Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Michel-Servet 1, 1211 Geneva, Switzerland.
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Michel-Servet 1, 1211 Geneva, Switzerland.
Cell Rep. 2018 Feb 6;22(6):1451-1461. doi: 10.1016/j.celrep.2018.01.025.
Correlated activity in the hippocampus drives synaptic plasticity that is necessary for the recruitment of neuronal ensembles underlying fear memory. Sustained neural activity, on the other hand, may trigger homeostatic adaptations. However, whether homeostatic plasticity affects memory function remains unknown. Here, we use optogenetics to induce cell autonomous homeostatic plasticity in CA1 pyramidal neurons and granule cells of the hippocampus. High-frequency spike trains applied for 10 min decreased the number of excitatory spine synapses and increased the number of inhibitory shaft synapses. This activity stopped dendritic spine formation via L-type voltage-dependent calcium channel activity and protein synthesis. Applied selectively to the ensemble of granule cells encoding a contextual fear memory, the spike trains impaired memory recall and facilitated extinction. Our results indicate that homeostatic plasticity triggered by optogenetic neuronal firing alters the balance between excitation and inhibition in favor of memory extinction.
海马体中的相关活动驱动着突触可塑性，这对于招募恐惧记忆所必需的神经元集合是必要的。另一方面，持续的神经活动可能会引发同型性适应。然而，同型性可塑性是否会影响记忆功能尚不清楚。在这里，我们使用光遗传学诱导海马体 CA1 锥体神经元和颗粒细胞中的自主同型性可塑性。应用 10 分钟的高频尖峰训练减少了兴奋性棘突突触的数量，并增加了抑制性轴突突触的数量。这种活动通过 L 型电压依赖性钙通道活性和蛋白质合成停止树突棘形成。选择性地应用于编码情境恐惧记忆的颗粒细胞集合，尖峰训练会损害记忆回忆并促进消退。我们的结果表明，光遗传学神经元放电引发的同型性可塑性改变了兴奋与抑制之间的平衡，有利于记忆消退。
