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[S2.2]: Regulation of ciliogenesis in mammalian development and disease
Author(s) -
GarciaGonzalo F.,
Corbit K.,
Wong S.Y.,
Seol A.D.,
Reiter J.F.
Publication year - 2010
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2010.07.014
Subject(s) - garcia , ciliogenesis , library science , citation , humanities , history , philosophy , computer science , biology , biochemistry , gene
Heightened cortical plasticity during postnatal critical periods wanes with age to consolidate neural circuits and behavior. Such rigidity in turn limits recovery from injury or developmental disorders. Identifying these mechanisms carries a broad impact for therapeutic approaches, but is often hampered by complex etiologies and distributed networks. An approachable model is the permanent loss of visual acuity (amblyopia) following sensory deprivation within primary visual cortex, which does not readily recover later in life. Here, we identify two classes of “molecular brakes” on (1) structural growth (acute myelin-related Nogo receptor signaling), and (2) neuromodulation (Lynx1 suppression of nicotinic cholinergic receptor signaling) that actively limit plasticity in adulthood. Removal of these brakes notably restores visual acuity to normal levels simply upon reopening the eye rendered amblyopic earlier in life. Given the widespread distribution of these factors, they may offer a more general model for understanding cognitive development and for treating disorders of similar origin in early postnatal life.