Cross‐modal restoration of ocular dominance plasticity in adult mice

2018 ◽  
Vol 47 (11) ◽  
pp. 1375-1384 ◽  
Author(s):  
Manuel Teichert ◽  
Marcel Isstas ◽  
Yitong Zhang ◽  
Jürgen Bolz
Keyword(s):  
Ocular Dominance ◽  
Ocular Dominance Plasticity ◽  
Adult Mice

scholarly journals Loss of P2Y12 Has Behavioral Effects in the Adult Mouse

2021 ◽  
Vol 22 (4) ◽  
pp. 1868
Author(s):  
Rebecca L. Lowery ◽  
Monique S. Mendes ◽  
Brandon T. Sanders ◽  
Allison J. Murphy ◽  
Brendan S. Whitelaw ◽  
...  
Keyword(s):  
Synaptic Plasticity ◽  
Ex Vivo ◽  
Purinergic Receptor ◽  
Ocular Dominance ◽  
Developmental Time ◽  
Brain Regions ◽  
Ocular Dominance Plasticity ◽  
Early Form ◽  
Adult Mice ◽  
Molecular Signals

While microglia have been established as critical mediators of synaptic plasticity, the molecular signals underlying this process are still being uncovered. Increasing evidence suggests that microglia utilize these signals in a temporally and regionally heterogeneous manner. Subsequently, it is necessary to understand the conditions under which different molecular signals are employed by microglia to mediate the physiological process of synaptic remodeling in development and adulthood. While the microglial purinergic receptor P2Y12 is required for ocular dominance plasticity, an adolescent form of experience-dependent plasticity, it remains unknown whether P2Y12 functions in other forms of plasticity at different developmental time points or in different brain regions. Using a combination of ex vivo characterization and behavioral testing, we examined how the loss of P2Y12 affects developmental processes and behavioral performance in adulthood in mice. We found P2Y12 was not required for an early form of plasticity in the developing visual thalamus and did not affect microglial migration into barrels in the developing somatosensory cortex. In adult mice, however, the loss of P2Y12 resulted in alterations in recognition and social memory, as well as anxiety-like behaviors, suggesting that while P2Y12 is not a universal regulator of synaptic plasticity, the loss of P2Y12 is sufficient to cause functional defects.

scholarly journals Age-Dependent Ocular Dominance Plasticity in Adult Mice

PLoS ONE ◽  
2008 ◽  
Vol 3 (9) ◽  
pp. e3120 ◽  
Author(s):  
Konrad Lehmann ◽  
Siegrid Löwel
Keyword(s):  
Ocular Dominance ◽  
Ocular Dominance Plasticity ◽  
Adult Mice ◽  
Age Dependent

scholarly journals Cross-modal restoration of juvenile-like ocular dominance plasticity after increasing GABAergic inhibition

2018 ◽  
Author(s):  
Manuel Teichert ◽  
Marcel Isstas ◽  
Franziska Wieske ◽  
Christine Winter ◽  
Jürgen Bolz
Keyword(s):  
Young Adult ◽  
Critical Period ◽  
Hplc Analysis ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Gabaergic Inhibition ◽  
Ocular Dominance Plasticity ◽  
Intrinsic Signal ◽  
Adult Mice ◽  
Contralateral Eye

AbstractIn juvenile and “young adult” mice monocular deprivation (MD) shifts the ocular dominance (OD) of binocular neurons in the primary visual cortex (V1) away from the deprived eye. However, OD plasticity is completely absent in mice older than 110 days, but can be reactivated by treatments which decrease GABA levels in V1. Typically, these OD shifts can be prevented by increasing GABAergic transmission with diazepam. We could recently demonstrate that both bilateral whisker and auditory deprivation (WD, AD), can also restore OD plasticity in mice older than 110 days, since MD for 7 days in WD mice caused a potentiation of V1 input through the ipsilateral (open) eye, the characteristic feature of OD plasticity of “young adult” mice. Here we examined whether WD for 7 days also decreases GABA levels. For this, we performed post mortem HPLC analysis of V1 tissue. Indeed, we found that WD significantly decreased GABA levels in V1. Surprisingly, enhancing GABAergic inhibition by diazepam did not abolish OD shifts in WD mice, as revealed by repeated intrinsic signal imaging. On the contrary, this treatment led to a depression of V1 input through the previously closed contralateral eye, the characteristic signature of OD plasticity in juvenile mice during the critical period. Interestingly, the same result was obtained after AD. Taken together, these results suggest that cross-modally restored OD plasticity does not only depend on reduction of GABA levels in V1, but also requires other, so far unknown mechanisms.

scholarly journals Cross-Modal Reinstatement of Thalamocortical Plasticity Accelerates Ocular Dominance Plasticity in Adult Mice

Cell Reports ◽  
2018 ◽  
Vol 24 (13) ◽  
pp. 3433-3440.e4 ◽  
Author(s):  
Gabriela Rodríguez ◽  
Darpan Chakraborty ◽  
Katrina M. Schrode ◽  
Rinki Saha ◽  
Isabel Uribe ◽  
...  
Keyword(s):  
Ocular Dominance ◽  
Ocular Dominance Plasticity ◽  
Adult Mice

Regulation of ocular dominance plasticity by biogenic amines: An activity mapping using c-FOS immunohistochemistry in rat visual cortex

1998 ◽  
Vol 31 ◽  
pp. S181
Author(s):  
Kazuhiko Nakadate ◽  
Kazuyuki Imamura ◽  
Masayuki Kobayashi ◽  
Peter A. Kaub ◽  
Yasuyoshi Watanabe
Keyword(s):  
Visual Cortex ◽  
Biogenic Amines ◽  
Ocular Dominance ◽  
Ocular Dominance Plasticity

scholarly journals Homeostatic plasticity mechanisms in mouse V1

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Neuronal Activity ◽  
Dynamic Range ◽  
Ocular Dominance ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
The Brain

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’.

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