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The development of cortical columns: role of Fragile X mental retardation protein
Author(s) -
Bureau Ingrid
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2008.167155
Subject(s) - neuroscience , fragile x syndrome , fmr1 , sensory system , glutamatergic , neuroplasticity , biological neural network , cerebral cortex , biology , sensory deprivation , cortex (anatomy) , psychology , fragile x , glutamate receptor , receptor , genetics , gene
Neuronal circuits in the brain are complex and precise. Here, I review aspects of the development of cortical columns in the rodent barrel cortex, focusing on the anatomical and functional data describing the maturation of ascending glutamatergic circuits. Projections from layer 4 to layer 3 develop into cortical columns with little macroscopic refinement. Depriving animals of normal sensory experience induces long‐term synaptic depression but does not perturb this pattern of development. Mouse models of mental retardation can help us understand the mechanisms of development of cortical columns. Fmr1 knock‐out (ko) mice, a model for Fragile X syndrome, lack Fragile X mental retardation protein (FMRP), a suppressor of translation present in synapses. Because FMRP expression is stimulated by neuronal activity, Fmr1 ‐ko mice provide a model to survey the role of sensory input in brain development. Layer 4 to layer 3 projections are altered in multiple ways in the young mutant mice: connection rate is low and layer 4 cell axons are spatially diffuse. Sensory deprivation rescues the connection rate phenotype. The interaction of FMRP and neuronal activity in the development of cortical circuits is discussed.