线粒体上的“热点”：大麻素通过破坏细胞呼吸来限制神经元活动。
(S)Pot on Mitochondria: Cannabinoids Disrupt Cellular Respiration to Limit Neuronal Activity.
机构信息
Department of Molecular Neurosciences, Center for Brain Research, Medical University of Vienna, 1090 Vienna, Austria; Department of Neuroscience, Karolinska Institutet, 17177 Stockholm, Sweden.
Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT 06510, USA.
出版信息
Cell Metab. 2017 Jan 10;25(1):8-10. doi: 10.1016/j.cmet.2016.12.020.
Classical views posit G protein-coupled cannabinoid receptor 1s (CB1Rs) at the cell surface with cytosolic Giα-mediated signal transduction. Hebert-Chatelain et al. (2016) instead place CBRs at mitochondria limiting neuronal respiration by soluble adenylyl cyclase-dependent modulation of complex I activity. Thus, neuronal bioenergetics link to synaptic plasticity and, globally, learning and memory.
经典观点认为，位于细胞表面的 G 蛋白偶联大麻素受体 1（CB1R）通过胞质 Giα 介导的信号转导发挥作用。然而，Hebert-Chatelain 等人（2016 年）则认为，CBR 位于线粒体，通过可溶性腺苷酸环化酶依赖性调节复合物 I 的活性来限制神经元呼吸。因此，神经元的生物能量学与突触可塑性以及整体的学习和记忆有关。
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