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首页> 外文期刊>Neuron >Microglial TNF-alpha Suppresses Cocaine-Induced Plasticity and Behavioral Sensitization
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Microglial TNF-alpha Suppresses Cocaine-Induced Plasticity and Behavioral Sensitization

机译：小胶质细胞的肿瘤坏死因子-α抑制可卡因诱导的可塑性和行为敏化。

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摘要

Repeated administration of cocaine results in the development of behavioral sensitization, accompanied by a decrease in excitatory synaptic strength in the nucleus accumbens (NAc) through an unknown mechanism. Furthermore, glial cells in the NAc are activated by drugs of abuse, but the contribution of glia to the development of addictive behaviors is unknown. Tumor necrosis factor alpha (TNF-alpha), an inflammatory cytokine released by activated glia, can drive the internalization of synaptic AMPA receptors on striatal medium spiny neurons. Here we show that repeated administration of cocaine activates striatal microglia and induces TNF-alpha production, which in turn depresses glutamatergic synaptic strength in the NAc core and limits the development of behavioral sensitization. Critically, following a period of abstinence, a weak TLR4 agonist can reactivate microglia, increase TNF-alpha production, depress striatal synaptic strength, and suppress cocaine-induced sensitization. Thus, cytokine signaling from microglia can regulate both the induction and expression of drug-induced behaviors.
机译：重复施用可卡因可导致行为致敏性的发展，并伴随着伏隔核（NAc）的兴奋性突触强度通过未知机制的降低。此外，NAc中的神经胶质细胞被滥用药物激活，但是神经胶质对成瘾行为发展的贡献尚不清楚。肿瘤坏死因子α（TNF-alpha）是由活化的神经胶质细胞释放的炎性细胞因子，可以驱动纹状体中棘神经元上突触AMPA受体的内在化。在这里，我们显示可卡因的重复给药可激活纹状体小胶质细胞并诱导TNF-α的产生，从而降低NAc核心的谷氨酸能突触强度并限制行为敏化的发展。至关重要的是，禁欲一段时间后，弱的TLR4激动剂可以重新激活小胶质细胞，增加TNF-α的产生，降低纹状体突触强度，并抑制可卡因诱导的致敏作用。因此，来自小胶质细胞的细胞因子信号传导可以调节药物诱导行为的诱导和表达。

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