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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Postsynaptic inositol 1,4,5-trisphosphate signaling maintains presynaptic function of parallel fiber-Purkinje cell synapses via BDNf
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Postsynaptic inositol 1,4,5-trisphosphate signaling maintains presynaptic function of parallel fiber-Purkinje cell synapses via BDNf

机译：突触后肌醇1,4,5-三磷酸信号传导通过BDNf维持平行纤维-浦肯野细胞突触的突触前功能

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摘要

The maintenance of synaptic functions is essential for neuronal information processing, but cellular mechanisms that maintain synapses in the adult brain are not well understood. Here, we report an activity-dependent maintenance mechanism of parallel fiber (PF)-Purkinje cell (PC) synapses in the cerebellum. When postsynaptic metabotropic glutamate receptor (mGluR) or inositol 1,4,5-trisphosphate (IP_3) signaling was chronically inhibited in vivo, PF-PC synaptic strength decreased because of a decreased transmitter release probability. The same effects were observed when PF activity was inhibited in vivo by the suppression of NMDA receptor-mediated inputs to granule cells. PF-PC synaptic strength similarly decreased after the in vivo application of an antibody against brain-derived neurotrophic factor (BDNF). Furthermore, the weakening of synaptic connection caused by the blockade of mGluR-IP_3 signaling was reversed by the in vivo application of BDNF. These results indicate that a signaling cascade comprising PF activity, postsynaptic mGluR-IP_3 signaling and subsequent BDNF signaling maintains presynaptic functions in the mature cerebellum.
机译：突触功能的维持对于神经元信息处理至关重要，但是在成年大脑中维持突触的细胞机制尚不十分清楚。在这里，我们报告小脑中的平行纤维（PF）-Purkinje细胞（PC）突触的活动依赖的维护机制。当体内慢性抑制突触后代谢型谷氨酸受体（mGluR）或肌醇1,4,5-三磷酸（IP_3）信号传导时，由于递质释放的可能性降低，PF-PC突触强度降低。当通过抑制NMDA受体介导的颗粒细胞输入抑制体内PF活性时，观察到相同的效果。在体内应用针对脑源性神经营养因子（BDNF）的抗体后，PF-PC突触强度同样降低。此外，体内应用BDNF可逆转由mGluR-IP_3信号传导阻滞引起的突触连接减弱。这些结果表明，包括PF活性，突触后mGluR-IP_3信号传导和随后的BDNF信号传导的信号传导级联在成熟小脑中维持突触前功能。

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