Spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex
Spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex
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DOI：
10.1152/jn.00551.2006
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发表时间：
2006-12-01
影响因子：
2.5
通讯作者：
Abarbanel, H. D. I.
中科院分区：
文献类型：
--
作者：
Haas, Julie S.;Nowotny, Thomas;Abarbanel, H. D. I.
抑制性中间神经元的活动组织和调节许多神经元过程，但抑制性突触可塑性的机制和后果仍不清楚。我们报道了内嗅皮层抑制性突触的棘波时序依赖性可塑性。在药物阻断兴奋的情况下，将时间t(Pre)的突触前刺激与在时间t(Post)诱发的突触后峰配对后，我们通过全细胞记录发现，剩余抑制反应的可塑性存在不对称的时间规律。反应强度随时间间隔Delta t=t(Post)-t(Pre)变化：对于Delta t>；0抑制反应增强，在延迟10ms时达到峰值。对于Delta t<；0，突触耦合再次受到抑制，最大影响接近10ms的延迟。我们还表明，突触强度的变化依赖于细胞内钙浓度的变化，并证明钙通过电压门控通道进入突触后细胞。使用网络模型，我们展示了这种新的可塑性形式如何有效地塑造网络行为，并具有显著的灵活性。
Actions of inhibitory interneurons organize and modulate many neuronal processes, yet the mechanisms and consequences of plasticity of inhibitory synapses remain poorly understood. We report on spike-timing-dependent plasticity of inhibitory synapses in the entorhinal cortex. After pairing presynaptic stimulations at time t(pre) with evoked postsynaptic spikes at time t(post) under pharmacological blockade of excitation we found, via whole cell recordings, an asymmetrical timing rule for plasticity of the remaining inhibitory responses. Strength of response varied as a function of the time interval Delta t = t(post) - t(pre): for Delta t > 0 inhibitory responses potentiated, peaking at a delay of 10 ms. For Delta t < 0, the synaptic coupling depressed, again with a maximal effect near 10 ms of delay. We also show that changes in synaptic strength depend on changes in intracellular calcium concentrations and demonstrate that the calcium enters the postsynaptic cell through voltage-gated channels. Using network models, we demonstrate how this novel form of plasticity can sculpt network behavior efficiently and with remarkable flexibility.