Presynaptic action potential waveform determines cortical synaptic latency
Presynaptic action potential waveform determines cortical synaptic latency
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DOI：
10.1113/jphysiol.2010.199653
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发表时间：
2011-03-01
影响因子：
5.5
通讯作者：
Debanne, Dominique
中科院分区：
文献类型：
--
作者：
Boudkkazi, Sami;Fronzaroli-Molinieres, Laure;Debanne, Dominique
非技术概述皮层突触的突触延迟由突触前释放概率决定。我们在这里表明，突触前动作电位的持续时间和幅度也决定了新皮层和海马兴奋性突触的突触潜伏期。扩大突触前尖峰与钾通道阻滞剂增加延迟1-2毫秒。减少突触前动作电位的幅度，部分阻断钠通道减少突触潜伏期相似的0.5毫秒。这些变化可能有助于稳定的突触定时在重复刺激。这些药物对突触时间的调节不能归因于轴突传导的调制。相反，这些作用与突触前钙电流动力学的改变是相容的。结果表明，皮层神经元的突触潜伏期不是恒定的，而是受突触前动作电位波形的动态调节，突触潜伏期由突触前释放概率（P-r）决定。短期和长期突触前可塑性与突触延迟的调制有关。我们在这里表明，突触前动作电位的持续时间和幅度也决定了新皮层和海马兴奋性突触的突触潜伏期。阻断电压门控钾（KV）通道与4-氨基吡啶或dendrotoxin-I，但不是四乙铵，诱导1-2 ms的潜伏期移位兴奋性突触连接形成的新皮层锥体神经元对。4-氨基吡啶或dendrotoxin-I，但不是四乙铵，增加了轴突中记录的动作电位的持续时间，这表明突触前尖峰持续时间是由轴突Kv 1钾通道控制的。在苔藓纤维-CA 3细胞突触处已经确定了潜伏期的尖峰宽度依赖性变化，并且有助于在重复刺激期间稳定突触定时。同时观察了突触前锋电位幅度对突触潜伏期的影响。减少突触前动作电位的幅度与15-30 nm TTX减少突触潜伏期相似的0.5毫秒。突触定时的钾和钠通道阻滞剂的调节不能归因于轴突传导的调制。相反，这些效果是兼容的突触前钙电流的动力学的修改。我们的结论是，在皮层神经元的突触潜伏期不是恒定的，而是动态调节突触前动作电位波形。
Non-technical summarySynaptic delay at cortical synapses is determined by the presynaptic release probability. We show here that the duration and amplitude of the presynaptic action potential also determine synaptic latency at neocortical and hippocampal excitatory synapses. Broadening the presynaptic spike with blockers of potassium channels increased latency by 1-2 ms. Decreasing the amplitude of the presynaptic action potential by partly blocking sodium channels reduced synaptic latency by similar to 0.5 ms. These changes may contribute to stabilization of synaptic timing during repetitive stimulation. The regulation of synaptic timing by these pharmacological agents could not be attributed to modulation of axonal conduction. Rather, the effects are compatible with modifications of the kinetics of the presynaptic calcium current. We conclude that synaptic latency at cortical neurons is not constant but dynamically regulated by presynaptic action potential waveform.Synaptic latency at cortical synapses is determined by the presynaptic release probability (P-r). Short- and long-term presynaptic plasticity is associated with modulation of synaptic delay. We show here that the duration and amplitude of the presynaptic action potential also determine synaptic latency at neocortical and hippocampal excitatory synapses. Blockade of voltage-gated potassium (Kv) channels with 4-aminopyridine or dendrotoxin-I, but not tetraethylammonium, induced a 1-2 ms shift in latency at excitatory synaptic connections formed by pairs of neocortical pyramidal neurons. 4-Aminopyridine or dendrotoxin-I, but not tetraethylammonium, increased the duration of the action potential recorded in the axon, suggesting that presynaptic spike duration is controlled by axonal Kv1 potassium channels. Spike width-dependent changes in latency have been identified at the mossy fibre-CA3 cell synapses and contribute to stabilization of synaptic timing during repetitive stimulation. The effects of presynaptic spike amplitude on synaptic latency were also examined. Decreasing the amplitude of the presynaptic action potential with 15-30 nm TTX reduced synaptic latency by similar to 0.5 ms. The regulation of synaptic timing by potassium and sodium channel blockers could not be attributed to modulation of axonal conduction. Rather, these effects are compatible with modifications of the kinetics of the presynaptic calcium current. We conclude that synaptic latency at cortical neurons is not constant but dynamically regulated by presynaptic action potential waveform.