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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >Inhibition of IL-6 trans-signaling in the brain increases sociability in the BTBR mouse model of autism
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Inhibition of IL-6 trans-signaling in the brain increases sociability in the BTBR mouse model of autism

机译：在自闭症的BTBR小鼠模型中，大脑中IL-6反信号的抑制增加了社交能力

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Autism is a severe neurodevelopmental disorder with a large population prevalence, characterized by abnormal reciprocal social interactions, communication deficits, and repetitive behaviors with restricted interests. The BTBR T+ Itpr3(tf) (BTBR) mice have emerged as strong candidates to serve as models of a range of autism relevant behaviors. Increasing evidences suggest that interleuldn (IL)-6, one of the most important neuroimmune factors, was involved in the pathophysiology of autism. It is of great importance to further investigate whether therapeutic interventions in autism can be achieved through the manipulation of IL-6. Our previous studies showed that IL-6 elevation in the brain could mediate autistic-like behaviors, possibly through the imbalances of neural circuitry and impairments of synaptic plasticity. In this study, we evaluate whether inhibiting IL-6 signaling in the brain is sufficient to modulate the autism-like behaviors on the BTBR mice. The results showed that chronic infusion of an analog of the endogenous IL-6 trans-signaling blocker sgp130Fc protein increased the sociability in BTBR mice. Furthermore, no change was observed in the number of excitatory synapse, level of synaptic proteins, density of dentitic spine and postsynaptic density in BTBR cortices after inhibiting IL-6 trans-signaling. However, inhibition of IL-6 trans-signaling increased the evoked glutamate release in synaptoneurosomes from the cerebral cortex of BTBR mice. Our findings suggest that inhibition of excessive production of IL-6 may have selective therapeutic efficacy in treating abnormal social behaviors in autism. (C) 2016 Elsevier B.V. All rights reserved.
机译：自闭症是一种严重的神经发育障碍，具有较高的人口患病率，其特征是异常的相互社交互动，沟通障碍和兴趣受限的重复行为。 BTBR T + Itpr3（tf）（BTBR）小鼠已成为各种自闭症相关行为模型的有力候选者。越来越多的证据表明，interleuldn（IL）-6是最重要的神经免疫因子之一，与自闭症的病理生理有关。进一步研究自闭症的治疗干预是否可以通过操纵IL-6来实现，这一点非常重要。我们以前的研究表明，大脑中IL-6的升高可能介导自闭症样的行为，可能是由于神经回路的不平衡和突触可塑性的损害。在这项研究中，我们评估抑制IL-6信号在大脑中是否足以调节BTBR小鼠的自闭症样行为。结果表明，长期输注内源性IL-6反信号传导阻断剂sgp130Fc蛋白的类似物可增加BTBR小鼠的社交能力。此外，在抑制IL-6信号转导后，BTBR皮质的兴奋性突触数量，突触蛋白水平，树突棘密度和突触后密度均未见变化。但是，IL-6反信号的抑制增加了BTBR小鼠大脑皮层突触神经小体中诱发的谷氨酸释放。我们的发现表明，抑制IL-6过量产生可能在治疗自闭症的异常社交行为方面具有选择性的治疗功效。 （C）2016 Elsevier B.V.保留所有权利。

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