Haas Julie S, Nowotny Thomas, Abarbanel H D I
Institute for Nonlinear Science, University of California-San Diego, 9500 Gilman Dr. MC0402, La Jolla, CA 92093-0402, USA.
J Neurophysiol. 2006 Dec;96(6):3305-13. doi: 10.1152/jn.00551.2006. Epub 2006 Aug 23.
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 Deltat = t(post) - t(pre): for Deltat > 0 inhibitory responses potentiated, peaking at a delay of 10 ms. For Deltat < 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.
抑制性中间神经元的活动组织并调节许多神经元过程,然而抑制性突触可塑性的机制和后果仍知之甚少。我们报告了内嗅皮层中抑制性突触的尖峰时间依赖性可塑性。在药理学阻断兴奋的情况下,将时间t(pre)的突触前刺激与时间t(post)诱发的突触后尖峰配对后,我们通过全细胞记录发现了剩余抑制性反应可塑性的不对称时间规则。反应强度随时间间隔Deltat = t(post) - t(pre)而变化:当Deltat > 0时,抑制性反应增强,在延迟10毫秒时达到峰值。当Deltat < 0时,突触耦合减弱,同样在延迟接近10毫秒时达到最大效果。我们还表明,突触强度的变化取决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,我们展示了这种新型可塑性形式如何能够高效且灵活地塑造网络行为。