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Two distinct mechanisms for experience-dependent homeostasis.
Michelle C D Bridi1, Roberto de Pasquale1, Crystal L Lantz2
1Mind/Brain Institute, Johns Hopkins University, Baltimore, MD, USA.
Nature Neuroscience
|May 16, 2018
Summary
Sensory deprivation enhances neuronal function through a novel Hebbian mechanism, not synaptic scaling. This process involves spontaneous firing and GluN2B receptor activation, revealing distinct homeostatic regulation pathways.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Homeostasis
Background:
- Synaptic scaling and plasticity thresholds predict enhanced neuronal function with decreased activity.
- Sensory deprivation models are used to study neuronal activity regulation.
Purpose of the Study:
- To investigate the mechanisms of synaptic plasticity during visual deprivation.
- To determine if synaptic scaling or other mechanisms regulate neuronal function under reduced activity.
Main Methods:
- Visual deprivation using dark exposure (DE) and binocular lid suture in animal models.
- Measurement of miniature excitatory postsynaptic current (mEPSC) amplitude.
- Blocking GluN2B receptor activation.
Main Results:
- Contrary to predictions, spontaneous firing during visual deprivation lowered the threshold for Hebbian plasticity and increased mEPSC amplitude.
- Blocking GluN2B receptors prevented mEPSC potentiation, indicating a Hebbian mechanism.
- Extreme activity reduction induced NMDA-receptor-independent changes consistent with synaptic scaling.
Conclusions:
- Visual deprivation potentiates mEPSCs via a Hebbian mechanism involving spontaneous firing and GluN2B receptors.
- Synaptic scaling operates under different, more extreme activity reduction ranges.
- Two distinct homeostatic mechanisms regulate synaptic strength based on neuronal activity levels.
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