Abstract
Experience-dependent brain plasticity typically declines after an early critical period during which circuits are established. Loss of plasticity with closure of the critical period limits improvement of function in adulthood, but the mechanisms that change the brain's plasticity remain poorly understood. Here, we identified an increase in expression of Lynx1 protein in mice that prevented plasticity in the primary visual cortex late in life. Removal of this molecular brake enhanced nicotinic acetylcholine receptor signaling. Lynx1 expression thus maintains stability of mature cortical networks in the presence of cholinergic innervation. The results suggest that modulating the balance between excitatory and inhibitory circuits reactivates visual plasticity and may present a therapeutic target.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adaptor Proteins, Signal Transducing
-
Aging
-
Amblyopia / metabolism
-
Animals
-
Cholinesterase Inhibitors / pharmacology
-
Dominance, Ocular
-
Evoked Potentials, Visual
-
Mecamylamine / pharmacology
-
Membrane Glycoproteins / genetics*
-
Membrane Glycoproteins / metabolism
-
Membrane Glycoproteins / physiology*
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Neural Inhibition
-
Neuronal Plasticity*
-
Neuropeptides / genetics*
-
Neuropeptides / metabolism
-
Neuropeptides / physiology*
-
Nicotinic Antagonists / pharmacology
-
Physostigmine / pharmacology
-
Receptors, Nicotinic / genetics
-
Receptors, Nicotinic / metabolism*
-
Sensory Deprivation
-
Signal Transduction
-
Vision, Ocular*
-
Visual Cortex / physiology*
-
Visual Pathways
Substances
-
Adaptor Proteins, Signal Transducing
-
Cholinesterase Inhibitors
-
Lynx1 protein, mouse
-
Membrane Glycoproteins
-
Neuropeptides
-
Nicotinic Antagonists
-
Receptors, Nicotinic
-
Mecamylamine
-
Physostigmine