Bernstein Center for Computational Neuroscience Berlin, Berlin, Germany.
Department for Electrical Engineering and Computer Science, Technische Universität Berlin, Berlin, Germany.
Elife. 2021 Apr 26;10:e59715. doi: 10.7554/eLife.59715.
Understanding the connectivity observed in the brain and how it emerges from local plasticity rules is a grand challenge in modern neuroscience. In the primary visual cortex (V1) of mice, synapses between excitatory pyramidal neurons and inhibitory parvalbumin-expressing (PV) interneurons tend to be stronger for neurons that respond to similar stimulus features, although these neurons are not topographically arranged according to their stimulus preference. The presence of such excitatory-inhibitory (E/I) neuronal assemblies indicates a stimulus-specific form of feedback inhibition. Here, we show that activity-dependent synaptic plasticity on input and output synapses of PV interneurons generates a circuit structure that is consistent with mouse V1. Computational modeling reveals that both forms of plasticity must act in synergy to form the observed E/I assemblies. Once established, these assemblies produce a stimulus-specific competition between pyramidal neurons. Our model suggests that activity-dependent plasticity can refine inhibitory circuits to actively shape cortical computations.
理解大脑中观察到的连接以及它如何从局部可塑性规则中出现,是现代神经科学的一个重大挑战。在小鼠的初级视觉皮层 (V1) 中,对于响应类似刺激特征的神经元,兴奋性锥体神经元和抑制性表达 parvalbumin (PV) 的中间神经元之间的突触往往更强,尽管这些神经元不是根据其刺激偏好进行地形排列的。兴奋性抑制性 (E/I) 神经元集合的存在表明存在一种具有刺激特异性的反馈抑制。在这里,我们表明 PV 中间神经元输入和输出突触上的活动依赖性突触可塑性产生了与小鼠 V1 一致的电路结构。计算模型表明,这两种形式的可塑性必须协同作用才能形成观察到的 E/I 集合。一旦建立,这些集合就在锥体神经元之间产生了一种刺激特异性竞争。我们的模型表明,活动依赖性可塑性可以细化抑制性回路,从而主动塑造皮层计算。