Caroni P, Becker M
Friedrich Miescher Institute, Basel, Switzerland.
J Neurosci. 1992 Oct;12(10):3849-61. doi: 10.1523/JNEUROSCI.12-10-03849.1992.
Axonal growth during development and regeneration coincides with the expression of growth-associated proteins (GAPs), including GAP-43 and tubulin-alpha 1. Following contact with the target region and synaptogenesis, GAPs are downregulated. However, high levels of GAP-43 are expressed in some neurons in the adult CNS, indicating that its function may not be restricted to axonal growth. To define the type of signals that regulate GAP levels during development, we have determined whether GAP downregulation coincides with a defined phase of synapse development and whether it is controlled by the postsynaptic target. Levels of GAP-43 mRNA in spinal motoneurons and protein at the neuromuscular junction were analyzed in the developing neuromuscular system of chick and rat. In both species, GAP-43 mRNA declined rapidly at a time corresponding to the onset of synapse elimination, and nerve terminal GAP-43 immunoreactivity became undetectable with a delay of 2-3 d. In rat motoneurons, GAP-43 and tubulin-alpha 1 mRNA levels declined with a similar time course, indicating that at least two GAPs are downregulated at the same time. Blockade of neuromuscular transmission with either a pre- or a postsynaptically acting toxin prevented GAP downregulation, indicating that target activity affects GAP mRNA levels in motoneurons. Finally, counteracting the activity-dependent decline of muscle insulin-like growth factors during synapse elimination by local subcutaneous injections prevented motoneuron GAP downregulation, suggesting that these growth factors may be involved in the regulation of motoneuron GAPs by the muscle. These results demonstrate that motoneurons undergo target-sensitive changes in GAPs at the onset of synapse elimination. In addition, these results raise the possibility that termination of a presynaptic growth mode may be a prerequisite for synapse elimination.
在发育和再生过程中,轴突生长与生长相关蛋白(GAPs)的表达同时发生,包括GAP - 43和微管蛋白α1。在与靶区域接触和突触形成后,GAPs表达下调。然而,在成体中枢神经系统的一些神经元中,GAP - 43表达水平较高,这表明其功能可能不限于轴突生长。为了确定在发育过程中调节GAP水平的信号类型,我们已经确定GAP下调是否与突触发育的特定阶段一致,以及它是否由突触后靶标控制。在鸡和大鼠发育中的神经肌肉系统中,分析了脊髓运动神经元中GAP - 43 mRNA的水平以及神经肌肉接头处的蛋白水平。在这两个物种中,GAP - 43 mRNA在对应于突触消除开始的时间迅速下降,并且神经末梢GAP - 43免疫反应性在延迟2 - 3天后变得不可检测。在大鼠运动神经元中,GAP - 43和微管蛋白α1 mRNA水平以相似的时间进程下降,表明至少两种GAPs同时下调。用突触前或突触后作用的毒素阻断神经肌肉传递可防止GAP下调,这表明靶标活动会影响运动神经元中的GAP mRNA水平。最后,通过局部皮下注射抵消突触消除期间肌肉胰岛素样生长因子的活性依赖性下降,可防止运动神经元GAP下调,这表明这些生长因子可能参与肌肉对运动神经元GAPs的调节。这些结果表明,在突触消除开始时,运动神经元的GAPs会发生靶标敏感的变化。此外,这些结果还提出了一种可能性,即突触前生长模式的终止可能是突触消除的先决条件。