scholarly journals Experience-Dependent Plasticity of Mouse Visual Cortex in the Absence of the Neuronal Activity-Dependent Markeregr1/zif268

2001 ◽  
Vol 21 (24) ◽  
pp. 9724-9732 ◽  
Author(s):  
Nobuko Mataga ◽  
Sayaka Fujishima ◽  
Brian G. Condie ◽  
Takao K. Hensch
Keyword(s):  
Visual Cortex ◽  
Neuronal Activity ◽  
Dependent Plasticity ◽  
Mouse Visual Cortex ◽  
Activity Dependent

The role of ZIF268/EGR-1 during activity-dependent plasticity of developing visual cortex

1998 ◽  
Vol 31 ◽  
pp. S324
Author(s):  
Nobuko Mataga ◽  
Brian G. Condie ◽  
Sayaka Fujishima ◽  
Takao K. Hensch
Keyword(s):  
Visual Cortex ◽  
Dependent Plasticity ◽  
Activity Dependent

scholarly journals Neurofilament Protein and Neuronal Activity Markers Define Regional Architectonic Parcellation in the Mouse Visual Cortex

2007 ◽  
Vol 17 (12) ◽  
pp. 2805-2819 ◽  
Author(s):  
E. Van der Gucht ◽  
P. R. Hof ◽  
L. Van Brussel ◽  
K. Burnat ◽  
L. Arckens
Keyword(s):  
Visual Cortex ◽  
Neuronal Activity ◽  
Neurofilament Protein ◽  
Mouse Visual Cortex

scholarly journals Arc restores juvenile plasticity in adult mouse visual cortex

2017 ◽  
Author(s):  
Kyle R. Jenks ◽  
Taekeun Kim ◽  
Elissa D. Pastuzyn ◽  
Hiroyuki Okuno ◽  
Andrew V. Taibi ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Neural Plasticity ◽  
Critical Period ◽  
Adult Mouse ◽  
Monocular Deprivation ◽  
Protein Synthesis Inhibitor ◽  
Adult Mice ◽  
Mouse Visual Cortex ◽  
Activity Dependent

AbstractThe molecular basis for the decline in experience-dependent neural plasticity over age remains poorly understood. In visual cortex, the robust plasticity induced in juvenile mice by brief monocular deprivation (MD) during the critical period is abrogated by genetic deletion of Arc, an activity-dependent regulator of excitatory synaptic modification. Here we report that augmenting Arc expression in adult mice prolongs juvenile-like plasticity in visual cortex, as assessed by recordings of ocular dominance (OD) plasticity in vivo. A distinguishing characteristic of juvenile OD plasticity is the weakening of deprived-eye responses, believed to be accounted for by the mechanisms of homosynaptic long-term depression (LTD). Accordingly, we also found increased LTD in visual cortex of adult mice with augmented Arc expression, and impaired LTD in visual cortex of juvenile mice that lack Arc or have been treated in vivo with a protein synthesis inhibitor. Further, we found that although activity-dependent expression of Arc mRNA does not change with age, expression of Arc protein is maximal during the critical period and declines in adulthood. Finally, we show that acute augmentation of Arc expression in wild type adult mouse visual cortex is sufficient to restore juvenile-like plasticity. Together, our findings suggest a unifying molecular explanation for the age- and activity-dependent modulation of synaptic sensitivity to deprivation.Significance StatementNeuronal plasticity peaks early in life during critical periods and normally declines with age, but the molecular changes that underlie this decline are not fully understood. Using the mouse visual cortex as a model, we found that activity-dependent expression of the neuronal protein Arc peaks early in life, and that loss of activity-dependent Arc expression parallels loss of synaptic plasticity in the visual cortex. Genetic overexpression of Arc prolongs the critical period of visual cortex plasticity and acute viral expression of Arc in adult mice can restore juvenile-like plasticity. These findings provide a mechanism for the loss of excitatory plasticity with age, and suggest that Arc may be an exciting therapeutic target for modulation of the malleability of neuronal circuits.

Reversible blockade of experience-dependent plasticity by calcineurin in mouse visual cortex

2005 ◽  
Vol 8 (6) ◽  
pp. 791-796 ◽  
Author(s):  
Yupeng Yang ◽  
Quentin S Fischer ◽  
Ying Zhang ◽  
Karsten Baumgärtel ◽  
Isabelle M Mansuy ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Dependent Plasticity ◽  
Mouse Visual Cortex

Gene expression changes and molecular pathways mediating activity-dependent plasticity in visual cortex

2006 ◽  
Vol 9 (5) ◽  
pp. 660-668 ◽  
Author(s):  
Daniela Tropea ◽  
Gabriel Kreiman ◽  
Alvin Lyckman ◽  
Sayan Mukherjee ◽  
Hongbo Yu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Visual Cortex ◽  
Molecular Pathways ◽  
Dependent Plasticity ◽  
Activity Dependent

scholarly journals Synaptic Mechanisms of Activity-Dependent Remodeling in Visual Cortex during Monocular Deprivation

2009 ◽  
Vol 2 ◽  
pp. JEN.S2559 ◽  
Author(s):  
Cynthia D. Rittenhouse ◽  
Ania K Majewska
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Neuronal Structure ◽  
Cortical Cells ◽  
Dependent Plasticity ◽  
Cortical Synapses ◽  
Activity Dependent ◽  
Synaptic Mechanisms

It has long been appreciated that in the visual cortex, particularly within a postnatal critical period for experience-dependent plasticity, the closure of one eye results in a shift in the responsiveness of cortical cells toward the experienced eye. While the functional aspects of this ocular dominance shift have been studied for many decades, their cortical substrates and synaptic mechanisms remain elusive. Nonetheless, it is becoming increasingly clear that ocular dominance plasticity is a complex phenomenon that appears to have an early and a late component. Early during monocular deprivation, deprived eye cortical synapses depress, while later during the deprivation open eye synapses potentiate. Here we review current literature on the cortical mechanisms of activity-dependent plasticity in the visual system during the critical period. These studies shed light on the role of activity in shaping neuronal structure and function in general and can lead to insights regarding how learning is acquired and maintained at the neuronal level during normal and pathological brain development.

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