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

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.

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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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Layer differences in the effect of monocular vision in light- and dark-reared kittens

Visual Neuroscience ◽

10.1017/s0952523801185147 ◽

2001 ◽

Vol 18 (5) ◽

pp. 811-820 ◽

Cited By ~ 20

Author(s):

CHRISTOPHER J. BEAVER ◽

QINGHUA JI ◽

NIGEL W. DAW

Keyword(s):

Visual Cortex ◽

Critical Period ◽

Ocular Dominance ◽

Large Change ◽

Monocular Deprivation ◽

Monocular Vision ◽

Ocular Dominance Plasticity ◽

The Difference ◽

Dark Rearing

We compared the effect of 2 days of monocular vision on the ocular dominance of cells in the visual cortex of light-reared kittens with the effect in dark-reared kittens at 6, 9, and 14 weeks of age, and analyzed the results by layer. The size of the ocular-dominance shift declined with age in all layers in light-reared animals. There was not a large change in the ocular-dominance shift with age in dark-reared animals in any layer, suggesting that dark rearing largely keeps the cortex in the immature 6-week state until 14 weeks or longer, although there was a slight decrease in layers II, III, and IV, and a slight increase in layers V and VI. At 14 weeks, the difference between light- and dark-reared animals was smallest in layer IV, larger in layers II/III, and largest in layers V/VI, suggesting that dark rearing has a large effect on intracortical synapses and a small effect on geniculocortical synapses. There was a significant ocular-dominance shift in layer IV at 14 weeks of age in both light- animals and dark-reared animals, showing that the critical period for ocular-dominance plasticity is not ended at this age. While the ocular-dominance shift after 26 h of monocular deprivation in 6-week animals was similar in light- and dark-reared animals, after 14 h it was smaller in dark-reared animals, showing that ocular-dominance changes occur more slowly in dark-reared animals at this age, in agreement with Mower (1991). Increases in selectivity for axis of movement after 26 h of monocular vision were seen in dark-reared animals at 6 weeks of age, but not at 9 or 14 weeks of age, showing that the critical period for axial selectivity ends earlier than the critical period for ocular dominance in dark-reared animals, as it does in light-reared animals.

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Visual plasticity and exercise revisited: no evidence for a “cycling lane”

10.1101/448498 ◽

2018 ◽

Cited By ~ 2

Author(s):

Abigail E Finn ◽

Alex S Baldwin ◽

Alexandre Reynaud ◽

Robert F Hess

Keyword(s):

Ocular Dominance ◽

Monocular Deprivation ◽

Visual Plasticity ◽

Deprivation Period ◽

Deprivation Effect ◽

Adult Humans ◽

Before And After ◽

Exercise Effect ◽

The Difference ◽

Enriched Environments

AbstractExperiments using enriched environments have shown that physical exercise modulates visual plasticity in rodents. A recent study (Lunghi & Sale, 2015, doi: 10.1016/j.cub.2015.10.026) investigated whether exercise also affects visual plasticity in adult humans. The plastic effect they measured was the shift in ocular dominance caused by 2 hours of monocular deprivation (e.g. by an eye patch). They used a binocular rivalry task to measure this shift. They found that the magnitude of the shift was increased by exercise during the deprivation period. This effect of exercise was later disputed by a study that used a different behavioural task (Zhouet al., 2017, doi: 10.1155/2017/4780876). Our goal was to determine whether the difference in task was responsible for that study’s failure to find an exercise effect. We set out to replicate Lunghi & Sale (2015). We measured ocular dominance with a rivalry task before and after 2 hours of deprivation. We measured data from two conditions in 30 subjects. On two separate days they either performed exercise or rested during the deprivation period. Contrary to the previous study, we find no significant effect of exercise. We hypothesise that exercise may affect rivalry dynamics in a way that interacts with the measurement of the deprivation effect.

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Obstructive Sleep Apnea in Acromegaly and the Effect of Treatment: A Systematic Review and Meta-Analysis

The Journal of Clinical Endocrinology & Metabolism ◽

10.1210/clinem/dgz116 ◽

2019 ◽

Vol 105 (3) ◽

pp. e23-e31 ◽

Cited By ~ 1

Author(s):

Matteo Parolin ◽

Francesca Dassie ◽

Luigi Alessio ◽

Alexandra Wennberg ◽

Marco Rossato ◽

...

Keyword(s):

Obstructive Sleep Apnea ◽

Sleep Apnea ◽

Meta Analysis ◽

Upper Airway ◽

Apnea Hypopnea Index ◽

Cross Sectional ◽

Obstructive Sleep ◽

Before And After ◽

The Difference

Abstract Background Obstructive sleep apnea (OSA) is a common disorder characterized by upper airway collapse requiring nocturnal ventilatory assistance. Multiple studies have investigated the relationship between acromegaly and OSA, reporting discordant results. Aim To conduct a meta-analysis on the risk for OSA in acromegaly, and in particular to assess the role of disease activity and the effect of treatments. Methods and Study Selection A search through literature databases retrieved 21 articles for a total of 24 studies (n = 734). Selected outcomes were OSA prevalence and apnea-hypopnea index (AHI) in studies comparing acromegalic patients with active (ACT) vs inactive (INACT) disease and pretreatment and posttreatment measures. Factors used for moderator and meta-regression analysis included the percentage of patients with severe OSA, patient sex, age, body mass index, levels of insulin-like growth factor 1, disease duration and follow-up, and therapy. Results OSA prevalence was similar in patients with acromegaly who had ACT and INACT disease (ES = −0.16; 95% CI, −0.47 to 0.15; number of studies [k] = 10; P = 0.32). In addition, AHI was similar in ACT and INACT acromegaly patients (ES = −0.03; 95% CI, −0.49 to 0.43; k = 6; P = 0.89). When AHI was compared before and after treatment in patients with acromegaly (median follow-up of 6 months), a significant improvement was observed after treatment (ES = −0.36; 95% CI, −0.49 to −0.23; k = 10; P < 0.0001). In moderator analysis, the percentage of patients with severe OSA in the populations significantly influenced the difference in OSA prevalence (P = 0.038) and AHI (P = 0.04) in ACT vs INACT patients. Conclusion Prevalence of OSA and AHI is similar in ACT and INACT patients in cross-sectional studies. However, when AHI was measured longitudinally before and after treatment, a significant improvement was observed after treatment.

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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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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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Rapid eye movement sleep promotes cortical plasticity in the developing brain

Science Advances ◽

10.1126/sciadv.1500105 ◽

2015 ◽

Vol 1 (6) ◽

pp. e1500105 ◽

Cited By ~ 59

Author(s):

Michelle C. Dumoulin Bridi ◽

Sara J. Aton ◽

Julie Seibt ◽

Leslie Renouard ◽

Tammi Coleman ◽

...

Keyword(s):

Eye Movement ◽

Developmental Plasticity ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Developing Brain ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Ocular Dominance Plasticity ◽

Extracellular Signal Regulated Kinase ◽

Extracellular Signal

Rapid eye movement sleep is maximal during early life, but its function in the developing brain is unknown. We investigated the role of rapid eye movement sleep in a canonical model of developmental plasticity in vivo (ocular dominance plasticity in the cat) induced by monocular deprivation. Preventing rapid eye movement sleep after monocular deprivation reduced ocular dominance plasticity and inhibited activation of a kinase critical for this plasticity (extracellular signal–regulated kinase). Chronic single-neuron recording in freely behaving cats further revealed that cortical activity during rapid eye movement sleep resembled activity present during monocular deprivation. This corresponded to times of maximal extracellular signal–regulated kinase activation. These findings indicate that rapid eye movement sleep promotes molecular and network adaptations that consolidate waking experience in the developing brain.

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