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首页> 外文期刊>Neuron >Neuronal Ig/Caspr Recognition Promotes the Formation of Axoaxonic Synapses in Mouse Spinal Cord
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Neuronal Ig/Caspr Recognition Promotes the Formation of Axoaxonic Synapses in Mouse Spinal Cord

机译:神经元Ig / Caspr识别促进小鼠脊髓中轴突突触的形成。

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摘要

Inhibitory microcircuits are wired with a precision that underlies their complex regulatory roles in neural information processing. In the spinal cord, one specialized class of GABAergic interneurons (GABApre) mediates presynaptic inhibitory control of sensory-motor synapses. The synaptic targeting of these GABAergic neurons exhibits an absolute dependence on proprioceptive sensory terminals, yet the molecular underpinnings of this specialized axoaxonic organization remain unclear. Here, we show that sensory expression of an NB2 (Contactin5)/Caspr4 coreceptor complex, together with spinal interneuron expression of NrCAM/CHL1, directs the high-density accumulation of GABAergic boutons on sensory terminals. Moreover, genetic elimination of NB2 results in a disproportionate stripping of inhibitory boutons from high-density GABApre-sensory synapses, suggesting that the preterminal axons of GABApre neurons compete for access to individual sensory terminals. Our findings define a recognition complex that contributes to the assembly and organization of a specialized GABAergic microcircuit.
机译:抑制性微电路的布线精确度是其在神经信息处理中复杂调控作用的基础。在脊髓中,一类特殊的GABA能中间神经元(GABApre)介导对感觉运动突触的突触前抑制控制。这些GABA能神经元的突触靶向表现出对本体感受性感觉末梢的绝对依赖性,但是这个专门的轴突轴突组织的分子基础仍然不清楚。在这里,我们显示了NB2(Contactin5)/ Caspr4受体复合体的感觉表达,以及NrCAM / CHL1的脊髓中间神经元表达,指导了GABA能性boutons在感觉末端的高密度积累。此外,NB2的遗传消除导致高密度GABApre神经元的突触抑制性条顿的过度剥离,这表明GABApre神经元的前轴突轴突竞争进入各个感觉末端。我们的发现定义了识别复合物,该复合物有助于专门的GABA能微电路的组装和组织。

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