scholarly journals A critical period for number-related plasticity in the visual cortex of blind individuals

2017 ◽  
Vol 17 (10) ◽  
pp. 644
Author(s):  
Shipra Kanjlia ◽  
Lisa Feigenson ◽  
Marina Bedny
1984 ◽  
Vol 52 (5) ◽  
pp. 941-960 ◽  
Author(s):  
L. Tong ◽  
R. E. Kalil ◽  
P. D. Spear

Previous experiments have found that neurons in the cat's lateral suprasylvian (LS) visual area of cortex show functional compensation following removal of visual cortical areas 17, 18, and 19 on the day of birth. Correspondingly, an enhanced retino-thalamic pathway to LS cortex develops in these cats. The present experiments investigated the critical periods for these changes. Unilateral lesions of areas 17, 18, and 19 were made in cats ranging in age from 1 day postnatal to 26 wk. When the cats were adult, single-cell recordings were made from LS cortex ipsilateral to the lesion. In addition, transneuronal autoradiographic methods were used to trace the retino-thalamic projections to LS cortex in many of the same animals. Following lesions in 18- and 26-wk-old cats, there is a marked reduction in direction-selective LS cortex cells and an increase in cells that respond best to stationary flashing stimuli. These results are similar to those following visual cortex lesions in adult cats. In contrast, the percentages of cells with these properties are normal following lesions made from 1 day to 12 wk of age. Thus the critical period for development of direction selectivity and greater responses to moving than to stationary flashing stimuli in LS cortex following a visual cortex lesion ends between 12 and 18 wk of age. Following lesions in 26-wk-old cats, there is a decrease in the percentage of cells that respond to the ipsilateral eye, which is similar to results following visual cortex lesions in adult cats. However, ocular dominance is normal following lesions made from 1 day to 18 wk of age. Thus the critical period for development of responses to the ipsilateral eye following a lesion ends between 18 and 26 wk of age. Following visual cortex lesions in 2-, 4-, or 8-wk-old cats, about 30% of the LS cortex cells display orientation selectivity to elongated slits of light. In contrast, few or no cells display this property in normal adult cats, cats with lesions made on the day of birth, or cats with lesions made at 12 wk of age or later. Thus an anomalous property develops for many LS cells, and the critical period for this property begins later (between 1 day and 2 wk) and ends earlier (between 8 and 12 wk) than those for other properties.(ABSTRACT TRUNCATED AT 400 WORDS)


2018 ◽  
Vol 120 (6) ◽  
pp. 3063-3076 ◽  
Author(s):  
Camilo Ferrer ◽  
Helen Hsieh ◽  
Lonnie P. Wollmuth

Parvalbumin-expressing (PV) GABAergic interneurons regulate local circuit dynamics. In terms of the excitation driving PV interneuron activity, the N-methyl-d-aspartate receptor (NMDAR)-mediated component onto PV interneurons tends to be smaller than that onto pyramidal neurons but makes a significant contribution to their physiology and development. In the visual cortex, PV interneurons mature during the critical period. We hypothesize that during the critical period, the NMDAR-mediated signaling and functional properties of glutamatergic synapses onto PV interneurons are developmentally regulated. We therefore compared the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)- and NMDAR-mediated synaptic responses before (postnatal days 15–20, P15–P20), during (P25–P40), and after (P50–P60) the visual critical period. AMPAR miniature excitatory postsynaptic currents (mEPSCs) showed a developmental decrease in frequency, whereas NMDAR mEPSCs were absent or showed extremely low frequencies throughout development. For evoked responses, we consistently saw a NMDAR-mediated component, suggesting pre- or postsynaptic differences between evoked and spontaneous neurotransmission. Evoked responses showed input-specific developmental changes. For intralaminar inputs, the NMDAR-mediated component significantly decreased with development. This resulted in adult intralaminar inputs almost exclusively mediated by AMPARs, suited for the computation of synaptic inputs with precise timing, and likely having NMDAR-independent forms of plasticity. In contrast, interlaminar inputs maintained a stable NMDAR-mediated component throughout development but had a shift in the AMPAR paired-pulse ratio from depression to facilitation. Adult interlaminar inputs with facilitating AMPAR responses and a substantial NMDAR component would favor temporal integration of synaptic responses and could be modulated by NMDAR-dependent forms of plasticity. NEW & NOTEWORTHY We show for the first time input-specific developmental changes in the N-methyl-d-aspartate receptor component and short-term plasticity of the excitatory drive onto layers 2/3 parvalbumin-expressing (PV) interneurons in the visual cortex during the critical period. These developmental changes would lead to functionally distinct adult intralaminar and interlaminar glutamatergic inputs that would engage PV interneuron-mediated inhibition differently.


1992 ◽  
Vol 67 (1) ◽  
pp. 197-202 ◽  
Author(s):  
N. W. Daw ◽  
K. Fox ◽  
H. Sato ◽  
D. Czepita

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.


2018 ◽  
Author(s):  
Theo Marins ◽  
Maite Russo ◽  
Erika Rodrigues ◽  
jorge Moll ◽  
Daniel Felix ◽  
...  

ABSTRACTEvidence of cross-modal plasticity in blind individuals has been reported over the past decades showing that non-visual information is carried and processed by classical “visual” brain structures. This feature of the blind brain makes it a pivotal model to explore the limits and mechanisms of brain plasticity. However, despite recent efforts, the structural underpinnings that could explain cross-modal plasticity in congenitally blind individuals remain unclear. Using advanced neuroimaging techniques, we mapped the thalamocortical connectivity and assessed cortical thickness and integrity of white matter of congenitally blind individuals and sighted controls to test the hypothesis that aberrant thalamocortical pattern of connectivity can pave the way for cross-modal plasticity. We described a direct occipital takeover by the temporal projections from the thalamus, which would carry non-visual information (e.g. auditory) to the visual cortex in congenitally blinds. In addition, the amount of thalamo-occipital connectivity correlated with the cortical thickness of primary visual cortex (V1), supporting a probably common (or related) reorganization phenomena. Our results suggest that aberrant thalamocortical connectivity as one possible mechanism of cross-modal plasticity in blinds, with potential impact on cortical thickness of V1.SIGNIFICANT STATEMENTCongenitally blind individuals often develop greater abilities on spared sensory modalities, such as increased acuity in auditory discrimination and voice recognition, when compared to sighted controls. These functional gains have been shown to rely on ‘visual’ cortical areas of the blind brain, characterizing the phenomenon of cross-modal plasticity. However, its anatomical underpinnings in humans have been unsuccessfully pursued for decades. Recent advances of non-invasive neuroimaging techniques allowed us to test the hypothesis of abnormal thalamocortical connectivity in congenitally blinds. Our results showed an expansion of the thalamic connections to the temporal cortex over those that project to the occipital cortex, which may explain, the cross-talk between the visual and auditory systems in congenitally blind individuals.


Cell ◽  
1999 ◽  
Vol 98 (6) ◽  
pp. 739-755 ◽  
Author(s):  
Z.Josh Huang ◽  
Alfredo Kirkwood ◽  
Tommaso Pizzorusso ◽  
Vittorio Porciatti ◽  
Bernardo Morales ◽  
...  

2018 ◽  
Vol 29 (7) ◽  
pp. 2859-2875 ◽  
Author(s):  
A W de Borst ◽  
B de Gelder

Abstract Cortical plasticity in congenitally blind individuals leads to cross-modal activation of the visual cortex and may lead to superior perceptual processing in the intact sensory domains. Although mental imagery is often defined as a quasi-perceptual experience, it is unknown whether it follows similar cortical reorganization as perception in blind individuals. In this study, we show that auditory versus tactile perception evokes similar intra-modal discriminative patterns in congenitally blind compared with sighted participants. These results indicate that cortical plasticity following visual deprivation does not influence broad intra-modal organization of auditory and tactile perception as measured by our task. Furthermore, not only the blind, but also the sighted participants showed cross-modal discriminative patterns for perception modality in the visual cortex. During mental imagery, both groups showed similar decoding accuracies for imagery modality in the intra-modal primary sensory cortices. However, no cross-modal discriminative information for imagery modality was found in early visual cortex of blind participants, in contrast to the sighted participants. We did find evidence of cross-modal activation of higher visual areas in blind participants, including the representation of specific-imagined auditory features in visual area V4.


2018 ◽  
Vol 35 ◽  
Author(s):  
TAKAO K. HENSCH ◽  
ELIZABETH M. QUINLAN

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.


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