scholarly journals Multiple Roles for Nogo Receptor 1 in Visual System Plasticity

2016 ◽  
Vol 22 (6) ◽  
pp. 653-666 ◽  
Author(s):  
Céleste-Élise Stephany ◽  
Michael G. Frantz ◽  
Aaron W. McGee

During the developmental critical period for visual plasticity, discordant vision alters the responsiveness of neurons in visual cortex. The subsequent closure of the critical period not only consolidates neural function but also limits recovery of acuity from preceding abnormal visual experience. Despite species-specific differences in circuitry of the visual system, these characteristics are conserved. The nogo-66 receptor 1 ( ngr1) is one of only a small number of genes identified thus far that is essential to closing the critical period. Mice lacking a functional ngr1 gene retain developmental visual plasticity as adults and their visual acuity spontaneously improves after prolonged visual deprivation. Experiments employing conditional mouse genetics have revealed that ngr1 restricts plasticity within distinct circuits for ocular dominance and visual acuity. However, the mechanisms by which NgR1 limits plasticity have not been elucidated, in part because the subcellular localization and signal transduction of the protein are only partially understood. Here we explore potential mechanisms for NgR1 function in relation to manipulations that reactivate visual plasticity in adults and propose lines of investigation to address relevant gaps in knowledge.

2021 ◽  
Vol 15 ◽  
Author(s):  
Lauren Lepow ◽  
Hirofumi Morishita ◽  
Rachel Yehuda

As psychedelic compounds gain traction in psychiatry, there is a need to consider the active mechanism to explain the effect observed in randomized clinical trials. Traditionally, biological psychiatry has asked how compounds affect the causal pathways of illness to reduce symptoms and therefore focus on analysis of the pharmacologic properties. In psychedelic-assisted psychotherapy (PAP), there is debate about whether ingestion of the psychedelic alone is thought to be responsible for the clinical outcome. A question arises how the medication and psychotherapeutic intervention together might lead to neurobiological changes that underlie recovery from illness such as post-traumatic stress disorder (PTSD). This paper offers a framework for investigating the neurobiological basis of PAP by extrapolating from models used to explain how a pharmacologic intervention might create an optimal brain state during which environmental input has enduring effects. Specifically, there are developmental “critical” periods (CP) with exquisite sensitivity to environmental input; the biological characteristics are largely unknown. We discuss a hypothesis that psychedelics may remove the brakes on adult neuroplasticity, inducing a state similar to that of neurodevelopment. In the visual system, progress has been made both in identifying the biological conditions which distinguishes the CP and in manipulating the active ingredients with the idea that we might pharmacologically reopen a critical period in adulthood. We highlight ocular dominance plasticity (ODP) in the visual system as a model for characterizing CP in limbic systems relevant to psychiatry. A CP framework may help to integrate the neuroscientific inquiry with the influence of the environment both in development and in PAP.


2015 ◽  
Vol 282 (1803) ◽  
pp. 20142756 ◽  
Author(s):  
Donald E. Mitchell ◽  
Nathan A. Crowder ◽  
Kaitlyn Holman ◽  
Matthew Smithen ◽  
Kevin R. Duffy

Extended periods of darkness have long been used to study how the mammalian visual system develops in the absence of any instruction from vision. Because of the relative ease of implementation of darkness as a means to eliminate visually driven neural activity, it has usually been imposed earlier in life and for much longer periods than was the case for other manipulations of the early visual input used for study of their influences on visual system development. Recently, it was shown that following a very brief (10 days) period of darkness imposed at five weeks of age, kittens emerged blind. Although vision as assessed by measurements of visual acuity eventually recovered, the time course was very slow as it took seven weeks for visual acuity to attain normal levels. Here, we document the critical period of this remarkable vulnerability to the effects of short periods of darkness by imposing 10 days of darkness on nine normal kittens at progressively later ages. Results indicate that the period of susceptibility to darkness extends only to about 10 weeks of age, which is substantially shorter than the critical period for the effects of monocular deprivation in the primary visual cortex, which extends beyond six months of age.


2021 ◽  
Author(s):  
Longqian Liu ◽  
Xiaohang Chen ◽  
Pengfan Chen ◽  
Yifan Wu ◽  
Jianglan Wang ◽  
...  

When human beings recognize the external world, more than 80% of the information come from visual function and visual system. Normal visual development and normal binocularity are the fundamental of good visual acuity and visual functions. Any abnormal visual experience would cause abnormality, such as refractive error, strabismus, amblyopia and other diseases. The patients with abnormal visual developments were reported to have abnormal, lonely, and other psycho problems. In this chapter, we will describe the normal developmental of visual function, summarize the abnormal developments and the correction or treatment.


The Auk ◽  
2019 ◽  
Vol 136 (3) ◽  
Author(s):  
Esteban Fernández-Juricic ◽  
Patrice E Baumhardt ◽  
Luke P Tyrrell ◽  
Amanda Elmore ◽  
Shelagh T DeLiberto ◽  
...  

Abstract Avian vision is fundamentally different from human vision; however, even within birds there are substantial between-species differences in visual perception in terms of visual acuity, visual coverage, and color vision. However, there are not many species that have all these visual traits described, which can constrain our ability to study the evolution of visual systems in birds. To start addressing this gap, we characterized multiple traits of the visual system (visual coverage, visual acuity, centers of acute vision, and color vision) of the Red-winged Blackbird (Agelaius phoeniceus), one of the most abundant and studied birds in North America. We found that Red-winged Blackbirds have: wide visual coverage; one center of acute vision per eye (fovea) projecting fronto-laterally with high density of single and double cones, making it the center of both chromatic and achromatic vision; a wide binocular field that does not have the input of the centers of acute vision; and an ultraviolet sensitive visual system. With this information, we parameterized a Red-winged Blackbird-specific perceptual model considering different plumage patches. We found that the male red epaulet was chromatically conspicuous but with minimal achromatic signal, but the male yellow patch had a lower chromatic but a higher achromatic signal, which may be explained by the pigment composition of the feathers. However, the female epaulet was not visually conspicuous in both the chromatic and achromatic dimensions compared with other female feather patches. We discuss the implications of this visual system configuration relative to the foraging, antipredator, mate choice, and social behaviors of Red-winged Blackbirds. Our findings can be used for comparative studies as well as for making more species-specific predictions about different visual behaviors for future empirical testing.


2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Alexander J. Lingley ◽  
Donald E. Mitchell ◽  
Nathan A. Crowder ◽  
Kevin R. Duffy

The capacity for neural plasticity in the mammalian central visual system adheres to a temporal profile in which plasticity peaks early in postnatal development and then declines to reach enduring negligible levels. Early studies to delineate the critical period in cats employed a fixed duration of monocular deprivation to measure the extent of ocular dominance changes induced at different ages. The largest deprivation effects were observed at about 4 weeks postnatal, with a steady decline in plasticity thereafter so that by about 16 weeks only small changes were measured. The capacity for plasticity is regulated by a changing landscape of molecules in the visual system across the lifespan. Studies in rodents and cats have demonstrated that the critical period can be altered by environmental or pharmacological manipulations that enhance plasticity at ages when it would normally be low. Immersion in complete darkness for long durations (dark rearing) has long been known to alter plasticity capacity by modifying plasticity-related molecules and slowing progress of the critical period. In this study, we investigated the possibility that brief darkness (dark exposure) imposed just prior to the critical period peak can enhance the level of plasticity beyond that observed naturally. We examined the level of plasticity by measuring two sensitive markers of monocular deprivation, namely, soma size of neurons and neurofilament labeling within the dorsal lateral geniculate nucleus. Significantly larger modification of soma size, but not neurofilament labeling, was observed at the critical period peak when dark exposure preceded monocular deprivation. This indicated that the natural plasticity ceiling is modifiable and also that brief darkness does not simply slow progress of the critical period. As an antecedent to traditional amblyopia treatment, darkness may increase treatment efficacy even at ages when plasticity is at its highest.


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)


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 ◽  
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.


2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Peter V. Sguigna ◽  
Morgan C. McCreary ◽  
Darrel L. Conger ◽  
Jennifer S. Graves ◽  
Leslie A. Benson ◽  
...  

2021 ◽  
pp. 821-833
Author(s):  
Shivram Kumar ◽  
Kelly D. Flemming

Visual loss may develop acutely, subacutely, or insidiously. The course may be transient, static, or progressive. This chapter reviews the causes, diagnosis, and treatment of various disorders resulting in visual loss or abnormal visual perception. In addition, it reviews clinical disorders of the eyelids and pupils. Disorders of visual perception involve visual acuity, color perception, visual field defects, and other visual changes. Historical information and physical findings on examination can help to localize the problem and define the cause.


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