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

2018 ◽  
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.

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

eLife ◽  
2018 ◽  
Vol 7 ◽  
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.

scholarly journals Short-term plasticity in the visual thalamus

2021 ◽  
Author(s):  
Jan W Kurzawski ◽  
Claudia Lunghi ◽  
Laura Biagi ◽  
Michela Tosetti ◽  
Maria Concetta Morrone ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Visual Processing ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Spatial Proximity ◽  
Short Term ◽  
Ocular Dominance Plasticity ◽  
Short Term Plasticity ◽  
Visual Thalamus ◽  
Plasticity Effect

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.

scholarly journals Enhancement of visual cortex plasticity by dark exposure

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160159 ◽  
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’.

scholarly journals Elastic Net Model of Ocular Dominance: Overall Stripe Pattern and Monocular Deprivation

1994 ◽  
Vol 6 (4) ◽  
pp. 615-621 ◽  
Author(s):  
Geoffrey J. Goodhill ◽  
David J. Willshaw
Keyword(s):  
Visual Cortex ◽  
Lateral Geniculate Nucleus ◽  
Primary Visual Cortex ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Elastic Net ◽  
Global Order ◽  
Stripe Pattern ◽  
Lateral Geniculate ◽  
Stripe Width

The elastic net (Durbin and Willshaw 1987) can account for the development of both topography and ocular dominance in the mapping from the lateral geniculate nucleus to primary visual cortex (Goodhill and Willshaw 1990). Here it is further shown for this model that (1) the overall pattern of stripes produced is strongly influenced by the shape of the cortex: in particular, stripes with a global order similar to that seen biologically can be produced under appropriate conditions, and (2) the observed changes in stripe width associated with monocular deprivation are reproduced in the model.

scholarly journals Homeostatic plasticity mechanisms in mouse V1

2017 ◽  
Vol 372 (1715) ◽  
pp. 20160504 ◽  
Author(s):  
Megumi Kaneko ◽  
Michael P. Stryker
Keyword(s):  
Visual Cortex ◽  
Primary Visual Cortex ◽  
Neuronal Activity ◽  
Dynamic Range ◽  
Ocular Dominance ◽  
Homeostatic Plasticity ◽  
Ocular Dominance Plasticity ◽  
The Brain

Mechanisms thought of as homeostatic must exist to maintain neuronal activity in the brain within the dynamic range in which neurons can signal. Several distinct mechanisms have been demonstrated experimentally. Three mechanisms that act to restore levels of activity in the primary visual cortex of mice after occlusion and restoration of vision in one eye, which give rise to the phenomenon of ocular dominance plasticity, are discussed. The existence of different mechanisms raises the issue of how these mechanisms operate together to converge on the same set points of activity. This article is part of the themed issue ‘Integrating Hebbian and homeostatic plasticity’.

Critical period for monocular deprivation in the cat visual cortex

1992 ◽  
Vol 67 (1) ◽  
pp. 197-202 ◽  
Author(s):  
N. W. Daw ◽  
K. Fox ◽  
H. Sato ◽  
D. Czepita
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Single Cells ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Significant Shift ◽  
Cat Visual Cortex

1. Cats were monocularly deprived for 3 mo starting at 8-9 mo, 12 mo, 15 mo, and several years of age. Single cells were recorded in both visual cortexes of each cat, and the ocular dominance and layer determined for each cell. Ocular dominance histograms were then constructed for layers II/III, IV, and V/VI for each group of animals. 2. There was a statistically significant shift in the ocular dominance for cells in layers II/III and V/VI for the animals deprived between 8-9 and 11-12 mo of age. There was a small but not statistically significant shift for cells in layer IV from the animals deprived between 8-9 and 11-12 mo of age, and for cells in layers V/VI from the animals deprived between 15 and 18 mo of age. There was no noticeable shift in ocular dominance for any other layers in any other group of animals. 3. We conclude that the critical period for monocular deprivation is finally over at approximately 1 yr of age for extragranular layers (layers II, III, V, and VI) in visual cortex of the cat.

scholarly journals The Order of Information Transfer into Short- Term Memory from Visual Pathways with Different Spatial-Frequency Tunings

2020 ◽  
Vol 13 (2) ◽  
pp. 72-89
Author(s):  
D.S. Alekseeva ◽  
V.V. Babenko ◽  
D.V. Yavna
Keyword(s):  
Spatial Frequency ◽  
Information Transfer ◽  
Short Term Memory ◽  
Frequency Tuning ◽  
Visual Pathways ◽  
Input Image ◽  
Target Face ◽  
Short Term ◽  
Term Memory ◽  
Spatial Frequencies

Visual perceptual representations are formed from the results of processing the input image in parallel pathways with different spatial-frequency tunings. It is known that these representations are created gradually, starting from low spatial frequencies. However, the order of information transfer from the perceptual representation to short-term memory has not yet been determined. The purpose of our study is to determine the principle of entering information of different spatial frequencies in the short-term memory. We used the task of unfamiliar faces matching. Digitized photographs of faces were filtered by six filters with a frequency tuning step of 1 octave. These filters reproduced the spatial-frequency characteristics of the human visual pathways. In the experiment, the target face was shown first. Its duration was variable and limited by a mask. Then four test faces were presented. Their presentation was not limited in time. The observer had to determine the face that corresponds to the target one. The dependence of the accuracy of the solution of the task on the target face duration for different ranges of spatial frequencies was determined. When the target stimuli were unfiltered (broadband) faces, the filtered faces were the test ones, and vice versa. It was found that the short-term memory gets information about an unfamiliar face in a certain order, starting from the medium spatial frequencies, and this sequence does not depend on the processing method (holistic or featural).

scholarly journals Critical periods in amblyopia

2018 ◽  
Vol 35 ◽  
Author(s):  
TAKAO K. HENSCH ◽  
ELIZABETH M. QUINLAN
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Molecular Mechanisms ◽  
Ocular Dominance ◽  
Molecular Genetic ◽  
Monocular Deprivation ◽  
Critical Periods ◽  
Developmental Constraints ◽  
Early Postnatal Development ◽  
Visual Cortical

AbstractThe shift in ocular dominance (OD) of binocular neurons induced by monocular deprivation is the canonical model of synaptic plasticity confined to a postnatal critical period. Developmental constraints on this plasticity not only lend stability to the mature visual cortical circuitry but also impede the ability to recover from amblyopia beyond an early window. Advances with mouse models utilizing the power of molecular, genetic, and imaging tools are beginning to unravel the circuit, cellular, and molecular mechanisms controlling the onset and closure of the critical periods of plasticity in the primary visual cortex (V1). Emerging evidence suggests that mechanisms enabling plasticity in juveniles are not simply lost with age but rather that plasticity is actively constrained by the developmental up-regulation of molecular ‘brakes’. Lifting these brakes enhances plasticity in the adult visual cortex, and can be harnessed to promote recovery from amblyopia. The reactivation of plasticity by experimental manipulations has revised the idea that robust OD plasticity is limited to early postnatal development. Here, we discuss recent insights into the neurobiology of the initiation and termination of critical periods and how our increasingly mechanistic understanding of these processes can be leveraged toward improved clinical treatment of adult amblyopia.

Experience-dependent changes in NMDAR1 expression in the visual cortex of an animal model for amblyopia

2004 ◽  
Vol 21 (4) ◽  
pp. 653-670 ◽  
Author(s):  
KATHRYN M. MURPHY ◽  
KEVIN R. DUFFY ◽  
DAVID G. JONES
Keyword(s):  
Visual Cortex ◽  
Neural Plasticity ◽  
Visual Deprivation ◽  
Monocular Deprivation ◽  
Homeostatic Plasticity ◽  
Cortical Circuits ◽  
Central Visual Field ◽  
Binocular Competition ◽  
Binocular Deprivation ◽  
Cortical Representations

When normal binocular visual experience is disrupted during postnatal development, it affects the maturation of cortical circuits and often results in the development of poor visual acuity known as amblyopia. Two main factors contribute to the development of amblyopia: visual deprivation and reduced binocular competition. We investigated the affect of these two amblyogenic factors on the expression of the NMDAR1 subunit in the visual cortex because activation of the NMDA receptor is a key mechanism of developmental neural plasticity. We found that disruption of binocular correlations by monocular deprivation promoted a topographic loss of NMDAR1 expression within the cortical representations of the central visual field and the vertical and horizontal meridians. In contrast, binocular deprivation, which primarily affects visual deprivation, promoted an increase in NMDAR1 expression throughout the visual cortex. These different changes in NMDAR1 expression can be described as topographic and homeostatic plasticity of NMDA expression, respectively. In addition, the changes in NMDA expression in the visual cortex provide a greater understanding of the neural mechanisms that underlie the development of amblyopia and the potential for visual recovery.

Blockade of Cyclic AMP-Dependent Protein Kinase Does Not Prevent the Reverse Ocular Dominance Shift in Kitten Visual Cortex

2003 ◽  
Vol 90 (6) ◽  
pp. 4027-4032 ◽  
Author(s):  
Satoshi Shimegi ◽  
Quentin S. Fischer ◽  
Yupeng Yang ◽  
Hiromichi Sato ◽  
Nigel W. Daw
Keyword(s):  
Visual Cortex ◽  
Protein Kinase ◽  
Intracellular Signaling ◽  
Ocular Dominance ◽  
Monocular Deprivation ◽  
Dependent Protein Kinase ◽  
Signaling Mechanism ◽  
Chronic Infusion ◽  
Dependent Protein ◽  
Od Distribution

Monocular deprivation (MD) during the critical period for the development of visual cortex causes a loss of binocular response of neurons and a shift to the open eye, a normal ocular dominance (OD) shift. However, when MD is combined with chronic inactivation of the visual cortex by muscimol, the OD distribution of the neurons shifts to the deprived eye (reverse OD shift). We have previously shown that the normal OD shift is abolished by chronic infusion of the protein kinase A (PKA) inhibitor, 8-chloroadenosine-3′, 5′-cyclic monophosphorothioate, Rpisomer (Rp-8-Cl-cAMPS), into kitten visual cortex. In this study, we investigated the effect of this inhibitor on the reverse OD shift. Combination of MD and muscimol infusion into the visual cortex of 6-wk-old kittens caused a reverse OD shift that was comparable to that seen in previous studies. However, a reverse OD shift was also seen with concurrent infusion of the PKA inhibitor with muscimol. The strongest OD shift was observed in layer IV regardless of the presence or absence of the PKA inhibitor. This suggests that the dissociation of pre- and postsynaptic activities, which occurs mainly at thalamocortical synapses, induces the reverse OD shift and that inhibition of PKA does not prevent it. Presumably, an inhibition of PKA has no effect in silent cortex. We conclude that 1) an activation of PKA is not required for the induction of the reverse OD shift, and 2) the intracellular signaling mechanism underlying MD-induced OD plasticity differs between normal and reverse OD shifts.

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