scholarly journals Precise levels of Nectin-3 and an interaction with Afadin are required for proper synapse formation in postnatal visual cortex

2019 ◽  
Author(s):  
Johanna Tomorsky ◽  
Philip R. L. Parker ◽  
Chris Q. Doe ◽  
Cristopher M. Niell
Keyword(s):  
Visual Cortex ◽  
Dendritic Spine ◽  
Cortical Neurons ◽  
Synapse Formation ◽  
Ocular Dominance ◽  
Developmental Time ◽  
Ocular Dominance Plasticity ◽  
Layer 2 ◽  
Eye Opening ◽  
Visual Cortical

AbstractBackgroundDeveloping cortical neurons express a tightly choreographed sequence of cytoskeletal and transmembrane proteins to form and strengthen specific synaptic connections during circuit formation. Nectin-3 is a cell-adhesion molecule with previously described roles in synapse formation and maintenance. This protein and its binding partner, Nectin-1, are selectively expressed in upper-layer neurons of mouse visual cortex, but their role in the development of cortical circuits is unknown.MethodsHere we block Nectin-3 expression (via shRNA) or overexpress Nectin-3 in developing layer 2/3 visual cortical neurons using in utero electroporation. We then assay dendritic spine densities at three developmental time points: eye opening (postnatal day (P)14), one week following eye opening after a period of heightened synaptogenesis (P21), and at the close of the critical period for ocular dominance plasticity (P35).ResultsKnockdown of Nectin-3 beginning at E15.5 or ∼P19 increased dendritic spine densities at P21 or P35, respectively. Conversely, overexpressing full length Nectin-3 at E15.5 led to decreased dendritic spine densities when all ages were considered together. Interestingly, an even greater decrease in dendritic spine densities, particularly at P21, was observed when we overexpressed Nectin-3 lacking its Afadin binding domain, indicating Afadin may facilitate spine morphogenesis after eye opening.ConclusionThese data collectively suggest that the proper levels of Nectin-3, as well as the interaction of Nectin-3 with Afadin, facilitate normal synapse formation after eye opening in layer 2/3 visual cortical neurons.

scholarly journals Precise levels of nectin-3 are required for proper synapse formation in postnatal visual cortex

2020 ◽  
Vol 15 (1) ◽  
Author(s):  
Johanna Tomorsky ◽  
Philip R. L. Parker ◽  
Chris Q. Doe ◽  
Cristopher M. Niell
Keyword(s):  
Visual Cortex ◽  
Dendritic Spine ◽  
Cortical Neurons ◽  
Synapse Formation ◽  
Ocular Dominance ◽  
Developmental Time ◽  
Basal Dendrites ◽  
Layer 2 ◽  
Eye Opening ◽  
Visual Cortical

Abstract Background Developing cortical neurons express a tightly choreographed sequence of cytoskeletal and transmembrane proteins to form and strengthen specific synaptic connections during circuit formation. Nectin-3 is a cell-adhesion molecule with previously described roles in synapse formation and maintenance. This protein and its binding partner, nectin-1, are selectively expressed in upper-layer neurons of mouse visual cortex, but their role in the development of cortical circuits is unknown. Methods Here we block nectin-3 expression (via shRNA) or overexpress nectin-3 in developing layer 2/3 visual cortical neurons using in utero electroporation. We then assay dendritic spine densities at three developmental time points: eye opening (postnatal day (P)14), one week following eye opening after a period of heightened synaptogenesis (P21), and at the close of the critical period for ocular dominance plasticity (P35). Results Knockdown of nectin-3 beginning at E15.5 or ~ P19 increased dendritic spine densities at P21 or P35, respectively. Conversely, overexpressing full length nectin-3 at E15.5 decreased dendritic spine densities when all ages were considered together. The effects of nectin-3 knockdown and overexpression on dendritic spine densities were most significant on proximal secondary apical dendrites. Interestingly, an even greater decrease in dendritic spine densities, particularly on basal dendrites at P21, was observed when we overexpressed nectin-3 lacking its afadin binding domain. Conclusion These data collectively suggest that the proper levels and functioning of nectin-3 facilitate normal synapse formation after eye opening on apical and basal dendrites in layer 2/3 of visual cortex.

scholarly journals Progressive maturation of silent synapses governs the duration of a critical period

2015 ◽  
Vol 112 (24) ◽  
pp. E3131-E3140 ◽  
Author(s):  
Xiaojie Huang ◽  
Sophia K. Stodieck ◽  
Bianka Goetze ◽  
Lei Cui ◽  
Man Ho Wong ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Neural Circuit ◽  
Ocular Dominance ◽  
Critical Periods ◽  
Ocular Dominance Plasticity ◽  
Silent Synapses ◽  
Synapse Maturation ◽  
Silent Synapse ◽  
Visual Cortical

During critical periods, all cortical neural circuits are refined to optimize their functional properties. The prevailing notion is that the balance between excitation and inhibition determines the onset and closure of critical periods. In contrast, we show that maturation of silent glutamatergic synapses onto principal neurons was sufficient to govern the duration of the critical period for ocular dominance plasticity in the visual cortex of mice. Specifically, postsynaptic density protein-95 (PSD-95) was absolutely required for experience-dependent maturation of silent synapses, and its absence before the onset of critical periods resulted in lifelong juvenile ocular dominance plasticity. Loss of PSD-95 in the visual cortex after the closure of the critical period reinstated silent synapses, resulting in reopening of juvenile-like ocular dominance plasticity. Additionally, silent synapse-based ocular dominance plasticity was largely independent of the inhibitory tone, whose developmental maturation was independent of PSD-95. Moreover, glutamatergic synaptic transmission onto parvalbumin-positive interneurons was unaltered in PSD-95 KO mice. These findings reveal not only that PSD-95–dependent silent synapse maturation in visual cortical principal neurons terminates the critical period for ocular dominance plasticity but also indicate that, in general, once silent synapses are consolidated in any neural circuit, initial experience-dependent functional optimization and critical periods end.

Cholinergic and noradrenergic afferents influence the functional properties of the postnatal visual cortex in rats

1999 ◽  
Vol 16 (6) ◽  
pp. 1015-1028 ◽  
Author(s):  
ROSITA SICILIANO ◽  
FRANCESCO FORNAI ◽  
IRENE BONACCORSI ◽  
LUCIANO DOMENICI ◽  
PAOLA BAGNOLI
Keyword(s):  
Visual Cortex ◽  
Functional Properties ◽  
Cortical Neurons ◽  
Developmental Plasticity ◽  
Signal To Noise Ratio ◽  
Ocular Dominance ◽  
Field Size ◽  
Cortical Cells ◽  
Visual Cortical ◽  
Na Depletion

Based on previous evidence that acetylcholine (ACh) and noradrenaline (NA) play a permissive role in developmental plasticity in the kitten visual cortex, we reinvestigated this topic in the postnatal visual cortex of rats with normal vision. In rats, the functional properties of visual cortical cells develop gradually between the second and the sixth postnatal week (Fagiolini et al., 1994). Cortical cholinergic depletion, by basal forebrain (BF) lesions at postnatal day (PD) 15 (eye opening), leads to a transient disturbance in the distribution of ocular dominance (Siciliano et al., 1997). In the present study, we investigated the development of visual cortical response properties following cytotoxic lesions of the locus coeruleus (LC) alone or in combination with lesions of cholinergic BF. The main result is that early NA depletion impairs the orientation selectivity of cortical neurons, causes a slight increase of their receptive-field size, and reduces the signal-to-noise ratio of cell responses. Similar effects are obtained following NA depletion in adult animals, although the effects of adult noradrenergic deafferentation are significantly more severe than those obtained after early NA depletion. Additional cholinergic depletion causes an additional transient change in ocular-dominance distribution similarly to that obtained after cholinergic deafferentation alone. Comparisons between depletion of NA on the one hand and depletion of both NA and ACh on the other suggest that the effects of combined deafferentation on the functional properties studied result from simple linear addition of the effects of depleting each afferent system alone.

Critical periods for functional and anatomical compensation in lateral suprasylvian visual area following removal of visual cortex in cats

1984 ◽  
Vol 52 (5) ◽  
pp. 941-960 ◽  
Author(s):  
L. Tong ◽  
R. E. Kalil ◽  
P. D. Spear
Keyword(s):  
Visual Cortex ◽  
Critical Period ◽  
Ocular Dominance ◽  
Direction Selectivity ◽  
Visual Area ◽  
Critical Periods ◽  
Cortex Lesion ◽  
Thalamic Projections ◽  
Adult Cats ◽  
Visual Cortical

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)

Regulation of ocular dominance plasticity by biogenic amines: An activity mapping using c-FOS immunohistochemistry in rat visual cortex

1998 ◽  
Vol 31 ◽  
pp. S181
Author(s):  
Kazuhiko Nakadate ◽  
Kazuyuki Imamura ◽  
Masayuki Kobayashi ◽  
Peter A. Kaub ◽  
Yasuyoshi Watanabe
Keyword(s):  
Visual Cortex ◽  
Biogenic Amines ◽  
Ocular Dominance ◽  
Ocular Dominance Plasticity

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’.

scholarly journals The Development of Active Binocular Vision under Normal and Alternate Rearing Conditions

2020 ◽  
Author(s):  
Lukas Klimmasch ◽  
Johann Schneider ◽  
Alexander Lelais ◽  
Bertram E. Shi ◽  
Jochen Triesch
Keyword(s):  
Visual Cortex ◽  
Binocular Vision ◽  
Cortical Neurons ◽  
Orientation Tuning ◽  
Active Perception ◽  
Efficient Coding ◽  
Rearing Conditions ◽  
Active Binocular Vision ◽  
Experimental Findings ◽  
Visual Cortical

AbstractThe development of binocular vision is an active learning process comprising the development of disparity tuned neurons in visual cortex and the establishment of precise vergence control of the eyes. We present a computational model for the learning and self-calibration of active binocular vision based on the Active Efficient Coding framework, an extension of classic efficient coding ideas to active perception. Under normal rearing conditions, the model develops disparity tuned neurons and precise vergence control, allowing it to correctly interpret random dot stereogramms. Under altered rearing conditions modeled after neurophysiological experiments, the model qualitatively reproduces key experimental findings on changes in binocularity and disparity tuning. Furthermore, the model makes testable predictions regarding how altered rearing conditions impede the learning of precise vergence control. Finally, the model predicts a surprising new effect that impaired vergence control affects the statistics of orientation tuning in visual cortical neurons.

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.

scholarly journals Postnatal Development of Onset Transient Responses in Macaque V1 and V2 Neurons

2008 ◽  
Vol 100 (3) ◽  
pp. 1476-1487 ◽  
Author(s):  
Bin Zhang ◽  
Earl L. Smith ◽  
Yuzo M. Chino
Keyword(s):  
Visual Cortex ◽  
Eye Movements ◽  
Primary Visual Cortex ◽  
Cortical Neurons ◽  
Newborn Infants ◽  
Neuronal Firing ◽  
Transient Responses ◽  
Visual Cortical ◽  
Better Than

Vision of newborn infants is limited by immaturities in their visual brain. In adult primates, the transient onset discharges of visual cortical neurons are thought to be intimately involved with capturing the rapid succession of brief images in visual scenes. Here we sought to determine the responsiveness and quality of transient responses in individual neurons of the primary visual cortex (V1) and visual area 2 (V2) of infant monkeys. We show that the transient component of neuronal firing to 640-ms stationary gratings was as robust and as reliable as in adults only 2 wk after birth, whereas the sustained component was more sluggish in infants than in adults. Thus the cortical circuitry supporting onset transient responses is functionally mature near birth, and our findings predict that neonates, known for their “impoverished vision,” are capable of initiating relatively mature fixating eye movements and of performing in detection of simple objects far better than traditionally thought.

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