Activity-Dependent Downscaling of Subthreshold Synaptic Inputs during Slow-Wave-Sleep-like Activity In Vivo.

Activity-Dependent Downscaling of Subthreshold Synaptic Inputs during Slow-Wave-Sleep-like Activity In Vivo.
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DOI:
10.1016/j.neuron.2018.01.047
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发表时间:
2018-03-21
期刊:
影响因子:
16.2
通讯作者:
Paulsen O
Paulsen O
中科院分区:
医学1区
文献类型:
--
作者:
González-Rueda A;Pedrosa V;Feord RC;Clopath C;Paulsen O

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活动依赖性突触可塑性对于皮层回路的精细化是至关重要的。突触稳态假说认为,突触连接在清醒时加强,在睡眠时缩小;然而,同样的可塑性规则如何解释这两种结果并不明显。使用全细胞记录和光遗传学刺激的突触前输入的麻醉小鼠,表现出慢波睡眠(SWS)样活动,我们表明,突触可塑性规则门控在体内的皮质动力学。虽然下状态支持传统的尖峰时间依赖性可塑性,但上状态偏向于抑郁,使得突触前刺激单独导致突触抑郁,而有助于突触后尖峰的连接受到保护,免受这种突触减弱的影响。我们发现,这种新的活动相关和输入特定的降尺度机制有两个重要的计算优势:(1)提高信噪比,(2)保存以前存储的信息。因此,这些突触可塑性规则提供了一个有吸引力的机制SWS相关的突触缩小和电路细化。传统的STDP只在体内的Down状态下出现在Up状态下,L4输入的突触激活导致突触抑制突触后锋电位防止Up状态介导的突触减弱这些新的可塑性规则改善了S/N比并保存了存储的信息。表明在体内慢波睡眠样活动期间突触前激活导致突触抑制,除非它有助于突触后尖峰。这个可塑性规则提供了一个有吸引力的机制,改善信号噪声比,并保留先前存储的信息的电路细化。
Activity-dependent synaptic plasticity is critical for cortical circuit refinement. The synaptic homeostasis hypothesis suggests that synaptic connections are strengthened during wake and downscaled during sleep; however, it is not obvious how the same plasticity rules could explain both outcomes. Using whole-cell recordings and optogenetic stimulation of presynaptic input in urethane-anesthetized mice, which exhibit slow-wave-sleep (SWS)-like activity, we show that synaptic plasticity rules are gated by cortical dynamics in vivo. While Down states support conventional spike timing-dependent plasticity, Up states are biased toward depression such that presynaptic stimulation alone leads to synaptic depression, while connections contributing to postsynaptic spiking are protected against this synaptic weakening. We find that this novel activity-dependent and input-specific downscaling mechanism has two important computational advantages: (1) improved signal-to-noise ratio, and (2) preservation of previously stored information. Thus, these synaptic plasticity rules provide an attractive mechanism for SWS-related synaptic downscaling and circuit refinement. Conventional STDP is seen only during Down states in vivo During Up states synaptic activation of L4 inputs leads to synaptic depression Postsynaptic spikes protect against Up state-mediated synaptic weakening These new plasticity rules improve S/N ratio and preserve stored information González-Rueda et al. show that presynaptic activation during slow-wave-sleep-like activity in vivo causes synaptic depression, unless it contributes to postsynaptic spiking. This plasticity rule offers an attractive mechanism for circuit refinement that improves signal-to-noise ratio and preserves previously stored information.
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