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首页> 外文期刊>Developmental neurobiology >Target‐dependent retrograde signaling mediates synaptic plasticity at the Drosophila Drosophila neuromuscular junction
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Target‐dependent retrograde signaling mediates synaptic plasticity at the Drosophila Drosophila neuromuscular junction

机译:目标依赖性逆行信号传导介导果蝇果蝇神经肌肉交界处的突触塑性

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Abstract Neurons that innervate multiple targets often establish synapses with target‐specific strengths, and local forms of synaptic plasticity. We have examined the molecular‐genetic mechanisms that allow a single Drosophila motoneuron, the ventral Common Exciter (vCE), to establish connections with target‐specific properties at its various synaptic partners. By driving transgenes in a subset of vCE’s targets, we found that individual target cells are able to independently control the properties of vCE's innervating branch and synapses. This is achieved by means of a trans‐synaptic growth factor secreted by the target cell. At the larval neuromuscular junction, postsynaptic glutamate receptor activity stimulates the release of the BMP4/5/6 homolog Glass bottom boat (Gbb). As larvae mature and motoneuron terminals grow, Gbb activates the R‐Smad transcriptional regulator phosphorylated Mad (pMad) to facilitate presynaptic development. We found that manipulations affecting glutamate receptors or Gbb within subsets of target muscles led to local effects either specific to the manipulated muscle or by a limited gradient within the presynaptic branches. While presynaptic development depends on pMad transcriptional activity within the motoneuron nucleus, we find that the Gbb growth factor may also act locally within presynaptic terminals. Local Gbb signaling and presynaptic pMad accumulation within boutons may therefore participate in a “synaptic tagging” mechanism, to influence synaptic growth and plasticity in Drosophila .
机译:摘要神经元,占用多个目标经常建立具有目标特异性强度的突触,以及局部突触可塑性的局部形式。我们研究了分子遗传机制,允许单个果蝇的术,腹侧常见激励率(VCE),在其各种突触伙伴处建立与靶特异性特性的关系。通过在VCE目标的子集中驾驶转基因,我们发现各个目标细胞能够独立地控制VCE的支配分支和突触的性质。这是通过靶细胞分泌的反式突触生长因子来实现的。在幼虫神经肌肉交界处,突触后谷氨酸受体活性刺激BMP4 / 5/6同源物玻璃底船(GBB)的释放。作为幼虫成熟和运动神经元终端生长,GBB激活R-Smad转录调节剂磷酸化MAD(PMAD)以促进突触前发育。我们发现影响谷氨酸受体或GBB在靶肌群子集内的操纵导致局部效应对被操纵的肌肉或突触前分支内的有限梯度。虽然突触前的发展取决于Motoneuron核内的PMAD转录活性,但我们发现GBB生长因子也可能在突触前终端内局部作用。因此,Bouton内的局部GBB信号和预突触PMAD积累可以参与“突触标记”机制,以影响果蝇中的突触生长和可塑性。

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