Long-Term Visual Training Increases Visual Acuity and Long-Term Monocular Deprivation Promotes Ocular Dominance Plasticity in Adult Standard Cage-Raised Mice

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

eLife ◽

10.7554/elife.54455 ◽

2020 ◽

Vol 9 ◽

Cited By ~ 3

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.

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Long-Term Potentiation and Long-Term Depression as Early Steps in Ocular Dominance Plasticity

Visual Development ◽

10.1007/0-387-30484-3_12 ◽

2006 ◽

pp. 235-242

Keyword(s):

Ocular Dominance ◽

Long Term Potentiation ◽

Ocular Dominance Plasticity ◽

Long Term Depression ◽

Term Potentiation

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Augmented Reality as a Tool for Studying Visual Plasticity: 2009 to 2018

Current Directions in Psychological Science ◽

10.1177/0963721419862290 ◽

2019 ◽

Vol 28 (6) ◽

pp. 574-580 ◽

Cited By ~ 1

Author(s):

Min Bao ◽

Stephen A. Engel

Keyword(s):

Augmented Reality ◽

Recent Progress ◽

Ocular Dominance ◽

Basic Research ◽

Psychological Research ◽

Ocular Dominance Plasticity ◽

Contrast Adaptation ◽

Visual Disorders ◽

Medicine Education

Augmented reality (AR) has developed rapidly since its conception less than 30 years ago and is now a hot topic for both consumers and scientists. Although much attention has been paid to its application in industry, medicine, education, and entertainment, the use of AR in psychological research has been less noted. In this article, we survey recent progress in basic research that uses AR to explore the plasticity of the adult visual system. We focus on a particular application of AR called altered reality, which has been used to shed new light on mechanisms of long-term contrast adaptation and ocular-dominance plasticity. The results suggest that AR could also be a useful tool for the treatment of visual disorders.

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Orientation Selectivity Is Reduced by Monocular Deprivation in Combination With PKA Inhibitors

Journal of Neurophysiology ◽

10.1152/jn.2002.88.4.1933 ◽

2002 ◽

Vol 88 (4) ◽

pp. 1933-1940 ◽

Cited By ~ 6

Author(s):

Chris J. Beaver ◽

Quentin S. Fischer ◽

Qinghua Ji ◽

Nigel W. Daw

Keyword(s):

Visual Cortex ◽

Protein Kinase ◽

Critical Period ◽

Ocular Dominance ◽

Receptive Fields ◽

Direction Selectivity ◽

Orientation Selectivity ◽

Monocular Deprivation ◽

Ocular Dominance Plasticity ◽

Kinase A

We have previously shown that the protein kinase A (PKA) inhibitor, 8-chloroadenosine-3′,5′–monophosphorothioate (Rp-8-Cl-cAMPS), abolishes ocular dominance plasticity in the cat visual cortex. Here we investigate the effect of this inhibitor on orientation selectivity. The inhibitor reduces orientation selectivity in monocularly deprived animals but not in normal animals. In other words, PKA inhibitors by themselves do not affect orientation selectivity, nor does monocular deprivation by itself, but monocular deprivation in combination with a PKA inhibitor does affect orientation selectivity. This result is found for the receptive fields in both deprived and nondeprived eyes. Although there is a tendency for the orientation selectivity in the nondeprived eye to be higher than the orientation selectivity in the deprived eye, the orientation selectivity in both eyes is considerably less than normal. The result is striking in animals at 4 wk of age. The effect of the monocular deprivation on orientation selectivity is reduced at 6 wk of age and absent at 9 wk of age, while the effect on ocular dominance shifts is less changed in agreement with previous results showing that the critical period for orientation/direction selectivity ends earlier than the critical period for ocular dominance. We conclude that closure of one eye in combination with inhibition of PKA reduces orientation selectivity during the period that orientation selectivity is still mutable and that the reduction in orientation selectivity is transferred to the nondeprived eye.

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Epigenetic treatments of adult rats promote recovery from visual acuity deficits induced by long-term monocular deprivation

European Journal of Neuroscience ◽

10.1111/j.1460-9568.2010.07261.x ◽

2010 ◽

Vol 31 (12) ◽

pp. 2185-2192 ◽

Cited By ~ 59

Author(s):

Davide Silingardi ◽

Manuela Scali ◽

Giulio Belluomini ◽

Tommaso Pizzorusso

Keyword(s):

Visual Acuity ◽

Monocular Deprivation ◽

Adult Rats

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Metabotropic glutamate receptor signaling is required for NMDA receptor-dependent ocular dominance plasticity and LTD in visual cortex

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1512878112 ◽

2015 ◽

Vol 112 (41) ◽

pp. 12852-12857 ◽

Cited By ~ 15

Author(s):

Michael S. Sidorov ◽

Eitan S. Kaplan ◽

Emily K. Osterweil ◽

Lothar Lindemann ◽

Mark F. Bear

Keyword(s):

Visual Cortex ◽

Glutamate Receptor ◽

Metabotropic Glutamate Receptor ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Excitatory Synapses ◽

Ocular Dominance Plasticity ◽

Metabotropic Glutamate

A feature of early postnatal neocortical development is a transient peak in signaling via metabotropic glutamate receptor 5 (mGluR5). In visual cortex, this change coincides with increased sensitivity of excitatory synapses to monocular deprivation (MD). However, loss of visual responsiveness after MD occurs via mechanisms revealed by the study of long-term depression (LTD) of synaptic transmission, which in layer 4 is induced by acute activation of NMDA receptors (NMDARs) rather than mGluR5. Here we report that chronic postnatal down-regulation of mGluR5 signaling produces coordinated impairments in both NMDAR-dependent LTD in vitro and ocular dominance plasticity in vivo. The data suggest that ongoing mGluR5 signaling during a critical period of postnatal development establishes the biochemical conditions that are permissive for activity-dependent sculpting of excitatory synapses via the mechanism of NMDAR-dependent LTD.

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

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.2105388118 ◽

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.

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Lateral geniculate neurons show robust ocular dominance plasticity

10.1101/097923 ◽

2017 ◽

Author(s):

Juliane Jäpel ◽

Mark Hübener ◽

Tobias Bonhoeffer ◽

Tobias Rose

Keyword(s):

Visual Cortex ◽

Visual System ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Ocular Dominance Plasticity ◽

Dependent Plasticity ◽

Two Photon ◽

Lateral Geniculate

AbstractExperience-dependent plasticity in the mature visual system is considered exclusively cortical. Using chronic two-photon Ca2+ imaging, we found evidence against this tenet: dLGN cells showed robust ocular dominance shifts after monocular deprivation. Most, but not all responses of dLGN cell boutons in binocular visual cortex were monocular during baseline. Following deprivation, however, deprived-eye dominated boutons became responsive to the non-deprived eye. Thus, plasticity of dLGN neurons contributes to cortical ocular dominance shifts.

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