Endocannabinoid Signaling Initiates a New Form of Memory-Related Plasticity at a Cortical Input to Hippocampus.
机构信息
Department of Anatomy and Neurobiology, University of California, Irvine, CA, USA.
Department of Neuroscience, The Scripps Research Institute, Jupiter, FL, USA.
出版信息
Cereb Cortex. 2018 Jul 1;28(7):2253-2266. doi: 10.1093/cercor/bhx126.
Endocannabinoids (ECBs) depress transmitter release at sites throughout the brain. Here, we describe another form of ECB signaling that triggers a novel form of long-term potentiation (LTP) localized to the lateral perforant path (LPP) which conveys semantic information from cortex to hippocampus. Two cannabinoid CB1 receptor (CB1R) signaling cascades were identified in hippocampus. The first is pregnenolone sensitive, targets vesicular protein Munc18-1 and depresses transmitter release; this cascade is engaged by CB1Rs in Schaffer-Commissural afferents to CA1 but not in the LPP, and it does not contribute to LTP. The second cascade is pregnenolone insensitive and LPP specific; it entails co-operative CB1R/β1-integrin signaling to effect synaptic potentiation via stable enhancement of transmitter release. The latter cascade is engaged during LPP-dependent learning. These results link atypical ECB signaling to the encoding of a fundamental component of episodic memory and suggest a novel route whereby endogenous and exogenous cannabinoids affect cognition.
内源性大麻素（ECB）会抑制整个大脑中递质的释放。在这里，我们描述了另一种 ECB 信号转导形式，它触发了一种新型的局部横向穿通路径（LPP）的长时程增强（LTP），这种形式将来自大脑皮层的语义信息传递到海马体。在海马体中确定了两种大麻素 CB1 受体（CB1R）信号级联。第一个级联是孕烯醇酮敏感的，靶向囊泡蛋白 Munc18-1 并抑制递质释放；该级联由 Schaffer-Commissural 传入纤维中的 CB1R 激活，但不在 LPP 中，并且它不参与 LTP。第二个级联是孕烯醇酮不敏感且 LPP 特异的；它需要通过 CB1R/β1-整合素的合作信号，通过稳定增强递质释放来实现突触增强，从而产生 LTP。后一个级联在 LPP 依赖性学习期间被激活。这些结果将非典型的 ECB 信号与情景记忆基本成分的编码联系起来，并提示了内源性和外源性大麻素影响认知的新途径。
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