Two distinct mechanisms for experience-dependent homeostasis.
Two distinct mechanisms for experience-dependent homeostasis.
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DOI：
10.1038/s41593-018-0150-0
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发表时间：
2018-06
影响因子：
25
通讯作者：
Kirkwood A
中科院分区：
文献类型：
--
作者：
Bridi MCD;de Pasquale R;Lantz CL;Gu Y;Borrell A;Choi SY;He K;Tran T;Hong SZ;Dykman A;Lee HK;Quinlan EM;Kirkwood A
放电率稳态的模型，如突触缩放和滑动突触可塑性修改阈值预测，减少神经元活动（例如，通过感觉剥夺）将增强突触功能。在两种形式的视觉剥夺（黑暗暴露（DE）和双眼眼睑缝合（BS））的皮层活动的操作显示，与预期相反，自发放电与视觉输入的损失是必要的，以降低阈值的赫布可塑性和增加mEPSC振幅。阻断由DE上调的GluN2B受体的激活也阻止mEPSC振幅的增加，表明DE主要通过Hebbian机制而不是通过突触缩放来增强mEPSC。然而，与突触缩放一致的mEPSC振幅的NMDAR非依赖性变化可由活动的极端减少诱导。因此，两种不同的机制在不同的神经元活动范围内运作，以稳态调节突触强度。
Models of firing rate homeostasis such as synaptic scaling and the sliding synaptic plasticity modification threshold predict that decreasing neuronal activity (e.g. by sensory deprivation) will enhance synaptic function. Manipulations of cortical activity during two forms of visual deprivation (dark exposure (DE) and binocular lid suture (BS)) revealed that, contrary to expectations, spontaneous firing in conjunction with loss of visual input is necessary to lower the threshold for Hebbian plasticity and increases mEPSC amplitude. Blocking activation of GluN2B receptors, which are up-regulated by DE, also prevents the increase in mEPSC amplitude, suggesting that DE potentiates mEPSCs primarily through a Hebbian mechanism, not through synaptic scaling. Nevertheless, NMDAR-independent changes in mEPSC amplitude consistent with synaptic scaling could be induced by extreme reductions of activity. Therefore, two distinct mechanisms operate within different ranges of neuronal activity to homeostatically regulate synaptic strength.
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