Bélair Eve-Lyne, Vallée Joanne, Robitaille Richard
Centre de Recherche en Sciences Neurologiques, Département de physiologie, Université de Montréal, Québec, Canada.
J Physiol. 2005 Nov 15;569(Pt 1):163-78. doi: 10.1113/jphysiol.2005.094805. Epub 2005 Sep 15.
Prolonged changes in motor neurone activity can result in long-term changes in synaptic transmission. We investigated whether mechanisms commonly thought to be involved in determining synaptic efficacy of vertebrate motor neurones are involved in these long-term changes. The nerve supplying the cutaneous pectoris muscle was chronically stimulated via skin surface electrodes in freely moving frogs for 5-7 days. Chronic stimulation induced a 50% reduction in evoked endplate potential (EPP) amplitude at stimulated neuromuscular junctions (NMJs). These changes appear to be presynaptic since miniature EPP (mEPP) amplitude was unchanged while mEPP frequency was decreased by 46% and paired-pulse facilitation was increased by 26%. High frequency facilitation (40 Hz, 2 s) was also increased by 89%. Moreover, stimulated NMJs presented a 92% decrease in synaptic depression (40 Hz, 2 s). An increase in mitochondrial metabolism was observed as indicated by a more pronounced labelling of active mitochondria (Mitotracker) in stimulated nerve terminals, which could account for their greater resistance to synaptic depression. NMJ length visualized by alpha-bungarotoxin staining of nAChRs was not affected. Presynaptic calcium signals measured with Calcium Green-1 were larger in stimulated NMJs at low frequency (0.2 Hz) and not different from control NMJs at higher frequency (40 Hz, 2 s and 30 s). These results suggest that some mechanisms downstream of calcium entry are responsible for the determination of synaptic output, such as a down-regulation of some calcium-binding proteins, which could explain the observed results. The possibility of a change in frequenin expression, a calcium-binding protein that is more prominently expressed in phasic synapses, was, however, refuted by our results.
运动神经元活动的长期变化可导致突触传递的长期改变。我们研究了通常被认为参与决定脊椎动物运动神经元突触效能的机制是否参与了这些长期变化。在自由活动的青蛙中,通过皮肤表面电极对供应胸皮肌的神经进行慢性刺激5 - 7天。慢性刺激导致受刺激的神经肌肉接头(NMJ)处诱发终板电位(EPP)幅度降低50%。这些变化似乎是突触前的,因为微小EPP(mEPP)幅度未改变,而mEPP频率降低了46%,双脉冲易化增加了26%。高频易化(40 Hz,2 s)也增加了89%。此外,受刺激的NMJ处突触抑制(40 Hz,2 s)降低了92%。观察到线粒体代谢增加,这表现为受刺激神经末梢中活性线粒体(线粒体追踪染料)的标记更明显,这可能解释了它们对突触抑制的更大抵抗力。通过α-银环蛇毒素对烟碱型乙酰胆碱受体(nAChRs)进行染色显示的NMJ长度未受影响。用钙绿-1测量的突触前钙信号在低频(0.2 Hz)受刺激的NMJ中较大,而在高频(40 Hz,2 s和30 s)时与对照NMJ无差异。这些结果表明,钙内流下游的一些机制负责突触输出的决定,例如某些钙结合蛋白的下调,这可以解释观察到的结果。然而,我们的结果否定了在相位突触中更显著表达的钙结合蛋白frequenin表达发生变化的可能性。