Erratum: Impairment of Synaptic Plasticity by Cannabis, Δ9-THC, and Synthetic Cannabinoids.
Erratum: Impairment of Synaptic Plasticity by Cannabis, Δ9-THC, and Synthetic Cannabinoids.
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勘误表：大麻、α9-THC 和合成大麻素对突触可塑性的损害。
DOI：
10.1101/cshperspect.a040428
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发表时间：
2020
影响因子：
5.4
通讯作者：
Lupica,CarlR
中科院分区：
文献类型：
--
作者：
Hoffman,AlexanderF;Hwang,Eun-Kyung;Lupica,CarlR
神经元通过短期和长期可塑性对突触输入进行动态和灵活编码的能力对于有机体学习和适应环境的能力至关重要。虽然突触的可塑性可能由突触前或突触后的机制编码，但目前的证据表明，学习的优化需要这两种形式的可塑性。内源性大麻素(ECB)通过激活中枢神经系统(CNS)中的大麻素CB1受体(CB1Rs)在调节突触传递中发挥重要作用，ECB系统直接或间接地参与了多种形式的突触可塑性。正因为如此，欧洲央行信号系统内的扰动可能会导致各种习得行为的损害。欧洲央行信号改变的一个因素是暴露于“外源性大麻素”，如大麻的主要精神活性成分Δ9-THC，或在许多情况下比Δ9-THc具有更高效力和效率的非法合成大麻素。因此，通过以欧洲央行系统为靶点，这些激动剂可以通过扰乱正在进行的欧洲央行功能而导致突触可塑性的广泛损害。在这里，我们回顾了Δ-9-Thc和合成大麻素类化合物损害各种神经元回路中突触可塑性的研究，并检查了证据表明这有助于它们干扰认知和行为的能力。
The ability of neurons to dynamically and flexibly encode synaptic inputs via short- and long-term plasticity is critical to an organism's ability to learn and adapt to the environment. Whereas synaptic plasticity may be encoded by pre- or postsynaptic mechanisms, current evidence suggests that optimization of learning requires both forms of plasticity. Endogenous cannabinoids (eCBs) play critical roles in modulating synaptic transmission via activation of cannabinoid CB1 receptors (CB1Rs) in many central nervous system (CNS) regions, and the eCB system has been implicated, either directly or indirectly, in several forms of synaptic plasticity. Because of this, perturbations within the eCB signaling system can lead to impairments in a variety of learned behaviors. One agent of altered eCB signaling is exposure to “exogenous cannabinoids” such as the primary psychoactive constituent of cannabis, Δ9-THC, or illicit synthetic cannabinoids that in many cases have higher potency and efficacy than Δ9-THC. Thus, by targeting the eCB system, these agonists can produce widespread impairment of synaptic plasticity by disrupting ongoing eCB function. Here, we review studies in which Δ9-THC and synthetic cannabinoids impair synaptic plasticity in a variety of neuronal circuits and examine evidence that this contributes to their well-documented ability to disrupt cognition and behavior.