Input-Specific Metaplasticity in the Visual Cortex Requires Homer1a-Mediated mGluR5 Signaling.
Neuron
; 104(4): 736-748.e6, 2019 11 20.
Article
in En
| MEDLINE
| ID: mdl-31563294
ABSTRACT
Effective sensory processing depends on sensory experience-dependent metaplasticity, which allows homeostatic maintenance of neural network activity and preserves feature selectivity. Following a strong increase in sensory drive, plasticity mechanisms that decrease the strength of excitatory synapses are preferentially engaged to maintain stability in neural networks. Such adaptation has been demonstrated in various model systems, including mouse primary visual cortex (V1), where excitatory synapses on layer 2/3 (L2/3) neurons undergo rapid reduction in strength when visually deprived mice are reexposed to light. Here, we report that this form of plasticity is specific to intracortical inputs to V1 L2/3 neurons and depends on the activity of NMDA receptors (NMDARs) and group I metabotropic glutamate receptor 5 (mGluR5). Furthermore, we found that expression of the immediate early gene (IEG) Homer1a (H1a) and its subsequent interaction with mGluR5s are necessary for this input-specific metaplasticity.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Visual Cortex
/
Signal Transduction
/
Receptor, Metabotropic Glutamate 5
/
Homer Scaffolding Proteins
/
Neuronal Plasticity
Limits:
Animals
Language:
En
Journal:
Neuron
Journal subject:
NEUROLOGIA
Year:
2019
Document type:
Article
Affiliation country:
United States