Ocular dominance plasticity: Molecular mechanisms revisited

2020 ◽  
Vol 528 (17) ◽  
pp. 3039-3074
Author(s):  
Takuji Kasamatsu ◽  
Kazuyuki Imamura
1998 ◽  
Vol 31 ◽  
pp. S181
Author(s):  
Kazuhiko Nakadate ◽  
Kazuyuki Imamura ◽  
Masayuki Kobayashi ◽  
Peter A. Kaub ◽  
Yasuyoshi Watanabe

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker

Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.


2013 ◽  
Vol 33 (29) ◽  
pp. 11774-11778 ◽  
Author(s):  
U. Matthies ◽  
J. Balog ◽  
K. Lehmann

2018 ◽  
Vol 35 ◽  
Author(s):  
TAKAO K. HENSCH ◽  
ELIZABETH M. QUINLAN

AbstractThe shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.


2019 ◽  
Vol 56 (9) ◽  
pp. 5987-5997 ◽  
Author(s):  
Elena Maria Boggio ◽  
Erich M. Ehlert ◽  
Leonardo Lupori ◽  
Elizabeth B. Moloney ◽  
Fred De Winter ◽  
...  

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