Chokshi Varun, Grier Bryce D, Dykman Andrew, Lantz Crystal L, Niebur Ernst, Quinlan Elizabeth M, Lee Hey-Kyoung
The Zanvyl-Krieger Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, United States.
Cell Molecular Developmental Biology and Biophysics (CMDB) Graduate Program, Johns Hopkins University, Baltimore, MD, United States.
Front Synaptic Neurosci. 2021 Apr 15;13:663282. doi: 10.3389/fnsyn.2021.663282. eCollection 2021.
The history of neural activity determines the synaptic plasticity mechanisms employed in the brain. Previous studies report a rapid reduction in the strength of excitatory synapses onto layer 2/3 (L2/3) pyramidal neurons of the primary visual cortex (V1) following two days of dark exposure and subsequent re-exposure to light. The abrupt increase in visually driven activity is predicted to drive homeostatic plasticity, however, the parameters of neural activity that trigger these changes are unknown. To determine this, we first recorded spike trains from V1 layer 4 (L4) of dark exposed (DE) mice of both sexes that were re-exposed to light through homogeneous or patterned visual stimulation. We found that delivering the spike patterns recorded to L4 of V1 slices was sufficient to reduce the amplitude of miniature excitatory postsynaptic currents (mEPSCs) of V1 L2/3 neurons in DE mice, but not in slices obtained from normal reared (NR) controls. Unexpectedly, the same stimulation pattern produced an up-regulation of mEPSC amplitudes in V1 L2/3 neurons from mice that received 2 h of light re-exposure (LE). A Poisson spike train exhibiting the same average frequency as the patterns recorded was equally effective at depressing mEPSC amplitudes in L2/3 neurons in V1 slices prepared from DE mice. Collectively, our results suggest that the history of visual experience modifies the responses of V1 neurons to stimulation and that rapid homeostatic depression of excitatory synapses can be driven by non-patterned input activity.
神经活动的历史决定了大脑中所采用的突触可塑性机制。先前的研究报告称，在经历两天黑暗暴露并随后重新暴露于光照后，初级视觉皮层（V1）第2/3层（L2/3）锥体神经元上兴奋性突触的强度会迅速降低。预计视觉驱动活动的突然增加会驱动稳态可塑性，然而，引发这些变化的神经活动参数尚不清楚。为了确定这一点，我们首先记录了通过均匀或图案化视觉刺激重新暴露于光照的两性黑暗暴露（DE）小鼠V1第4层（L4）的尖峰序列。我们发现，将记录的尖峰模式传递到V1切片的L4足以降低DE小鼠V1 L2/3神经元微小兴奋性突触后电流（mEPSCs）的幅度，但对于从正常饲养（NR）对照获得的切片则不然。出乎意料的是，相同的刺激模式使接受2小时光照重新暴露（LE）的小鼠V1 L2/3神经元的mEPSC幅度上调。展示与记录模式相同平均频率的泊松尖峰序列在抑制由DE小鼠制备的V1切片中L2/3神经元的mEPSC幅度方面同样有效。总体而言，我们的结果表明，视觉经验的历史会改变V1神经元对刺激 的反应，并且兴奋性突触的快速稳态抑制可由无模式输入活动驱动。
