Rebalancing strength between synapses Activation of a neuronal pathway is often associated with inhibition of surrounding pathways. How locally coordinated synaptic plasticity occurs in vivo is not known, nor is its role in shaping neuronal responses. El-Boustani et al. paired optogenetic stimulation of single neurons with a visual input and were able to shift the neuron's receptive field toward the target location. Spines that expressed structural long-term potentiation had receptive fields overlapping the target stimulus but were surrounded by spines that expressed receptive fields away from the target. Science, this issue p. 1349 Arc-mediated local synaptic plasticity reorganizes responses on dendrites to mediate functional neuronal plasticity in vivo. Plasticity of cortical responses in vivo involves activity-dependent changes at synapses, but the manner in which different forms of synaptic plasticity act together to create functional changes in neurons remains unknown. We found that spike timing–induced receptive field plasticity of visual cortex neurons in mice is anchored by increases in the synaptic strength of identified spines. This is accompanied by a decrease in the strength of adjacent spines on a slower time scale. The locally coordinated potentiation and depression of spines involves prominent AMPA receptor redistribution via targeted expression of the immediate early gene product Arc. Hebbian strengthening of activated synapses and heterosynaptic weakening of adjacent synapses thus cooperatively orchestrate cell-wide plasticity of functional neuronal responses.

中文翻译：

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体内视觉皮层神经元的局部协调突触可塑性

突触之间的重新平衡强度神经元通路的激活通常与周围通路的抑制有关。体内如何局部协调的突触可塑性尚不清楚，它在塑造神经元反应中的作用也不清楚。El-Boustani 等人。将单个神经元的光遗传学刺激与视觉输入配对，并能够将神经元的感受野移向目标位置。表达结构性长期增强的脊椎具有与目标刺激重叠的感受野，但被表达远离目标的感受野的刺包围。科学，这个问题 p。1349 Arc 介导的局部突触可塑性重组对树突的反应，以介导体内功能性神经元可塑性。体内皮质反应的可塑性涉及突触的活动依赖性变化，但不同形式的突触可塑性共同作用以在神经元中产生功能变化的方式仍然未知。我们发现，尖峰时间诱导的小鼠视觉皮层神经元的感受野可塑性是由已识别棘突突触强度的增加所锚定的。这伴随着在较慢的时间尺度上相邻棘的强度降低。刺的局部协调增强和抑制涉及通过直接早期基因产物 Arc 的靶向表达显着的 AMPA 受体重新分布。激活的突触的 Hebbian 强化和相邻突触的异质突触减弱，从而协同协调功能性神经元反应的全细胞可塑性。