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Robert F Hess - One of the best experts on this subject based on the ideXlab platform.
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action video gaming does not influence short term Ocular Dominance plasticity in visually normal adults
eNeuro, 2020Co-Authors: Xiaoxin Chen, Yiya Chen, Zhimo Yao, Shijia Chen, Deying Kong, Junhan Wei, Yu Mao, Wenman Lin, Seung Hyun Min, Robert F HessAbstract:Action video gaming can promote neural plasticity. Short-term monOcular patching drives neural plasticity in the visual system of human adults. For instance, short-term monOcular patching of 0.5-5 h briefly enhances the patched eye's contribution in binOcular vision (i.e., short-term Ocular Dominance plasticity). In this study, we investigate whether action video gaming can influence this plasticity in adults with normal vision. We measured participants' eye Dominance using a binOcular phase combination task before and after 2.5 h of monOcular patching. Participants were asked to play action video games, watch action video game movies, or play non-action video games during the period of monOcular patching. We found that participants' change of Ocular Dominance after monOcular patching was not significantly different either for playing action video games versus watching action video game movies (Comparison 1) or for playing action video games versus playing non-action video games (Comparison 2). These results suggest that action video gaming does not either boost or eliminate short-term Ocular Dominance plasticity, and that the neural site for this type of plasticity might be in the early visual pathway.
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Ocular Dominance plasticity a binOcular combination task finds no cumulative effect with repeated patching
Vision Research, 2019Co-Authors: Seung Hyun Min, Alex S Baldwin, Robert F HessAbstract:Abstract Short-term monOcular deprivation strengthens the contribution of the deprived eye to binOcular vision. This change has been observed in adults with normal vision or amblyopia. The change in Ocular Dominance is transient and recovers over approximately one hour. This shift has been measured with various visual tasks, including binOcular rivalry and binOcular combination. We investigated whether the Ocular Dominance shift could be accumulated across multiple periods of monOcular deprivation over consecutive days. We used a binOcular phase combination task to measure the shift in eye Dominance. We patched the dominant eye of ten adults with normal vision for two hours across five consecutive days. Our results show no cumulative effect after repeated sessions of short-term monOcular deprivation.
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the shift in Ocular Dominance from short term monOcular deprivation exhibits no dependence on duration of deprivation
Scientific Reports, 2018Co-Authors: Seung Hyun Min, Alex S Baldwin, Alexandre Reynaud, Robert F HessAbstract:Deprivation of visual information from one eye for a 120-minute period in normal adults results in a temporary strengthening of the patched eye’s contribution to binOcular vision. This plasticity for Ocular Dominance in adults has been demonstrated by binOcular rivalry as well as binOcular fusion tasks. Here, we investigate how its dynamics depend on the duration of the monOcular deprivation. Using a binOcular combination task, we measure the magnitude and recovery of Ocular Dominance change after durations of monOcular deprivation ranging from 15 to 300 minutes. Surprisingly, our results show that the dynamics are of an all-or-none form. There was virtually no significant dependence on the duration of the initial deprivation.
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the cortical mechanisms underlying Ocular Dominance plasticity in adults are not orientationally selective
Neuroscience, 2017Co-Authors: Yonghua Wang, Jiawei Zhou, Zhimo Yao, Robert F HessAbstract:Abstract Recently, it has been shown that short-term monOcular deprivation in adult humans can temporally shift the Ocular Dominance in favor of the deprived eye. It is not clear whether this form of Ocular Dominance plasticity can be explained by cortical contrast adaptation, which is known to be orientationally selective. Here we show that if only one eye is deprived of a limited band of orientations for a short period of 2.5 h, the deprived eye’s contribution to binOcular function at all orientations rather than just those corresponding to the previously deprived orientations is strengthened. This isotropic enhancement is quite different from the orientational enhancement previously reported and suggests a separate neuroplastic mechanism specific to binOcular function.
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aerobic exercise effects on Ocular Dominance plasticity with a phase combination task in human adults
Neural Plasticity, 2017Co-Authors: Jiawei Zhou, Alexandre Reynaud, Robert F HessAbstract:Several studies have shown that short-term monOcular patching can induce Ocular Dominance plasticity in normal adults, in which the patched eye becomes stronger in binOcular viewing. There is a recent study showing that exercise enhances this plasticity effect when assessed with binOcular rivalry. We address one question, is this enhancement from exercise a general effect such that it is seen for measures of binOcular processing other than that revealed using binOcular rivalry? Using a binOcular phase combination task in which we directly measure each eye’s contribution to the binOcularly fused percept, we show no additional effect of exercise after short-term monOcular occlusion and argue that the enhancement of Ocular Dominance plasticity from exercise could not be demonstrated with our approach.
Michael P Stryker - One of the best experts on this subject based on the ideXlab platform.
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distinctive features of adult Ocular Dominance plasticity
The Journal of Neuroscience, 2008Co-Authors: Masaaki Sato, Michael P StrykerAbstract:Sensory experience profoundly shapes neural circuitry of juvenile brain. Although the visual cortex of adult rodents retains a capacity for plasticity in response to monOcular visual deprivation, the nature of this plasticity and the neural circuit changes that accompany it remain enigmatic. Here, we investigate differences between adult and juvenile Ocular Dominance plasticity using Fourier optical imaging of intrinsic signals in mouse visual cortex. This comparison reveals that adult plasticity takes longer than in the juvenile mouse, is of smaller magnitude, has a greater contribution from the increase in response to the open eye, and has less effect on the hemisphere ipsilateral to the deprived eye. BinOcular deprivation also causes different changes in the adult. Adult plasticity is similar to juvenile plasticity in its dependence on signaling through NMDA receptors. We propose that adult Ocular Dominance plasticity arises from compensatory mechanisms that counterbalance the loss of afferent activity caused by visual deprivation.
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autophosphorylation of αcamkii is required for Ocular Dominance plasticity
Neuron, 2002Co-Authors: Sharif A Taha, Jessica L Hanover, Alcino J Silva, Michael P StrykerAbstract:Abstract Experience is a powerful sculptor of developing neural connections. In the primary visual cortex (V1), cortical connections are particularly susceptible to the effects of sensory manipulation during a postnatal critical period. At the molecular level, this activity-dependent plasticity requires the transformation of synaptic depolarization into changes in synaptic weight. The molecule α calcium-calmodulin kinase type II (αCaMKII) is known to play a central role in this transformation. Importantly, αCaMKII function is modulated by autophosphorylation, which promotes Ca 2+ -independent kinase activity. Here we show that mice possessing a mutant form of αCaMKII that is unable to autophosphorylate show impairments in Ocular Dominance plasticity. These results confirm the importance of αCaMKII in visual cortical plasticity and suggest that synaptic changes induced by monOcular deprivation are stored specifically in glutamatergic synapses made onto excitatory neurons.
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rapid Ocular Dominance plasticity requires cortical but not geniculate protein synthesis
Neuron, 2002Co-Authors: Sharif A Taha, Michael P StrykerAbstract:Synaptic plasticity is a multistep process in which rapid, early phases eventually give way to slower, more enduring stages. Diverse forms of synaptic change share a common requirement for protein synthesis in the late stages of plasticity, which are often associated with structural rearrangements. Ocular Dominance plasticity in the primary visual cortex (V1) is a long-lasting form of activity-dependent plasticity comprised of well-defined physiological and anatomical stages. The molecular events underlying these stages remain poorly understood. Using the protein synthesis inhibitor cycloheximide, we investigated a role for protein synthesis in Ocular Dominance plasticity. Suppression of cortical, but not geniculate, protein synthesis impaired rapid Ocular Dominance plasticity, while leaving neuronal responsiveness intact. These findings suggest that structural changes underlying Ocular Dominance plasticity occur rapidly following monOcular occlusion, and cortical changes guide subsequent alterations in thalamocortical afferents.
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Ocular Dominance peaks at pinwheel center singularities of the orientation map in cat visual cortex
Journal of Neurophysiology, 1997Co-Authors: Michael C. Crair, Edward S Ruthazer, Deda C Gillespie, Michael P StrykerAbstract:Crair, Michael C., Edward S. Ruthazer, Deda C. Gillespie, and Michael P. Stryker. Ocular Dominance peaks at pinwheel center singularities of the orientation map in cat visual cortex. J. Neurophysio...
Konrad Lehmann - One of the best experts on this subject based on the ideXlab platform.
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social hierarchy regulates Ocular Dominance plasticity in adult male mice
Brain Structure & Function, 2019Co-Authors: Jenny Balog, Franziska Hintz, Marcel Isstas, Manuel Teichert, Christine Winter, Konrad LehmannAbstract:We here show that social rank, as assessed by competition for a running wheel, influences Ocular Dominance plasticity in adult male mice. Dominant animals showed a clear Ocular Dominance shift after 4 days of MD, whereas their submissive cagemates did not. NMDA receptor activation, reduced GABA inhibition, and serotonin transmission were necessary for this plasticity, but not sufficient to explain the difference between dominant and submissive animals. In contrast, prefrontal dopamine concentration was higher in dominant than submissive mice, and systemic manipulation of dopamine transmission bidirectionally changed Ocular Dominance plasticity. Thus, we could show that a social hierarchical relationship influences Ocular Dominance plasticity in the visual cortex via higher-order cortices, most likely the medial prefrontal cortex. Further studies will be needed to elucidate the precise mechanisms by which this regulation takes place.
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social experience modulates Ocular Dominance plasticity differentially in adult male and female mice
NeuroImage, 2014Co-Authors: Jenny Balog, Christine Winter, Ulrike Matthies, Lisa Naumann, Mareike Voget, Konrad LehmannAbstract:Environmental factors have long been known to regulate brain plasticity. We investigated the potential influence of social experience on Ocular Dominance plasticity. Fully adult female or male mice were monOcularly deprived for four days and kept a) either alone or in pairs of the same sex and b) either in a small cage or a large, featureless arena. While mice kept alone did not show Ocular Dominance plasticity, no matter whether in a cage or in an arena, paired female mice in both environmental conditions displayed a shift of Ocular Dominance towards the open eye. Paired male mice, in contrast, showed no plasticity in the cage, but a very strong Ocular Dominance shift in the arena. This effect was not due to increased locomotion, since the covered distance was similar in single and paired male mice in the arena, and furnishing cages with a running wheel did not enable Ocular Dominance plasticity in cage-housed mice. Confirming recent results in rats, the plasticity-enhancing effect of the social environment was shown to be mediated by serotonin. Our results demonstrate that social experience has a strong effect on cortical plasticity that is sex-dependent. This has potential consequences both for animal research and for human education and rehabilitation.
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Ocular Dominance plasticity in mouse visual cortex is age-dependent.
2013Co-Authors: Konrad Lehmann, Siegrid LöwelAbstract:Representative experiments of animals in all four age groups studied (PD25, PD95, PD130 and PD215) are displayed. Optical imaging maps of responses to the ipsi- and contralateral eye in the binOcular region of mouse visual cortex in both control animals (left column: a, c, e, g) and monOcularly deprived animals (right column: b, d, f, h) are shown. Both colour-coded polar maps of retinotopy (top) and grey-scale coded response magnitude maps (below) are illustrated. For each experiment, the histogram of Ocular Dominance scores, the average Ocular Dominance index (ODI) and the corresponding 2-D Ocular Dominance maps (ODI values colour-coded according to the scheme shown in the lower right corner of the figure: blue represents negative, red positive values) is included. Note that in control animals of all ages, activity patches evoked by the stimulation of the contralateral eye were consistently darker than those after stimulation of the ipsilateral eye (a, c, e, g) and that 2-D Ocular Dominance maps are red and yellow indicating contralateral Dominance. In contrast, monOcular deprivation for 4 days in PD25 animals (b) or for 7 days in PD95 animals (d) induced a significant Ocular Dominance shift so that the response magnitude maps of both ipsi- (open) and contralateral (deprived) eye are now equally dark, the histograms of Ocular Dominance scores shift to the left (compare a to b and c to d) and colder colours prevail in the 2-D Ocular Dominance maps. In the two older animal groups, PD130 and PD215 mice, monOcular deprivation for 7 days (f) or 14 days (h) fail to induce Ocular Dominance shifts and both histograms of Ocular Dominance scores and 2-D Ocular Dominance maps are similar to control animals (compare e to f and g to h). The scale bar is 1 mm and applies to all panels showing maps. Abbreviations: MD = monOcular deprivation, OD = Ocular Dominance, contra = contralateral eye, ipsi = ipsilateral eye.
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age dependent Ocular Dominance plasticity in adult mice
PLOS ONE, 2008Co-Authors: Konrad Lehmann, Siegrid LöwelAbstract:Background: Short monOcular deprivation (4 days) induces a shift in the Ocular Dominance of binOcular neurons in the juvenile mouse visual cortex but is ineffective in adults. Recently, it has been shown that an Ocular Dominance shift can still be elicited in young adults (around 90 days of age) by longer periods of deprivation (7 days). Whether the same is true also for fully mature animals is not yet known. Methodology/Principal Findings: We therefore studied the effects of different periods of monOcular deprivation (4, 7, 14 days) on Ocular Dominance in C57Bl/6 mice of different ages (25 days, 90–100 days, 109–158 days, 208–230 days) using optical imaging of intrinsic signals. In addition, we used a virtual optomotor system to monitor visual acuity of the open eye in the same animals during deprivation. We observed that Ocular Dominance plasticity after 7 days of monOcular deprivation was pronounced in young adult mice (90–100 days) but significantly weaker already in the next age group (109–158 days). In animals older than 208 days, Ocular Dominance plasticity was absent even after 14 days of monOcular deprivation. Visual acuity of the open eye increased in all age groups, but this interOcular plasticity also declined with age, although to a much lesser degree than the optically detected Ocular Dominance shift. Conclusions/Significance: These data indicate that there is an age-dependence of both Ocular Dominance plasticity and the enhancement of vision after monOcular deprivation in mice: Ocular Dominance plasticity in binOcular visual cortex is most pronounced in young animals, reduced but present in adolescence and absent in fully mature animals older than 110 days of age. Mice are thus not basically different in Ocular Dominance plasticity from cats and monkeys which is an absolutely essential prerequisite for their use as valid model systems of human visual disorders.
Siegrid Löwel - One of the best experts on this subject based on the ideXlab platform.
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Ocular Dominance plasticity in mouse visual cortex is age-dependent.
2013Co-Authors: Konrad Lehmann, Siegrid LöwelAbstract:Representative experiments of animals in all four age groups studied (PD25, PD95, PD130 and PD215) are displayed. Optical imaging maps of responses to the ipsi- and contralateral eye in the binOcular region of mouse visual cortex in both control animals (left column: a, c, e, g) and monOcularly deprived animals (right column: b, d, f, h) are shown. Both colour-coded polar maps of retinotopy (top) and grey-scale coded response magnitude maps (below) are illustrated. For each experiment, the histogram of Ocular Dominance scores, the average Ocular Dominance index (ODI) and the corresponding 2-D Ocular Dominance maps (ODI values colour-coded according to the scheme shown in the lower right corner of the figure: blue represents negative, red positive values) is included. Note that in control animals of all ages, activity patches evoked by the stimulation of the contralateral eye were consistently darker than those after stimulation of the ipsilateral eye (a, c, e, g) and that 2-D Ocular Dominance maps are red and yellow indicating contralateral Dominance. In contrast, monOcular deprivation for 4 days in PD25 animals (b) or for 7 days in PD95 animals (d) induced a significant Ocular Dominance shift so that the response magnitude maps of both ipsi- (open) and contralateral (deprived) eye are now equally dark, the histograms of Ocular Dominance scores shift to the left (compare a to b and c to d) and colder colours prevail in the 2-D Ocular Dominance maps. In the two older animal groups, PD130 and PD215 mice, monOcular deprivation for 7 days (f) or 14 days (h) fail to induce Ocular Dominance shifts and both histograms of Ocular Dominance scores and 2-D Ocular Dominance maps are similar to control animals (compare e to f and g to h). The scale bar is 1 mm and applies to all panels showing maps. Abbreviations: MD = monOcular deprivation, OD = Ocular Dominance, contra = contralateral eye, ipsi = ipsilateral eye.
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age dependent Ocular Dominance plasticity in adult mice
PLOS ONE, 2008Co-Authors: Konrad Lehmann, Siegrid LöwelAbstract:Background: Short monOcular deprivation (4 days) induces a shift in the Ocular Dominance of binOcular neurons in the juvenile mouse visual cortex but is ineffective in adults. Recently, it has been shown that an Ocular Dominance shift can still be elicited in young adults (around 90 days of age) by longer periods of deprivation (7 days). Whether the same is true also for fully mature animals is not yet known. Methodology/Principal Findings: We therefore studied the effects of different periods of monOcular deprivation (4, 7, 14 days) on Ocular Dominance in C57Bl/6 mice of different ages (25 days, 90–100 days, 109–158 days, 208–230 days) using optical imaging of intrinsic signals. In addition, we used a virtual optomotor system to monitor visual acuity of the open eye in the same animals during deprivation. We observed that Ocular Dominance plasticity after 7 days of monOcular deprivation was pronounced in young adult mice (90–100 days) but significantly weaker already in the next age group (109–158 days). In animals older than 208 days, Ocular Dominance plasticity was absent even after 14 days of monOcular deprivation. Visual acuity of the open eye increased in all age groups, but this interOcular plasticity also declined with age, although to a much lesser degree than the optically detected Ocular Dominance shift. Conclusions/Significance: These data indicate that there is an age-dependence of both Ocular Dominance plasticity and the enhancement of vision after monOcular deprivation in mice: Ocular Dominance plasticity in binOcular visual cortex is most pronounced in young animals, reduced but present in adolescence and absent in fully mature animals older than 110 days of age. Mice are thus not basically different in Ocular Dominance plasticity from cats and monkeys which is an absolutely essential prerequisite for their use as valid model systems of human visual disorders.
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Theory meets experiment: correlated neural activity helps determine Ocular Dominance column periodicity
Trends in Neurosciences, 1995Co-Authors: Geoffrey J. Goodhill, Siegrid LöwelAbstract:The development of Ocular Dominance columns in primary visual cortex has attracted much interest from both experimentalists and theoreticians. One key parameter of these columns is their periodicity - it is thus important to understand how this is determined. Novel experimental work demonstrates that the periodicity is influenced by the temporal patterning of afferent activity, as predicted by recent theoretical work.
Mark F Bear - One of the best experts on this subject based on the ideXlab platform.
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nmda receptor dependent Ocular Dominance plasticity in adult visual cortex
Neuron, 2003Co-Authors: Nathaniel B Sawtell, Mikhail Y Frenkel, Benjamin D Philpot, Kazu Nakazawa, Susumu Tonegawa, Mark F BearAbstract:The binOcular region of mouse visual cortex is strongly dominated by inputs from the contralateral eye. Here we show in adult mice that depriving the dominant contralateral eye of vision leads to a persistent, NMDA receptor-dependent enhancement of the weak ipsilateral-eye inputs. These data provide in vivo evidence for metaplasticity as a mechanism for binOcular competition and demonstrate that an Ocular Dominance shift can occur solely by the mechanisms of response enhancement. They also show that adult mouse visual cortex has a far greater potential for experience-dependent plasticity than previously appreciated. These insights may force a revision in how data on Ocular Dominance plasticity in mutant mice have been interpreted.
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molecular basis for induction of Ocular Dominance plasticity
Journal of Neurobiology, 1999Co-Authors: Mark F Bear, Cynthia D RittenhouseAbstract:The most dramatic example of experience-dependent cortical plasticity is the shift in Ocular Dominance that occurs in visual cortex as a consequence of monOcular deprivation during early postnatal life. Many of the basic properties of this type of synaptic plasticity have been described in detail. The important challenge that remains is to understand the molecular basis for these properties. By combining theoretical analysis with experiments in vivo and in vitro, some of the elementary molecular mechanisms for visual cortical plasticity have now been uncovered.
