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

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.

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

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.

scholarly journals All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

2021 ◽  
Vol 118 (37) ◽  
pp. e2105388118
Author(s):  
Daniel Severin ◽  
Su Z. Hong ◽  
Seung-Eon Roh ◽  
Shiyong Huang ◽  
Jiechao Zhou ◽  
...  
Keyword(s):  
Cortical Plasticity ◽  
Classical Model ◽  
Ocular Dominance ◽  
Pyramidal Cells ◽  
Initial Step ◽  
Monocular Deprivation ◽  
Cortical Circuits ◽  
Ocular Dominance Plasticity ◽  
Layer 2 ◽  
Mouse Visual Cortex

Disinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience. Our investigation on disinhibitory mechanisms in the classical model of ocular dominance plasticity uncovered an unexpected form of experience-dependent circuit plasticity. In the layer 2/3 of mouse visual cortex, monocular deprivation triggers a complete, “all-or-none,” elimination of connections from pyramidal cells onto nearby parvalbumin-positive interneurons (Pyr→PV). This binary form of circuit plasticity is unique, as it is transient, local, and discrete. It lasts only 1 d, and it does not manifest as widespread changes in synaptic strength; rather, only about half of local connections are lost, and the remaining ones are not affected in strength. Mechanistically, the deprivation-induced loss of Pyr→PV is contingent on a reduction of the protein neuropentraxin2. Functionally, the loss of Pyr→PV is absolutely necessary for ocular dominance plasticity, a canonical model of deprivation-induced model of cortical remodeling. We surmise, therefore, that this all-or-none loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.

scholarly journals Exercise does not enhance short-term deprivation-induced ocular dominance plasticity: evidence from dichoptic surround suppression

2020 ◽  
Author(s):  
Alex S Baldwin ◽  
Hayden M Green ◽  
Abigail E Finn ◽  
Nicholas Gant ◽  
Robert F Hess
Keyword(s):  
Meta Analysis ◽  
Ocular Dominance ◽  
Relative Strength ◽  
Monocular Deprivation ◽  
Sinusoidal Grating ◽  
Surround Suppression ◽  
Ocular Dominance Plasticity ◽  
Exercise Condition ◽  
Before And After ◽  
The Difference

AbstractThe input from the two eyes is combined in the brain. In this combination, the relative strength of the input from each eye is determined by the ocular dominance. Recent work has shown that this dominance can be temporarily shifted. Covering one eye with an eye patch for a few hours makes its contribution stronger. It has been proposed that this shift can be enhanced by exercise. Here, we test this hypothesis using a dichoptic surround suppression task, and with exercise performed according to American College of Sport Medicine guidelines. We measured detection thresholds for patches of sinusoidal grating shown to one eye. When an annular mask grating was shown simultaneously to the other eye, thresholds were elevated. The difference in the elevation found in each eye is our measure of relative eye dominance. We made these measurements before and after 120 minutes of monocular deprivation (with an eye patch). In the control condition, subjects rested during this time. For the exercise condition, 30 minutes of exercise were performed at the beginning of the patching period. This was followed by 90 minutes of rest. We find that patching results in a shift in ocular dominance that can be measured using dichoptic surround suppression. However, we find no effect of exercise on the magnitude of this shift. We further performed a meta-analysis on the four studies that have examined the effects of exercise on the dominance shift. Looking across these studies, we find no evidence for such an effect.

scholarly journals Pull-Push Neuromodulation of Cortical Plasticity Enables Rapid Bi-Directional Shifts in Ocular Dominance

2019 ◽  
Author(s):  
Su Z. Hong ◽  
Shiyong Huang ◽  
Daniel Severin ◽  
Alfredo Kirkwood
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation ◽  
Visual Cortical

SUMMARYNeuromodulatory systems are essential for remodeling glutamatergic connectivity during experience-dependent cortical plasticity. This permissive/enabling function of neuromodulators has been associated with their capacity to facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability. In vitro studies indicate that neuromodulators can also affect the expression of Hebbian plasticity in a pull-push manner: receptors coupled to the G-protein Gs promote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense of LTD. Here we show that the pull-push mechanism can be recruited in vivo by pairing brief monocular stimulation with pharmacological or chemogenetical activation of Gs- or Gq-coupled receptors to respectively enhance or reduce visual cortical responses. These changes were stable, can be induced in adults after the termination of the critical period for juvenile ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

scholarly journals Enhancement of visual cortex plasticity by dark exposure

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160159 ◽  
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’.

scholarly journals All-or-none disconnection of pyramidal inputs onto parvalbumin-positive interneurons gates ocular dominance plasticity

2021 ◽  
Author(s):  
Daniel Severin ◽  
Su Z. Hong ◽  
Seung-Eon Roh ◽  
Jiechao Zhou ◽  
Michelle C. D. Bridi ◽  
...  
Keyword(s):  
Critical Period ◽  
Cortical Plasticity ◽  
Classical Model ◽  
Ocular Dominance ◽  
Pyramidal Cells ◽  
Initial Step ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Reversible Loss ◽  
Underlying Mechanisms

ABSTRACTDisinhibition is an obligatory initial step in the remodeling of cortical circuits by sensory experience, yet the underlying mechanisms remain unclear. Our investigation of mechanisms for disinhibition in the classical model of ocular dominance plasticity (ODP) uncovered an unexpected novel form of experience-dependent circuit plasticity. In layer 2/3 of mouse visual cortex monocular deprivation triggers an “all-or-none” elimination of approximately half the connections from local pyramidal cells onto parvalbumin-positive interneurons (Pyr→PV), without affecting the strength of the remaining connections. This loss of Pyr→PV connections is transient, lasting one day only, has a critical period commensurate with the ODP critical period, and is contingent on a reduction of neuropentraxin2 (NPTX2), which normally stabilizes Pyr→PV connections. Bidirectional manipulations of NPTX2 functionality that prevent/promote the elimination Pyr→PV connections also promote/prevent ODP. We surmise, therefore, that this rapid and reversible loss of local Pyr→PV circuitry gates experience-dependent cortical plasticity.

scholarly journals Pull-push neuromodulation of cortical plasticity enables rapid bi-directional shifts in ocular dominance

eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Su Z Hong ◽  
Shiyong Huang ◽  
Daniel Severin ◽  
Alfredo Kirkwood
Keyword(s):  
Cortical Plasticity ◽  
Ocular Dominance ◽  
Long Term Potentiation ◽  
Monocular Deprivation ◽  
Ocular Dominance Plasticity ◽  
Hebbian Plasticity ◽  
Term Potentiation

Neuromodulatory systems are essential for remodeling glutamatergic connectivity during experience-dependent cortical plasticity. This permissive/enabling function of neuromodulators has been associated with their capacity to facilitate the induction of Hebbian forms of long-term potentiation (LTP) and depression (LTD) by affecting cellular and network excitability. In vitro studies indicate that neuromodulators also affect the expression of Hebbian plasticity in a pull-push manner: receptors coupled to the G-protein Gs promote the expression of LTP at the expense of LTD, and Gq-coupled receptors promote LTD at the expense of LTP. Here we show that pull-push mechanisms can be recruited in vivo by pairing brief monocular stimulation with pharmacological or chemogenetical activation of Gs- or Gq-coupled receptors to respectively enhance or reduce neuronal responses in primary visual cortex. These changes were stable, inducible in adults after the termination of the critical period for ocular dominance plasticity, and can rescue deficits induced by prolonged monocular deprivation.

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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