Chen Simon X, Kim An Na, Peters Andrew J, Komiyama Takaki
1] Neurobiology Section, University of California, San Diego, La Jolla, California, USA. [2] Center for Neural Circuits and Behavior, University of California, San Diego, La Jolla, California, USA. [3] Department of Neurosciences, University of California, San Diego, La Jolla, California, USA.
1] Neurobiology Section, University of California, San Diego, La Jolla, California, USA. [2] Center for Neural Circuits and Behavior, University of California, San Diego, La Jolla, California, USA. [3] Department of Neurosciences, University of California, San Diego, La Jolla, California, USA. [4] Japan Science and Technology Agency, PRESTO, University of California, San Diego, La Jolla, California, USA.
Nat Neurosci. 2015 Aug;18(8):1109-15. doi: 10.1038/nn.4049. Epub 2015 Jun 22.
Motor skill learning induces long-lasting reorganization of dendritic spines, principal sites of excitatory synapses, in the motor cortex. However, mechanisms that regulate these excitatory synaptic changes remain poorly understood. Here, using in vivo two-photon imaging in awake mice, we found that learning-induced spine reorganization of layer (L) 2/3 excitatory neurons occurs in the distal branches of their apical dendrites in L1 but not in the perisomatic dendrites. This compartment-specific spine reorganization coincided with subtype-specific plasticity of local inhibitory circuits. Somatostatin-expressing inhibitory neurons (SOM-INs), which mainly inhibit distal dendrites of excitatory neurons, showed a decrease in axonal boutons immediately after the training began, whereas parvalbumin-expressing inhibitory neurons (PV-INs), which mainly inhibit perisomatic regions of excitatory neurons, exhibited a gradual increase in axonal boutons during training. Optogenetic enhancement and suppression of SOM-IN activity during training destabilized and hyperstabilized spines, respectively, and both manipulations impaired the learning of stereotyped movements. Our results identify SOM inhibition of distal dendrites as a key regulator of learning-related changes in excitatory synapses and the acquisition of motor skills.
运动技能学习会在运动皮层中诱导树突棘（兴奋性突触的主要位点）发生持久的重组。然而，调节这些兴奋性突触变化的机制仍知之甚少。在这里，我们通过在清醒小鼠中进行体内双光子成像发现，学习诱导的第2/3层兴奋性神经元的树突棘重组发生在其位于第1层的顶端树突的远端分支中，而不是在胞体周围的树突中。这种特定区域的树突棘重组与局部抑制性回路的亚型特异性可塑性相吻合。表达生长抑素的抑制性神经元（SOM-INs）主要抑制兴奋性神经元的远端树突，在训练开始后其轴突终扣立即减少，而表达小白蛋白的抑制性神经元（PV-INs）主要抑制兴奋性神经元的胞体周围区域，在训练期间其轴突终扣逐渐增加。在训练期间对SOM-IN活性进行光遗传学增强和抑制分别使树突棘不稳定和超稳定，并且这两种操作均损害了刻板运动的学习。我们的结果表明，SOM对远端树突的抑制是兴奋性突触学习相关变化和运动技能习得的关键调节因子。
Zotero 插件
