Bialowas Andrzej, Rama Sylvain, Zbili Mickaël, Marra Vincenzo, Fronzaroli-Molinieres Laure, Ankri Norbert, Carlier Edmond, Debanne Dominique
INSERM, UMR_S 1072, Marseille, France; Aix-Marseille Université, UNIS, Marseille, France.
Eur J Neurosci. 2015 Feb;41(3):293-304. doi: 10.1111/ejn.12787. Epub 2014 Nov 13.
Synaptic transmission usually depends on action potentials (APs) in an all-or-none (digital) fashion. Recent studies indicate, however, that subthreshold presynaptic depolarization may facilitate spike-evoked transmission, thus creating an analog modulation of spike-evoked synaptic transmission, also called analog-digital (AD) synaptic facilitation. Yet, the underlying mechanisms behind this facilitation remain unclear. We show here that AD facilitation at rat CA3-CA3 synapses is time-dependent and requires long presynaptic depolarization (5-10 s) for its induction. This depolarization-induced AD facilitation (d-ADF) is blocked by the specific Kv1.1 channel blocker dendrotoxin-K. Using fast voltage-imaging of the axon, we show that somatic depolarization used for induction of d-ADF broadened the AP in the axon through inactivation of Kv1.1 channels. Somatic depolarization enhanced spike-evoked calcium signals in presynaptic terminals, but not basal calcium. In conclusion, axonal Kv1.1 channels determine glutamate release in CA3 neurons in a time-dependent manner through the control of the presynaptic spike waveform.
突触传递通常以全或无（数字）方式依赖于动作电位（APs）。然而，最近的研究表明，阈下突触前去极化可能促进峰电位诱发的传递，从而对峰电位诱发的突触传递产生模拟调制，也称为模拟-数字（AD）突触易化。然而，这种易化背后的潜在机制仍不清楚。我们在此表明，大鼠CA3-CA3突触处的AD易化是时间依赖性的，其诱导需要长时间的突触前去极化（5-10秒）。这种去极化诱导的AD易化（d-ADF）被特异性Kv1.1通道阻滞剂树突毒素-K阻断。使用轴突的快速电压成像，我们表明用于诱导d-ADF的体细胞去极化通过Kv1.1通道的失活使轴突中的AP变宽。体细胞去极化增强了突触前终末峰电位诱发的钙信号，但不增强基础钙信号。总之，轴突Kv1.1通道通过控制突触前峰电位波形以时间依赖性方式决定CA3神经元中的谷氨酸释放。
