Short-term plasticity in the visual thalamus

While there is evidence that the visual cortex retains a potential for plasticity in adulthood, less is known about the subcortical stages of visual processing. Here we asked whether short-term ocular dominance plasticity affects the visual thalamus. We addressed this question in normally sighted adult humans, using ultra-high field (7T) magnetic resonance imaging combined with the paradigm of short-term monocular deprivation. With this approach, we previously demonstrated transient shifts of perceptual eye dominance and ocular dominance in visual cortex (Binda et al., 2018). Here we report evidence for short-term plasticity in the ventral division of the pulvinar (vPulv), where the deprived eye representation was enhanced over the non-deprived eye. This pulvinar plasticity effect was similar as previously seen in visual cortex and it was correlated with the ocular dominance shift measured behaviorally. In contrast, there was no short-term plasticity effect in Lateral Geniculate Nucleus (LGN), where results were reliably different from vPulv, despite their spatial proximity. We conclude that the visual thalamus retains potential for short-term plasticity in adulthood; the plasticity effect differs across thalamic subregions, possibly reflecting differences in their cortical connectivity.

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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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Short-term plasticity of the human adult visual cortex measured with 7T BOLD

10.1101/323741 ◽

2018 ◽

Cited By ~ 1

Author(s):

Paola Binda ◽

Jan W. Kurzawski ◽

Claudia Lunghi ◽

Laura Biagi ◽

Michela Tosetti ◽

...

Keyword(s):

Visual Cortex ◽

Frequency Tuning ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Homeostatic Plasticity ◽

Short Term ◽

Parvocellular Pathway ◽

Human Adult ◽

Spatial Frequencies ◽

Ventral Pathway

AbstractVisual cortex, particularly V1, is considered to be resilient to plastic changes in adults. In particular, ocular dominance is assumed to be hard-wired after the end of the critical period. We show that short-term (2h) monocular deprivation in adult humans boosts the BOLD response to the deprived eye, changing ocular dominance of V1 vertices, consistently with homeostatic plasticity. The boost is strongest in V1, present in V2, V3 & V4 but absent in V3a and MT. Assessment of spatial frequency tuning in V1 by a population Receptive-Field technique shows that deprivation primarily boosts high spatial frequencies, consistent with a primary involvement of the parvocellular pathway. Crucially, the V1 deprivation effect correlates across participants with the perceptual increase of the deprived eye dominance assessed with binocular rivalry, suggesting a common origin. Our results demonstrate that visual cortex, particularly the ventral pathway, retains a high potential for homeostatic plasticity in the human adult.

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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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Response to short-term deprivation of the human adult visual cortex measured with 7T BOLD

eLife ◽

10.7554/elife.40014 ◽

2018 ◽

Vol 7 ◽

Cited By ~ 20

Author(s):

Paola Binda ◽

Jan W Kurzawski ◽

Claudia Lunghi ◽

Laura Biagi ◽

Michela Tosetti ◽

...

Keyword(s):

Visual Cortex ◽

Frequency Tuning ◽

Sensory Deprivation ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Homeostatic Plasticity ◽

Short Term ◽

Structural Reorganization ◽

Parvocellular Pathway ◽

Human Adult

Sensory deprivation during the post-natal ‘critical period’ leads to structural reorganization of the developing visual cortex. In adulthood, the visual cortex retains some flexibility and adapts to sensory deprivation. Here we show that short-term (2 hr) monocular deprivation in adult humans boosts the BOLD response to the deprived eye, changing ocular dominance of V1 vertices, consistent with homeostatic plasticity. The boost is strongest in V1, present in V2, V3 and V4 but absent in V3a and hMT+. Assessment of spatial frequency tuning in V1 by a population Receptive-Field technique shows that deprivation primarily boosts high spatial frequencies, consistent with a primary involvement of the parvocellular pathway. Crucially, the V1 deprivation effect correlates across participants with the perceptual increase of the deprived eye dominance assessed with binocular rivalry, suggesting a common origin. Our results demonstrate that visual cortex, particularly the ventral pathway, retains a high potential for homeostatic plasticity in the human adult.

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Aerobic Exercise Effects on Ocular Dominance Plasticity with a Phase Combination Task in Human Adults

Neural Plasticity ◽

10.1155/2017/4780876 ◽

2017 ◽

Vol 2017 ◽

pp. 1-7 ◽

Cited By ~ 8

Author(s):

Jiawei Zhou ◽

Alexandre Reynaud ◽

Robert F. Hess

Keyword(s):

Aerobic Exercise ◽

Binocular Rivalry ◽

Ocular Dominance ◽

General Effect ◽

Short Term ◽

Ocular Dominance Plasticity ◽

Plasticity Effect ◽

Phase Combination ◽

Human Adults ◽

Normal Adults

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.

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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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Enhancement of visual cortex plasticity by dark exposure

Philosophical Transactions of the Royal Society B Biological Sciences ◽

10.1098/rstb.2016.0159 ◽

2017 ◽

Vol 372 (1715) ◽

pp. 20160159 ◽

Cited By ~ 13

Author(s):

Irina Erchova ◽

Asta Vasalauskaite ◽

Valentina Longo ◽

Frank Sengpiel

Keyword(s):

Visual Cortex ◽

Critical Period ◽

Time Course ◽

Ocular Dominance ◽

Monocular Deprivation ◽

Homeostatic Plasticity ◽

Ocular Dominance Plasticity ◽

Intrinsic Signals ◽

Significant Difference ◽

Dark Exposure

Dark rearing is known to delay the time course of the critical period for ocular dominance plasticity in the visual cortex. Recent evidence suggests that a period of dark exposure (DE) may enhance or reinstate plasticity even after closure of the critical period, mediated through modification of the excitatory–inhibitory balance and/or removal of structural brakes on plasticity. Here, we investigated the effects of a week of DE on the recovery from a month of monocular deprivation (MD) in the primary visual cortex (V1) of juvenile mice. Optical imaging of intrinsic signals revealed that ocular dominance in V1 of mice that had received DE recovered slightly more quickly than of mice that had not, but the level of recovery after three weeks was similar in both groups. Two-photon calcium imaging showed no significant difference in the recovery of orientation selectivity of excitatory neurons between the two groups. Parvalbumin-positive (PV+) interneurons exhibited a smaller ocular dominance shift during MD but again no differences in subsequent recovery. The percentage of PV+ cells surrounded by perineuronal nets, a structural brake on plasticity, was lower in mice with than those without DE. Overall, DE causes a modest enhancement of mouse visual cortex plasticity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

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Ocular Dominance Plasticity: Measurement Reliability and Variability

10.1101/2020.07.27.211144 ◽

2020 ◽

Author(s):

Seung Hyun Min ◽

Ling Gong ◽

Alex S. Baldwin ◽

Alexandre Reynaud ◽

Zhifen He ◽

...

Keyword(s):

Ocular Dominance ◽

Measurement Methods ◽

Monocular Deprivation ◽

Short Term ◽

Ocular Dominance Plasticity ◽

Physiological Basis ◽

Eye Dominance ◽

Phase Combination ◽

One And Many ◽

Test Retest Reliability

AbstractIn 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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Astrocytic glutamate uptake coordinates experience-dependent, eye-specific refinement in developing visual cortex

10.1101/2020.05.25.113613 ◽

2020 ◽

Author(s):

Grayson Sipe ◽

Jeremy Petravicz ◽

Rajeev Rikhye ◽

Rodrigo Garcia ◽

Nikolaos Mellios ◽

...

Keyword(s):

Visual Cortex ◽

Glutamate Uptake ◽

Ocular Dominance ◽

Glutamate Transporter ◽

Monocular Deprivation ◽

Spine Density ◽

Ocular Dominance Plasticity ◽

Contralateral Eye ◽

Cortical Inputs ◽

And Function

ABSTRACTThe uptake of glutamate by astrocytes actively shapes synaptic transmission, however its role in the development and plasticity of neuronal circuits remains poorly understood. The astrocytic glutamate transporter, GLT1 is the predominant source of glutamate clearance in the adult mouse cortex. Here, we examined the structural and functional development of the visual cortex in GLT1 heterozygous (HET) mice using two-photon microscopy, immunohistochemistry and slice electrophysiology. We find that though eye-specific thalamic axonal segregation is intact, binocular refinement in the primary visual cortex is disrupted. Eye-specific responses to visual stimuli in GLT1 HET mice show altered binocular matching, with abnormally high responses to ipsilateral compared to contralateral eye stimulation and a greater mismatch between preferred orientation selectivity of ipsilateral and contralateral eye responses. Furthermore, the balance of excitation and inhibition in cortical circuits is dysregulated with an increase in somatostatin positive interneurons, decrease in parvalbumin positive interneurons, and increase in dendritic spine density in the basal dendrites of layer 2/3 excitatory neurons. Monocular deprivation induces atypical ocular dominance plasticity in GLT1 HET mice, with an unusual depression of ipsilateral open eye responses; however, this change in ipsilateral responses correlates well with an upregulation of GLT1 protein following monocular deprivation. These results demonstrate that a key function of astrocytic GLT1 function during development is the experience-dependent refinement of ipsilateral eye inputs relative to contralateral eye inputs in visual cortex.SIGNIFICANCEWe show that astrocytic glutamate uptake via the transporter GLT1 is necessary for activity-dependent regulation of cortical inputs. Dysregulation of GLT1 expression and function leads to a disruption of binocular refinement and matching in visual cortex. Inputs from the ipsilateral eye are stronger, and monocular deprivation, which upregulates GLT1 expression in a homeostatic fashion, causes a paradoxical reduction of ipsilateral, non-deprived eye, responses. These results provide new evidence for the importance of glutamate transport in cortical development, function, and plasticity.

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