Homeostatic plasticity mechanisms are required for juvenile, but not adult, ocular dominance plasticity

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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Rem2 regulates distinct homeostatic mechanisms in visual circuit plasticity

10.1101/208975 ◽

2017 ◽

Author(s):

Anna R. Moore ◽

Sarah E. Richards ◽

Katelyn Kenny ◽

Leandro de Oliveira Royer ◽

Urann Chan ◽

...

Keyword(s):

Cortical Neurons ◽

Neural Circuit ◽

Ocular Dominance ◽

Scaling Up ◽

Homeostatic Plasticity ◽

Intrinsic Excitability ◽

Neuronal Membrane ◽

List Type ◽

Ocular Dominance Plasticity

SUMMARYActivity-regulated genes sculpt neural circuits in response to sensory experience. These calcium-sensitive genes generally fall into two categories: transcription factors and proteins that function at synapses. Yet little is known about activity-regulated, cytosolic proteins that transduce signals between the neuronal membrane and the nucleus. Using the visual system as a model, we investigated the role of the activity-regulated, non-canonical Ras-like GTPase Rem2 in vivo. We demonstrate that Rem2-/- mice fail to exhibit normal ocular dominance plasticity during the critical period. At the circuit level, cortical layer 2/3 neurons in Rem2-/- mice show deficits in both postsynaptic scaling up of excitatory synapses and misregulation of intrinsic excitability. Further, we reveal that Rem2 plays a novel, cell-autonomous role in regulating neuronal intrinsic excitability. Thus, Rem2 is a critical regulator of neural circuit function and distinct homeostatic plasticity mechanisms in vivo.HIGHLIGHTSRem2 is required in excitatory cortical neurons for normal ocular dominance plasticityRem2 regulates postsynaptic homoeostatic synaptic scaling upRem2 alters the intrinsic excitability of neurons in a cell-autonomous manner

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Can ocular dominance plasticity provide a general index to visual plasticity to personalize treatment in amblyopia?

10.1101/2020.03.26.20044701 ◽

2020 ◽

Author(s):

Chunwen Tao ◽

Zhifen He ◽

Yiya Chen ◽

Jiawei Zhou ◽

Robert F. Hess

Keyword(s):

Visual Acuity ◽

Cortical Plasticity ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Homeostatic Plasticity ◽

Ocular Dominance Plasticity ◽

Anisometropic Amblyopia ◽

Occlusion Therapy ◽

General Index ◽

Before And After

AbstractPurposeRecently, Lunghi et al showed that amblyopic eye’s visual acuity per se after 2 months of occlusion therapy could be predicted by a homeostatic plasticity, i.e., the temporary shift of ocular dominance observed after a 2-hour monocular deprivation, in children with anisometropic amblyopia(Lunghi et al., 2016). In this study, we assess whether the visual acuity improvement of the amblyopic eye measured after 2 months of occlusion therapy could be predicted by this plasticity.MethodsSeven children (6.86 ± 1.46 years old; SD) with anisometropic amblyopia participated in this study. All patients were newly diagnosed and had no treatment history before participating in our study. They had finished 2 months of refractive adaptation and then received a 4-hour daily fellow eye patching therapy with an opaque patch for a 2-month period. Best-corrected visual acuity of the amblyopic eye was measured before and after the patching therapy. The homeostatic plasticity was assessed by measuring the temporary shift of ocular dominance observed after 2 hours of occlusion for the amblyopic eye before the treatment started. A binocular phase combination paradigm was used for this test.ResultsWe found that there was no significant correlation between the temporary shift of ocular dominance observed after 2 hours of occlusion for the amblyopic eye before the treatment started and the visual acuity gain obtained by the amblyopic eye from 2-month of classical patching therapy. This result involving the short-term patching of the amblyopic eye is consistent with a reanalysis of Lunghi et al’ s data.ConclusionsOcular dominance plasticity does not provide an index of cortical plasticity in the general sense such that it could be used to predict acuity outcomes from longer term classical patching.

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Enhancement of visual cortex plasticity by dark exposure

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2016.0159 ◽

2017 ◽

Vol 372 (1715) ◽

pp. 20160159 ◽

Cited By ~ 13

Author(s):

Irina Erchova ◽

Asta Vasalauskaite ◽

Valentina Longo ◽

Frank Sengpiel

Keyword(s):

Visual Cortex ◽

Critical Period ◽

Time Course ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Homeostatic Plasticity ◽

Ocular Dominance Plasticity ◽

Intrinsic Signals ◽

Significant Difference ◽

Dark Exposure

Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory–inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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Sleep Slow Oscillations and Spindles encode ocular dominance plasticity and promote its consolidation in adult humans

10.1101/2021.03.31.437408 ◽

2021 ◽

Author(s):

Danilo Menicucci ◽

Claudia Lunghi ◽

Andrea Zaccaro ◽

Maria Concetta Morrone ◽

Angelo Gemignani

Keyword(s):

Cortical Plasticity ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Homeostatic Plasticity ◽

Ocular Dominance Plasticity ◽

Slow Oscillations ◽

Adult Humans ◽

The Individual ◽

Visual Cortical

Sleep and plasticity are highly interrelated, as sleep slow oscillations and sleep spindles are associated with consolidation of Hebbian-based processes. However, in adult humans, visual cortical plasticity is mainly sustained by homeostatic mechanisms, for which the role of sleep is still largely unknown. Here we demonstrate that non-REM sleep stabilizes homeostatic plasticity of ocular dominance in adult humans. We found that the effect of short-term monocular deprivation (boost of the deprived eye) was preserved at the morning awakening (>6 hours after deprivation). Subjects exhibiting stronger consolidation had increased sleep spindle density in frontopolar electrodes, suggesting distributed consolidation processes. Crucially, the individual susceptibility to visual homeostatic plasticity was encoded by changes in sleep slow oscillation rate and shape and spindle power in occipital sites, consistent with an early visual cortical site of ocular dominance homeostatic plasticity.

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