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吗啡戒断会募集外侧缰核细胞因子信号,从而减少突触兴奋和社交性。

Morphine withdrawal recruits lateral habenula cytokine signaling to reduce synaptic excitation and sociability.

机构信息

The Department of Fundamental Neuroscience, The University of Lausanne, Lausanne, Switzerland.

Department of Physiology, The University of Bern, Bern, Switzerland.

出版信息

Nat Neurosci. 2019 Jul;22(7):1053-1056. doi: 10.1038/s41593-019-0421-4. Epub 2019 Jun 17.

Abstract

The lateral habenula encodes aversive stimuli contributing to negative emotional states during drug withdrawal. Here we report that morphine withdrawal in mice leads to microglia adaptations and diminishes glutamatergic transmission onto raphe-projecting lateral habenula neurons. Chemogenetic inhibition of this circuit promotes morphine withdrawal-like social deficits. Morphine withdrawal-driven synaptic plasticity and reduced sociability require tumor necrosis factor-α (TNF-α) release and neuronal TNF receptor 1 activation. Hence, habenular cytokines control synaptic and behavioral adaptations during drug withdrawal.

摘要

外侧缰核编码厌恶刺激,有助于药物戒断期间的负面情绪状态。在这里,我们报告说,吗啡戒断会导致小鼠小胶质细胞适应性改变,并减少谷氨酸能传递到投射到中缝核的外侧缰核神经元。该回路的化学遗传抑制会促进吗啡戒断样社交缺陷。吗啡戒断驱动的突触可塑性和社交能力下降需要肿瘤坏死因子-α(TNF-α)释放和神经元 TNF 受体 1 激活。因此,缰核细胞因子控制药物戒断期间的突触和行为适应性。

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