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Mark F Bear - One of the best experts on this subject based on the ideXlab platform.
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recovery from the anatomical effects of long term Monocular Deprivation in cat lateral geniculate nucleus
The Journal of Comparative Neurology, 2018Co-Authors: Kevin R Duffy, Donald E Mitchell, Mingfai Fong, Mark F BearAbstract:Monocular Deprivation (MD) imposed early in postnatal life elicits profound structural and functional abnormalities throughout the primary visual pathway. The ability of MD to modify neurons within the visual system is restricted to a so-called critical period that, for cats, peaks at about one postnatal month and declines thereafter so that by about 3 months of age MD has little effect. Recovery from the consequences of MD likewise adheres to a critical period that ends by about 3 months of age, after which the effects of Deprivation are thought to be permanent and without capacity for reversal. The attenuation of plasticity beyond early development is a formidable obstacle for conventional therapies to stimulate recovery from protracted visual Deprivation. In the current study we examined the efficacy of dark exposure and retinal inactivation with tetrodotoxin to promote anatomical recovery in the dorsal lateral geniculate nuclues (dLGN) from long-term MD started at the peak of the critical period. Whereas 10 days of dark exposure or binocular retinal inactivation were not better at promoting recovery than conventional treatment with reverse occlusion, inactivation of only the non-deprived (fellow) eye for 10 days produced a complete restoration of neuron soma size, and also reversed the significant loss of neurofilament protein within originally deprived dLGN layers. These results reveal a capacity for neural plasticity and recovery that is larger than anything previously observed following protracted MD in cat, and they highlight a possibility for alternative therapies applied at ages thought to be recalcitrant to recovery.
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the ratio of nr2a b nmda receptor subunits determines the qualities of ocular dominance plasticity in visual cortex
Proceedings of the National Academy of Sciences of the United States of America, 2009Co-Authors: Kathleen K A Cho, Lena A Khibnik, Benjamin D Philpot, Mark F BearAbstract:Bidirectional synaptic plasticity during development ensures that appropriate synapses in the brain are strengthened and maintained while inappropriate connections are weakened and eliminated. This plasticity is well illustrated in mouse visual cortex, where Monocular Deprivation during early postnatal development leads to a rapid depression of inputs from the deprived eye and a delayed strengthening of inputs from the non-deprived eye. The mechanisms that control these bidirectional synaptic modifications remain controversial. Here we demonstrate, both in vitro and in vivo, that genetic deletion or reduction of the NR2A NMDA receptor subunit impairs activity-dependent weakening of synapses and enhances the strengthening of synapses. Although brief Monocular Deprivation in juvenile WT mice normally causes a profound depression of the deprived-eye response without a change in the non-deprived eye response, NR2A-knockout mice fail to exhibit Deprivation-induced depression and instead exhibit precocious potentiation of the non-deprived eye inputs. These data support the hypothesis that a reduction in the NR2A/B ratio during Monocular Deprivation is permissive for the compensatory potentiation of non-deprived inputs.
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bidirectional modifications of visual acuity induced by Monocular Deprivation in juvenile and adult rats
The Journal of Neuroscience, 2006Co-Authors: Arnold J Heynen, Erik Sklar, Mark F BearAbstract:Recent electrophysiological studies of rodent visual cortex suggest that, in addition to deprived-eye depression, Monocular Deprivation (MD) also shifts ocular dominance by potentiation of open-eye responses. We used computer-based, two-choice discrimination tasks to assess the behavioral significance of these findings in rats. As expected, prolonged MD, from postnatal day 21 until adulthood (>150 d) markedly decreased visual acuity through the deprived eye. However, we also found that the acuity through the nondeprived eye was significantly enhanced compared with normally reared controls. Interestingly, when the deprived eye was opened in adults, there was a gradual but incomplete recovery of acuity in the deprived eye preceded by a loss of the enhanced acuity in the nondeprived eye. These changes were reversed by again reclosing the eye. These findings suggest that the bidirectional changes in visually evoked responses after MD are behaviorally meaningful and that significant plasticity is exhibited well into adulthood.
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how Monocular Deprivation shifts ocular dominance in visual cortex of young mice
Neuron, 2004Co-Authors: Mikhail Y Frenkel, Mark F BearAbstract:Abstract We used a chronic recording method to document the kinetics of ocular dominance (OD) plasticity induced by temporary lid closure in young mice. We find that Monocular Deprivation (MD) induces two separate modifications: (1) rapid, Deprivation-induced response depression and (2) delayed, Deprivation-enabled, experience-dependent response potentiation. To gain insight into how altering retinal activity triggers these cortical responses, we compared the effects of MD by lid closure with Monocular inactivation (MI) by intravitreal injection of tetrodotoxin. We find that MI fails to induce deprived-eye response depression but promotes potentiation of responses driven by the normal eye. These effects of MI in juvenile mice closely resemble the effects of MD in adult mice. Understanding how MI and MD differentially affect activity in the visual system of young mice may provide key insight into how the critical period ends.
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molecular mechanism for loss of visual cortical responsiveness following brief Monocular Deprivation
Nature Neuroscience, 2003Co-Authors: Arnold J Heynen, Bongjune Yoon, Hee Jung Chung, Richard L Huganir, Mark F BearAbstract:A dramatic form of experience-dependent synaptic plasticity is revealed in visual cortex when one eye is temporarily deprived of vision during early postnatal life. Monocular Deprivation (MD) alters synaptic transmission such that cortical neurons cease to respond to stimulation of the deprived eye, but how this occurs is poorly understood. Here we show in rat visual cortex that brief MD sets in motion the same molecular and functional changes as the experimental model of homosynaptic long-term depression (LTD), and that prior synaptic depression by MD occludes subsequent induction of LTD. The mechanisms of LTD, about which there is now a detailed understanding, therefore contribute to visual cortical plasticity.
Tommaso Pizzorusso - One of the best experts on this subject based on the ideXlab platform.
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European Journal of Neuroscience, Vol. 11, pp. 204–212, 1999 © European Neuroscience Association TrkA activation in the rat visual cortex by antirat trkA IgG prevents the effect of Monocular Deprivation
2016Co-Authors: Tommaso Pizzorusso, Nicoletta Berardi, Francesco M. Rossi, Ro Viegi, Kristine Venstrom, Louis F. Reichardt, Lamberto MaffeiAbstract:It has been recently shown that intraventricular injections of nerve growth factor (NGF) prevent the effects of Monocular Deprivation in the rat. We have tested the localization and the molecular nature of the NGF receptor(s) responsible for this effect by activating cortical trkA receptors in Monocularly deprived rats by cortical infusion of a specific agonist of NGF on trkA, the bivalent antirat trkA IgG (RTA-IgG). TrkA protein was detected by immunoblot in the rat visual cortex during the critical period. Rats were Monocularly deprived for 1 week (P21–28) and RTA-IgG or control rabbit IgG were delivered by osmotic minipumps. The effects of Monocular Deprivation on the ocular dominance of visual cortical neurons were assessed by extracellular single cell recordings. We found that the shift towards the ipsilateral, non-deprived eye was largely prevented by RTA-IgG. Infusion of RTA-IgG combined with antibody that blocks p75NTR (REX), slightly reduced RTA-IgG effectiveness in preventing Monocular Deprivation effects. These results suggest that NGF action in visual cortical plasticity is mediated by cortical TrkA receptors with p75NTR exerting a facilitatory role
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schwann cells transplanted in the lateral ventricles prevent the functional and anatomical effects of Monocular Deprivation in the rat nerve growth factor amblyopia ocular dominance lateral geniculate nucleus neurotrophin
2016Co-Authors: Tommaso Pizzorusso, Michela Fagiolini, Lamberto MaffeiAbstract:We investigated whether the transplant of Schwann cells prevents the physiological and morphological effects of Monocular Deprivation in the rat. On the day of eye opening in rats (postnatal day 14), we transplanted Schwann ceils in the lateral ventricles and sutured the eyelids of one eye. After 20-30 days, at the end of the critical period for the visual system development, we analyzed the functional properties of visual cortical neurons. Spontaneous discharge, orientation selectivity, and receptive field size of visual cortical neurons in transplanted animals were in the normal range. Transplanta- tion of Schwann cells prevented the detrimental effects of Monocular Deprivation on ocular dominance and binocularity of cortical neurons. Visual acuity of the deprived eye estimated by visually evoked potentials was also normal. Schwann cells derived from adult animals were as effective as those derived from neonates. The effects of Schwann cells on Monocular Deprivation were dependent upon the number of cells present in the transplant so that 106 Schwann cells were sufficient to prevent the effect of Monocular Deprivation, whereas 105 and 3.3 x 105 Schwann cells were ineffective, and 6.3 x 105 cells gave variable results. Shrinkage of the deprived lateral genic- ulate neurons was prevented by a transplant of 106 cells. In rats transplanted with hybridoma cells producing an antibody that functionally blocks nerve growth factor (NGF), we found that the effect of cotransplanted Schwann cells on Monocular de- privation was partly counteracted. We conclude that trans- plantation of Schwann cells prevents both functional and anatomical effects of Monocular Deprivation, presumably act- ing through the production of NGF. We propose that trans- plants of Schwann cells could be a promising technique for clinical applications.
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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, 2010Co-Authors: Davide Silingardi, Manuela Scali, Giulio Belluomini, Tommaso PizzorussoAbstract:In mammals the development of the visual system may be altered during a sensitive period by modifying the visual input to one or both eyes. These plastic processes are reduced after the end of the sensitive period. It has been proposed that reduced levels of plasticity are at the basis of the lack of recovery from early visual Deprivation observed in adult animals. A developmental downregulation of experience-dependent regulation of histone acetylation has recently been found to be involved in closing the sensitive period. Therefore, we tested whether pharmacological epigenetic treatments increasing histone acetylation could be used to reverse visual acuity deficits induced by long-term Monocular Deprivation initiated during the sensitive period. We found that chronic intraperitoneal administration of valproic acid or sodium butyrate (two different histone deacetylases inhibitors) to long-term Monocularly deprived adult rats coupled with reverse lid-suturing caused a complete recovery of visual acuity, tested electrophysiologically and behaviorally. Thus, manipulations of the epigenetic machinery can be used to promote functional recovery from early alterations of sensory input in the adult cortex.
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reduced responsiveness to long term Monocular Deprivation of parvalbumin neurons assessed by c fos staining in rat visual cortex
PLOS ONE, 2009Co-Authors: Marco Mainardi, Nicoletta Berardi, Lamberto Maffei, Silvia Landi, Tommaso PizzorussoAbstract:Background It is generally assumed that visual cortical cells homogeneously shift their ocular dominance (OD) in response to Monocular Deprivation (MD), however little experimental evidence directly supports this notion. By using immunohistochemistry for the activity-dependent markers c-Fos and Arc, coupled with staining for markers of inhibitory cortical sub-populations, we studied whether long-term MD initiated at P21 differentially affects visual response of inhibitory neurons in rat binocular primary visual cortex. Methodology/Principal Findings The inhibitory markers GAD67, parvalbumin (PV), calbindin (CB) and calretinin (CR) were used. Visually activated Arc did not colocalize with PV and was discarded from further studies. MD decreased visually induced c-Fos activation in GAD67 and CR positive neurons. The CB population responded to MD with a decrease of CB expression, while PV cells did not show any effect of MD on c-Fos expression. The persistence of c-Fos expression induced by deprived eye stimulation in PV cells is not likely to be due to a particularly low threshold for activity-dependent c-Fos induction. Indeed, c-Fos induction by increasing concentrations of the GABAA antagonist picrotoxin in visual cortical slices was similar between PV cells and the other cortical neurons. Conclusion These data indicate that PV cells are particularly refractory to MD, suggesting that different cortical subpopulation may show different response to MD.
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reactivation of ocular dominance plasticity in the adult visual cortex
Science, 2002Co-Authors: Tommaso Pizzorusso, James W. Fawcett, Paolo Medini, Nicoletta Berardi, Sabrina Chierzi, Lamberto MaffeiAbstract:In young animals, Monocular Deprivation leads to an ocular dominance shift, whereas in adults after the critical period there is no such shift. Chondroitin sulphate proteoglycans (CSPGs) are components of the extracellular matrix (ECM) inhibitory for axonal sprouting. We tested whether the developmental maturation of the ECM is inhibitory for experience-dependent plasticity in the visual cortex. The organization of CSPGs into perineuronal nets coincided with the end of the critical period and was delayed by dark rearing. After CSPG degradation with chondroitinase-ABC in adult rats, Monocular Deprivation caused an ocular dominance shift toward the nondeprived eye. The mature ECM is thus inhibitory for experience-dependent plasticity, and degradation of CSPGs reactivates cortical plasticity.
Robert F. Hess - One of the best experts on this subject based on the ideXlab platform.
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some psychophysical tasks measure ocular dominance plasticity more reliably than others
Journal of Vision, 2021Co-Authors: Seung Hyun Min, Alex S. Baldwin, Alexandre Reynaud, Ling Gong, Jiawei Zhou, Robert F. HessAbstract:In the recent decade, studies have shown that short-term Monocular Deprivation strengthens the deprived eye's contribution to binocular vision. However, the magnitude of the change in eye dominance after Monocular Deprivation (i.e., the patching effect) has been found to be different between different methods and within the same method. There are three possible explanations for the discrepancy. First, the mechanisms underlying the patching effect that are probed by different measurement tasks might exist at different neural sites. Second, the test-retest variability of the same test can produce inconsistent results. Third, the magnitude of the patching effect itself within the same observer can vary across separate days or experimental sessions. To explore these possibilities, we assessed the test-retest reliability of the three most commonly used tasks (binocular rivalry, binocular combination, and dichoptic masking) and the repeatability of the shift in eye dominance after short-term Monocular Deprivation for each of the task. Two variations for binocular phase combination were used, at one and many contrasts of the stimuli. Also, two variations for dichoptic masking were employed; the orientation of the mask grating was either horizontal or vertical. Thus, five different tasks were evaluated. We hoped to resolve some of the inconsistencies reported in the literature concerning this form of visual plasticity. In this study, we also aimed to recommend a measurement method that would allow us to better understand its physiological basis and the underpinning of visual disorders.
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ocular dominance plasticity measurement reliability and variability
bioRxiv, 2020Co-Authors: Seung Hyun Min, Alex S. Baldwin, Alexandre Reynaud, Ling Gong, Jiawei Zhou, Robert F. HessAbstract:Abstract In the last decade, studies have shown that short-term Monocular Deprivation strengthens the deprived eye’s contribution to binocular vision. However, the magnitude of the change in eye dominance after Monocular Deprivation (i.e., the patching effect) has been found to be different between for different methods and within the same method. There are three possible explanations for the discrepancy. First, the mechanisms underlying the patching effect that are probed by different measurement tasks might exist at different neural sites. Second, test-retest variability in the measurement might have led to inconsistencies, even within the same method. Third, the patching effect itself in the same subject might fluctuate across separate days or experimental sessions. To explore these possibilities, we assessed the test-retest reliability of the three most commonly used tasks (binocular rivalry, binocular combination, and dichoptic masking) and the repeatability of the shift in eye dominance after short-term Monocular Deprivation for each of the task. Two variations for binocular phase combination were used, at one and many contrasts of the stimuli. Also, two variations of the dichoptic masking task was tested, in which the orientation of the mask grating was either horizontal or vertical. This makes five different measurement methods in all. We hope to resolve some of the inconsistencies reported in the literature concerning this form of visual plasticity. In this study, we also aim to recommend a measurement method that will allow us to better understand its physiological basis and the underpinning of visual disorders.
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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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temporary Monocular occlusion facilitates binocular fusion during rivalry
Journal of Vision, 2019Co-Authors: Yasha Sheynin, Sebastien Proulx, Robert F. HessAbstract:A few hours of Monocular patching temporarily enhances the deprived eye's contribution to binocular vision, constituting a form of adult brain plasticity. Although the mechanism for this plasticity is currently unknown, several imaging studies present evidence that Monocular Deprivation achieves its effects by changing excitatory-inhibitory balance in the visual cortex. Much of the past work on adult Monocular patching utilized binocular rivalry to quantify the patching-induced shift in perceptual eye dominance, extracting periods of exclusive visibility (in which one eye's signal is suppressed from perception) to assess each eye's contribution to binocular vision while overlooking the occurrence of mixed visibility (in which information from both eyes is combined). In this paper, we discuss two experiments to investigate the effects of short-term Monocular occlusion on the relative predominance of mixed and exclusive percepts during binocular rivalry. In addition to the known perceptual eye-dominance shift, we hypothesized patching would also increase the perception of mixtures during rivalry due to Deprivation-induced changes in excitatory-inhibitory balance. Our data point to two previously unknown effects of Monocular Deprivation: (a) a significant increase in the overall fraction and median duration of mixed visibility during rivalry that is detectable up to at least an hour after removing the patch and (b) the overall fraction of superimposition; rather than piecemeal, mixed percepts are specifically enhanced after Monocular Deprivation. In addition to strengthening the contribution of the deprived eye, our results show that temporary Monocular patching enhances the visibility of fused binocular percepts, likely the result of attenuated interocular inhibition.
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cholinergic potentiation alters perceptual eye dominance plasticity induced by a few hours of Monocular patching in adults
Frontiers in Neuroscience, 2019Co-Authors: Yasha Sheynin, Mira Chamoun, Alex S. Baldwin, Robert F. Hess, Pedro Rosaneto, Elvire VaucherAbstract:A few hours of Monocular Deprivation with a diffuser eye patch temporarily strengthens the contribution of the deprived eye to binocular vision. This shift in favour of the deprived eye is characterized as a form of adult visual plasticity. Studies in animal and human models suggest that neuromodulators can enhance adult brain plasticity in general. Specifically, acetylcholine has been shown to improve certain aspects of visual function and plasticity in adulthood. We investigated whether a single administration of donepezil (a cholinesterase inhibitor) could further augment the temporary shift in perceptual eye dominance that occurs after two hours of Monocular patching. Twelve healthy adults completed two experimental sessions while taking either donepezil (5 mg, oral) or a placebo (lactose) pill. We measured perceptual eye dominance using a binocular phase combination task before and after two hours of Monocular Deprivation with a diffuser eye patch. Participants in both groups demonstrated a significant shift in favour of the patched eye after Monocular Deprivation, however our results indicate that donepezil significantly reduces the magnitude and duration of the shift. We also investigated the possibility that donepezil reduces the amount of time needed to observe a shift in perceptual eye dominance relative to placebo control. For this experiment, seven subjects completed two sessions where we reduced the duration of Deprivation to one hour. Donepezil reduces the magnitude and duration of the patching-induced shift in perceptual eye dominance in this experiment as well. To verify whether the effects we observed using the binocular phase combination task were also observable in a different measure of sensory eye dominance, six subjects completed an identical experiment using a binocular rivalry task. These results also indicate that cholinergic enhancement impedes the shift that results from short-term Deprivation. In summary, our study demonstrates that enhanced cholinergic potentiation interferes with the consolidation of the perceptual eye dominance plasticity induced by several hours of Monocular Deprivation.
Donald E Mitchell - One of the best experts on this subject based on the ideXlab platform.
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recovery from the anatomical effects of long term Monocular Deprivation in cat lateral geniculate nucleus
The Journal of Comparative Neurology, 2018Co-Authors: Kevin R Duffy, Donald E Mitchell, Mingfai Fong, Mark F BearAbstract:Monocular Deprivation (MD) imposed early in postnatal life elicits profound structural and functional abnormalities throughout the primary visual pathway. The ability of MD to modify neurons within the visual system is restricted to a so-called critical period that, for cats, peaks at about one postnatal month and declines thereafter so that by about 3 months of age MD has little effect. Recovery from the consequences of MD likewise adheres to a critical period that ends by about 3 months of age, after which the effects of Deprivation are thought to be permanent and without capacity for reversal. The attenuation of plasticity beyond early development is a formidable obstacle for conventional therapies to stimulate recovery from protracted visual Deprivation. In the current study we examined the efficacy of dark exposure and retinal inactivation with tetrodotoxin to promote anatomical recovery in the dorsal lateral geniculate nuclues (dLGN) from long-term MD started at the peak of the critical period. Whereas 10 days of dark exposure or binocular retinal inactivation were not better at promoting recovery than conventional treatment with reverse occlusion, inactivation of only the non-deprived (fellow) eye for 10 days produced a complete restoration of neuron soma size, and also reversed the significant loss of neurofilament protein within originally deprived dLGN layers. These results reveal a capacity for neural plasticity and recovery that is larger than anything previously observed following protracted MD in cat, and they highlight a possibility for alternative therapies applied at ages thought to be recalcitrant to recovery.
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binocular eyelid closure promotes anatomical but not behavioral recovery from Monocular Deprivation
Vision Research, 2015Co-Authors: Kevin R Duffy, Dalia H Bukhamseen, Matthew Smithen, Donald E MitchellAbstract:Deprivation of patterned vision of frontal eyed mammals early in postnatal life alters structural and functional attributes of neurones in the central visual pathways, and can produce severe impairments of the vision of the deprived eye that resemble the visual loss observed in human amblyopia. A traditional approach to treatment of amblyopia has been the occlusion of the stronger fellow eye in order to force use of the weaker eye and thereby strengthen its connections in the visual cortex. Although this Monocular treatment strategy can be effective at promoting recovery of visual acuity of the amblyopic eye, such binocular visual functions as stereoscopic vision often remain impaired due in part to the lack of concordant vision during the period of unilateral occlusion. The recent development of binocular approaches for treatment of amblyopia that improve the possibility for binocular interaction have achieved success in promoting visual recovery. The full and rapid recovery of visual acuity observed in amblyopic kittens placed in complete darkness is an example of a binocular treatment whose success may in part derive from a restored balance of visually-driven neural activity. In the current study we examined as an alternative to dark rearing the efficacy of binocular lid suture (BLS) to stimulate anatomical and visual recovery from a preceding amblyogenic period of Monocular Deprivation. In the dorsal lateral geniculate nucleus (dLGN) of Monocularly deprived kittens, darkness or BLS for 10days produced a complete recovery of neurone soma size within initially deprived layers. The growth of neurone somata within initially deprived dLGN layers after darkness or BLS was accompanied by an increase in neurotrophin-4/5 labeling within these layers. Although anatomical recovery was observed in both recovery conditions, BLS failed to promote any improvement of the visual acuity of the deprived eye no matter whether it followed immediately or was delayed with respect to the prior period of Monocular Deprivation. Notwithstanding the lack of visual recovery with BLS, all animals in the BLS condition that were subsequently placed in darkness exhibited a substantial recovery of visual acuity in the amblyopic eye. We conclude that the balanced binocular visual input provided by BLS does not stimulate the collection of neural events necessary to support recovery from amblyopia. The complete absence of visually-driven activity that occurs with dark rearing evidently plays an important role in the recovery process.
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postnatal development of function in the mammalian visual system
Comprehensive Physiology, 2011Co-Authors: Donald E Mitchell, Brian TimneyAbstract:The sections in this article are: 1 Development of Visual Perception 1.1 Methods of Study 1.2 Development of Spatial Resolution 1.3 Development of Depth Perception and Stereopsis 1.4 Overview 2 Development of Visual Neural Processes 2.1 Retina 2.2 Lateral Geniculate Nucleus 2.3 Visual Cortex 3 Consequences of Binocular Visual Deprivation 3.1 Forms of Binocular Deprivation 3.2 Effects on Perception 4 Effects of Selected Visual Experience on Neural Processes and Perception 5 Conditions that Influence Ocular Dominance 5.1 Monocular Deprivation 5.2 Artificial Strabismus 5.3 Alternating Monocular Deprivation 6 Conditions that Influence Other Receptive-Field Properties 6.1 Orientation Selectivity 6.2 Movement and Direction Selectivity 6.3 Effects of Unusual Visual Input on Cortical Development 7 Genetic and Experiential Factors in Visual Development 7.1 Functional Role of Visual Experience
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neural mechanisms of recovery following early visual Deprivation
Philosophical Transactions of the Royal Society B, 2009Co-Authors: Donald E Mitchell, Frank SengpielAbstract:Natural patterned early visual input is essential for the normal development of the central visual pathways and the visual capacities they sustain. Without visual input, the functional development of the visual system stalls not far from the state at birth, and if input is distorted or biased the visual system develops in an abnormal fashion resulting in specific visual deficits. Monocular Deprivation, an extreme form of biased exposure, results in large anatomical and physiological changes in terms of territory innervated by the two eyes in primary visual cortex (V1) and to a loss of vision in the deprived eye reminiscent of that in human Deprivation amblyopia. We review work that points to a special role for binocular visual input in the development of V1 and vision. Our unique approach has been to provide animals with mixed visual input each day, which consists of episodes of normal and biased (Monocular) exposures. Short periods of concordant binocular input, if continuous, can offset much longer episodes of Monocular Deprivation to allow normal development of V1 and prevent amblyopia. Studies of animal models of patching therapy for amblyopia reveal that the benefits are both heightened and prolonged by daily episodes of binocular exposure.
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correlated binocular activity guides recovery from Monocular Deprivation
Nature, 2002Co-Authors: Peter C Kind, Donald E Mitchell, Bashir Ahmed, Colin Blakemore, Tobias Bonhoeffer, Frank SengpielAbstract:Monocular Deprivation (MD) has much more rapid and severe effects on the ocular dominance of neurons in the primary visual cortex (V1) than does binocular Deprivation1. This finding underlies the widely held hypothesis that the developmental plasticity of ocular dominance reflects competitive interactions for synaptic space between inputs from the two eyes2. According to this view, the relative levels of evoked activity in afferents representing the two eyes determine functional changes in response to altered visual experience. However, if the deprived eye of a Monocularly deprived kitten is simply reopened, there is substantial physiological and behavioural recovery, leading to the suggestion that absolute activity levels, or some other non-competitive mechanisms, determine the degree of recovery from MD3, 4, 5, 6, 7. Here we provide evidence that correlated binocular input is essential for such recovery. Recovery is far less complete if the two eyes are misaligned after a period of MD. This is a powerful demonstration of the importance of cooperative, associative mechanisms in the developing visual cortex.
Lamberto Maffei - One of the best experts on this subject based on the ideXlab platform.
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European Journal of Neuroscience, Vol. 11, pp. 204–212, 1999 © European Neuroscience Association TrkA activation in the rat visual cortex by antirat trkA IgG prevents the effect of Monocular Deprivation
2016Co-Authors: Tommaso Pizzorusso, Nicoletta Berardi, Francesco M. Rossi, Ro Viegi, Kristine Venstrom, Louis F. Reichardt, Lamberto MaffeiAbstract:It has been recently shown that intraventricular injections of nerve growth factor (NGF) prevent the effects of Monocular Deprivation in the rat. We have tested the localization and the molecular nature of the NGF receptor(s) responsible for this effect by activating cortical trkA receptors in Monocularly deprived rats by cortical infusion of a specific agonist of NGF on trkA, the bivalent antirat trkA IgG (RTA-IgG). TrkA protein was detected by immunoblot in the rat visual cortex during the critical period. Rats were Monocularly deprived for 1 week (P21–28) and RTA-IgG or control rabbit IgG were delivered by osmotic minipumps. The effects of Monocular Deprivation on the ocular dominance of visual cortical neurons were assessed by extracellular single cell recordings. We found that the shift towards the ipsilateral, non-deprived eye was largely prevented by RTA-IgG. Infusion of RTA-IgG combined with antibody that blocks p75NTR (REX), slightly reduced RTA-IgG effectiveness in preventing Monocular Deprivation effects. These results suggest that NGF action in visual cortical plasticity is mediated by cortical TrkA receptors with p75NTR exerting a facilitatory role
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schwann cells transplanted in the lateral ventricles prevent the functional and anatomical effects of Monocular Deprivation in the rat nerve growth factor amblyopia ocular dominance lateral geniculate nucleus neurotrophin
2016Co-Authors: Tommaso Pizzorusso, Michela Fagiolini, Lamberto MaffeiAbstract:We investigated whether the transplant of Schwann cells prevents the physiological and morphological effects of Monocular Deprivation in the rat. On the day of eye opening in rats (postnatal day 14), we transplanted Schwann ceils in the lateral ventricles and sutured the eyelids of one eye. After 20-30 days, at the end of the critical period for the visual system development, we analyzed the functional properties of visual cortical neurons. Spontaneous discharge, orientation selectivity, and receptive field size of visual cortical neurons in transplanted animals were in the normal range. Transplanta- tion of Schwann cells prevented the detrimental effects of Monocular Deprivation on ocular dominance and binocularity of cortical neurons. Visual acuity of the deprived eye estimated by visually evoked potentials was also normal. Schwann cells derived from adult animals were as effective as those derived from neonates. The effects of Schwann cells on Monocular Deprivation were dependent upon the number of cells present in the transplant so that 106 Schwann cells were sufficient to prevent the effect of Monocular Deprivation, whereas 105 and 3.3 x 105 Schwann cells were ineffective, and 6.3 x 105 cells gave variable results. Shrinkage of the deprived lateral genic- ulate neurons was prevented by a transplant of 106 cells. In rats transplanted with hybridoma cells producing an antibody that functionally blocks nerve growth factor (NGF), we found that the effect of cotransplanted Schwann cells on Monocular de- privation was partly counteracted. We conclude that trans- plantation of Schwann cells prevents both functional and anatomical effects of Monocular Deprivation, presumably act- ing through the production of NGF. We propose that trans- plants of Schwann cells could be a promising technique for clinical applications.
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reduced responsiveness to long term Monocular Deprivation of parvalbumin neurons assessed by c fos staining in rat visual cortex
PLOS ONE, 2009Co-Authors: Marco Mainardi, Nicoletta Berardi, Lamberto Maffei, Silvia Landi, Tommaso PizzorussoAbstract:Background It is generally assumed that visual cortical cells homogeneously shift their ocular dominance (OD) in response to Monocular Deprivation (MD), however little experimental evidence directly supports this notion. By using immunohistochemistry for the activity-dependent markers c-Fos and Arc, coupled with staining for markers of inhibitory cortical sub-populations, we studied whether long-term MD initiated at P21 differentially affects visual response of inhibitory neurons in rat binocular primary visual cortex. Methodology/Principal Findings The inhibitory markers GAD67, parvalbumin (PV), calbindin (CB) and calretinin (CR) were used. Visually activated Arc did not colocalize with PV and was discarded from further studies. MD decreased visually induced c-Fos activation in GAD67 and CR positive neurons. The CB population responded to MD with a decrease of CB expression, while PV cells did not show any effect of MD on c-Fos expression. The persistence of c-Fos expression induced by deprived eye stimulation in PV cells is not likely to be due to a particularly low threshold for activity-dependent c-Fos induction. Indeed, c-Fos induction by increasing concentrations of the GABAA antagonist picrotoxin in visual cortical slices was similar between PV cells and the other cortical neurons. Conclusion These data indicate that PV cells are particularly refractory to MD, suggesting that different cortical subpopulation may show different response to MD.
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reactivation of ocular dominance plasticity in the adult visual cortex
Science, 2002Co-Authors: Tommaso Pizzorusso, James W. Fawcett, Paolo Medini, Nicoletta Berardi, Sabrina Chierzi, Lamberto MaffeiAbstract:In young animals, Monocular Deprivation leads to an ocular dominance shift, whereas in adults after the critical period there is no such shift. Chondroitin sulphate proteoglycans (CSPGs) are components of the extracellular matrix (ECM) inhibitory for axonal sprouting. We tested whether the developmental maturation of the ECM is inhibitory for experience-dependent plasticity in the visual cortex. The organization of CSPGs into perineuronal nets coincided with the end of the critical period and was delayed by dark rearing. After CSPG degradation with chondroitinase-ABC in adult rats, Monocular Deprivation caused an ocular dominance shift toward the nondeprived eye. The mature ECM is thus inhibitory for experience-dependent plasticity, and degradation of CSPGs reactivates cortical plasticity.
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Monocular Deprivation decreases the expression of messenger rna for brain derived neurotrophic factor in the rat visual cortex
Neuroscience, 1995Co-Authors: Yuri Bozzi, Tommaso Pizzorusso, Federico Cremisi, F M Rossi, Giuseppina Barsacchi, Lamberto MaffeiAbstract:Abstract We found that Deprivation of pattern vision in one eye, that leaves luminance detection performance unaffected, is sufficient to reduce brain-derived neurotrophic factor (but not trkB) messenger RNA in the visual cortex of young and adult rats. Monocular Deprivation by means of eyelids' suture was performed during or after the critical period and the cortical amount of brain-derived neurotrophic factor messenger RNA was analysed by in situ hybridization and RNAase protection after 15–30 days of Deprivation. A reduction of brain-derived neurotrophic factor messenger RNA was observed in the visual cortex contralateral to the deprived eye in rats Monocularly deprived during the critical period. The same reduction was also found in rats Monocularly deprived after the end of the critical period, when anatomical or physiological signs of Monocular Deprivation are absent. The pharmacological blockade of retinal activity equally affected the expression of brain-derived neurotrophic factor messenger RNA in young and adults. Quantitative RNAase protection assays revealed that the cortical level of brain-derived neurotrophic factor messenger RNA was reduced to the same extent when intraocular injections of tetrodotoxin were performed within or after the critical period. A developmental study of brain-derived neurotrophic factor messenger RNA expression in rat visual cortex showed a marked increase around the time of natural eye-opening followed by a plateau from postnatal day 20 until adult age. Messenger RNA for the kinasic domain of brain-derived neurotrophic factor receptor (trkB) was found in the dorsal lateral geniculate nucleus and the visual cortex during development and in adults. Our results suggest that the reduction of brain-derived neurotrophic factor messenger RNA induced by Monocular Deprivation is related to the absence of pattern vision rather than to the competitive interactions that underlie the effects of Monocular Deprivation during the critical period.