| Autor: |
Bridi MCD; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., de Pasquale R; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., Lantz CL; Department of Biology, University of Maryland, College Park, MD, USA., Gu Y; Neuroscience and Cognitive Sciences Program, University of Maryland, College Park, MD, USA., Borrell A; Neuroscience and Cognitive Sciences Program, University of Maryland, College Park, MD, USA., Choi SY; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., He K; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., Tran T; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., Hong SZ; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., Dykman A; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA., Lee HK; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA.; Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA., Quinlan EM; Department of Biology, University of Maryland, College Park, MD, USA. equinlan@umd.edu.; Neuroscience and Cognitive Sciences Program, University of Maryland, College Park, MD, USA. equinlan@umd.edu., Kirkwood A; Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA. kirkwood@jhu.edu.; Department of Neuroscience, Johns Hopkins University, Baltimore, MD, USA. kirkwood@jhu.edu. |
| Abstrakt: |
Models of firing rate homeostasis such as synaptic scaling and the sliding synaptic plasticity modification threshold predict that decreasing neuronal activity (for example, by sensory deprivation) will enhance synaptic function. Manipulations of cortical activity during two forms of visual deprivation, dark exposure (DE) and binocular lid suture, revealed that, contrary to expectations, spontaneous firing in conjunction with loss of visual input is necessary to lower the threshold for Hebbian plasticity and increase miniature excitatory postsynaptic current (mEPSC) amplitude. Blocking activation of GluN2B receptors, which are upregulated by DE, also prevented the increase in mEPSC amplitude, suggesting that DE potentiates mEPSCs primarily through a Hebbian mechanism, not through synaptic scaling. Nevertheless, NMDA-receptor-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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