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首页> 外文期刊>The Journal of Neuroscience: The Official Journal of the Society for Neuroscience >Differential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis.
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Differential effects of neurotrophins and schwann cell-derived signals on neuronal survival/growth and synaptogenesis.

机译：神经营养蛋白和雪旺细胞衍生信号对神经元存活/生长和突触形成的差异作用。

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摘要

Recent studies have shown that the survival of mammalian motoneurons in vitro is promoted by neurotrophins (NTs) and cAMP. There is also evidence that neurotrophins enhance transmitter release. We thus investigated whether these agents also promote synaptogenesis. Cultured Xenopus spinal cord neurons were treated with a mixture of BDNF, glia-derived neurotrophic factor, NT-3, and NT-4, in addition to forskolin and IBMX or the cell-permeant form of cAMP, to elevate the cAMP level. The outgrowth and survival of neurons were dramatically increased by this trophic stimulation. However, when these neurons were cocultured with muscle cells, the trophic agents resulted in a failure of synaptogenesis. Specifically, the induction of ACh receptor (AChR) clustering in cultured muscle cells was inhibited at nerve-muscle contacts, in sharp contrast to control, untreated cocultures. Because AChR clustering induced by agrin or growth factor-coated beads in muscle cells was unaffected by trophic stimulation, its effect on synaptogenesis is presynaptic in origin. In the control, agrin was deposited along the neurite and at nerve-muscle contacts. This was significantly downregulated in cultures treated with trophic stimuli. Reverse transcriptase-PCR analyses showed that this decrease in agrin deposition was caused by an inhibition of agrin synthesis by trophic stimuli. Both agrin synthesis and induction of AChR clustering were restored under trophic stimulation when Schwann cell-conditioned medium was introduced. These results suggest that trophic stimulation maintains spinal neurons in the growth state, and Schwann cell-derived factors allow them to switch to the synaptogenic state.
机译：最近的研究表明，神经营养蛋白（NTs）和cAMP促进了哺乳动物运动神经元的体外存活。也有证据表明神经营养蛋白增强了递质的释放。因此，我们调查了这些药物是否也促进突触形成。除福司可林和IBMX或cAMP的细胞渗透性形式外，还用BDNF，胶质细胞衍生的神经营养因子，NT-3和NT-4的混合物处理培养的非洲爪蟾脊髓神经元，以提高cAMP水平。这种营养刺激极大地增加了神经元的生长和存活。但是，当这些神经元与肌肉细胞共培养时，营养剂导致突触发生失败。具体而言，在神经肌肉接触时，培养的肌肉细胞中ACh受体（AChR）簇的诱导受到抑制，这与未处理的对照共培养物形成鲜明对比。由于凝集素或生长因子包被的珠在肌肉细胞中诱导的AChR簇不受营养刺激的影响，因此其对突触形成的影响是突触的起源。在对照中，凝集素沿神经突并在神经-肌肉接触处沉积。在用营养刺激处理的培养物中，这显着下调。逆转录-PCR分析表明，凝集素沉积的这种减少是由于营养刺激抑制凝集素合成而引起的。当引入Schwann细胞条件培养基时，在营养刺激下恢复了凝集素的合成和AChR簇的诱导。这些结果表明，营养刺激将脊髓神经元维持在生长状态，而施旺细胞衍生的因子使它们转换为突触形成状态。

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