Prakriya M, Mennerick S
Department of Psychiatry, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Neuron. 2000 Jun;26(3):671-82. doi: 10.1016/s0896-6273(00)81203-9.
Sodium channels (NaChs) play a central role in action potential generation and are uniquely poised to influence the efficacy of transmitter release. We evaluated the effect of partial NaCh blockade on two aspects of synaptic efficacy First, we evaluated whether NaCh blockade accounts for the ability of certain drugs to selectively depress glutamate release. Second, we evaluated the contribution of NaChs to intraneuronal variability in glutamate release probability (p(r)). The antiglutamate drug riluzole nearly completely depresses glutamate excitatory postsynaptic currents (EPSCs) at concentrations that barely affect GABAergic inhibitory postsynaptic currents (IPSCs). NaCh inhibition explains the selective depression. Unlike other presynaptic depressants, partial NaCh blockade increases paired-pulse EPSC depression. This result is explained by selective depression of low-p(r) synapses. We conclude that local variations in the action potential contribute to p(r) variability among excitatory synapses.
钠通道（NaChs）在动作电位产生过程中起核心作用，并且在影响递质释放效率方面具有独特的作用。我们评估了部分钠通道阻断对突触效能两个方面的影响。首先，我们评估钠通道阻断是否解释了某些药物选择性抑制谷氨酸释放的能力。其次，我们评估了钠通道对谷氨酸释放概率（p(r)）的神经元内变异性的贡献。抗谷氨酸药物利鲁唑在几乎不影响γ-氨基丁酸能抑制性突触后电流（IPSCs）的浓度下，几乎完全抑制谷氨酸兴奋性突触后电流（EPSCs）。钠通道抑制解释了这种选择性抑制。与其他突触前抑制剂不同，部分钠通道阻断会增加双脉冲EPSC抑制。这一结果可通过低p(r)突触的选择性抑制来解释。我们得出结论，动作电位的局部变化导致兴奋性突触之间p(r)的变异性。
