scholarly journals Structural Changes and Astrocyte Response of the Lateral Geniculate Nucleus in a Ferret Model of Ocular Hypertension

2020 ◽  
Vol 21 (4) ◽  
pp. 1339
Author(s):  
Takashi Fujishiro ◽  
Megumi Honjo ◽  
Hiroshi Kawasaki ◽  
Ryo Asaoka ◽  
Reiko Yamagishi ◽  
...  

We investigated structural changes and astrocyte responses of the lateral geniculate nucleus (LGN) in a ferret model of ocular hypertension (OH). In 10 ferrets, OH was induced via the injection of cultured conjunctival cells into the anterior chamber of the right eye; six normal ferrets were used as controls. Anterograde axonal tracing with cholera toxin B revealed that atrophic damage was evident in the LGN layers receiving projections from OH eyes. Immunohistochemical analysis with antibodies against NeuN, glial fibrillary acidic protein (GFAP), and Iba-1 was performed to specifically label neurons, astrocytes, and microglia in the LGN. Significantly decreased NeuN immunoreactivity and increased GFAP and Iba-1 immunoreactivities were observed in the LGN layers receiving projections from OH eyes. Interestingly, the changes in the immunoreactivities were significantly different among the LGN layers. The C layers showed more severe damage than the A and A1 layers. Secondary degenerative changes in the LGN were also observed, including neuronal damage and astrocyte reactions in each LGN layer. These results suggest that our ferret model of OH is valuable for investigating damages during the retina–brain transmission of the visual pathway in glaucoma. The vulnerability of the C layers was revealed for the first time.

1996 ◽  
Vol 13 (3) ◽  
pp. 585-590 ◽  
Author(s):  
Ivan Suner ◽  
Pasko Rakic

AbstractWe examined the numerical correlation between total populations of neurons in the lateral geniculate nucleus (LGN) and the primary visual cortex (area 17 of Brodmann) in ten cerebral hemispheres of five normal rhesus monkeys using an unbiased three-dimensional counting method. There were 1.4 ± 0.2 million and 341 ±54 million neurons in the LGN and area 17, respectively. In each animal, a larger LGN on one side was in register with a larger area 17 of the cortex on the same side. Furthermore, asymmetry in the number of neurons in both the LGN and area 17 favored the right side. However, because of small variations across subjects, correlation between the total neuron number in LGN and area 17 was weak (r = 0.29). These results suggest that the final numbers of neurons in these visual centers may be established independently or by multiple factors controlling elimination of initially overproduced neurons.


2002 ◽  
Vol 357 (1428) ◽  
pp. 1695-1708 ◽  
Author(s):  
S. Murray Sherman ◽  
R. W. Guillery

The lateral geniculate nucleus is the best understood thalamic relay and serves as a model for all thalamic relays. Only 5–10% of the input to geniculate relay cells derives from the retina, which is the driving input. The rest is modulatory and derives from local inhibitory inputs, descending inputs from layer 6 of the visual cortex, and ascending inputs from the brainstem. These modulatory inputs control many features of retinogeniculate transmission. One such feature is the response mode, burst or tonic, of relay cells, which relates to the attentional demands at the moment. This response mode depends on membrane potential, which is controlled effectively by the modulator inputs. The lateral geniculate nucleus is a first–order relay, because it relays subcortical (i.e. retinal) information to the cortex for the first time. By contrast, the other main thalamic relay of visual information, the pulvinar region, is largely a higher–order relay, since much of it relays information from layer 5 of one cortical area to another. All thalamic relays receive a layer–6 modulatory input from cortex, but higher–order relays in addition receive a layer–5 driver input. Corticocortical processing may involve these corticothalamocortical ‘re–entry’ routes to a far greater extent than previously appreciated. If so, the thalamus sits at an indispensable position for the modulation of messages involved in corticocortical processing.


2019 ◽  
Vol 75 (5) ◽  
pp. 272-276
Author(s):  
Lucia Hlavatá ◽  
Ľubica Ďuďáková ◽  
Jana Moravíková ◽  
Anna Zobanová ◽  
Bohdan Kousal ◽  
...  

Introduction: Achromatopsia is an autosomal recessive retinal disorder with an estimated prevalence ranging from 1 in 30.000 to 50.000. The disease is caused by mutations in six different genes. The aim of the study was to perform molecular genetic analysis in 11 unrelated probands with a clinical diagnosis of achromatopsia and to describe clinical findings in those that were found to carry biallelic pathogenic mutations. Methods: All probands and their parents underwent ophthalmic examination. Mutation detection was performed using Sanger sequencing of CNGB3 exons 6, 7, 9-13, which have been found to harbour most diseasecausing mutations in patients with achromatopsia of European origin. Results: Three known pathogenic variants in CNGB3 were identified in 2 probands. Proband 1 was a compound heterozygote for the c.819_826del; p.(Arg274Valfs*13) and c.1006G>T; p.(Glu336*). Proband 2 carried the c.1148del; p.(Thr383Ilefs*13) in a homozygous state. The best corrected visual acuity in proband 1 (aged 19 years) was 0.1 in both eyes, in proband 2 (aged 8 years) 0.05 in the right eye and 0.1 in the left eye. Both individuals had nystagmus, photophobia, and absence of colour discrimination. Fundus examination appeared normal however spectral-domain optical coherence tomography revealed subtle bilaterally symmetrical structural changes in the fovea. Conclusion: Molecular genetic analysis of Czech patients with achromatopsia was performed for the first time. Identification of diseasecausing mutations in achromatopsia is important for establishing an early diagnosis, participation in clinical trials assessing gene therapies and may be also used for preimplantation genetic diagnosis.


2016 ◽  
Vol 27 (2) ◽  
pp. 135-157 ◽  
Author(s):  
Theodore G. Weyand

AbstractProviding the critical link between the retina and visual cortex, the well-studied lateral geniculate nucleus (LGN) has stood out as a structure in search of a function exceeding the mundane ‘relay’. For many mammals, it is structurally impressive: Exquisite lamination, sophisticated microcircuits, and blending of multiple inputs suggest some fundamental transform. This impression is bolstered by the fact that numerically, the retina accounts for a small fraction of its input. Despite such promise, the extent to which an LGN neuron separates itself from its retinal brethren has proven difficult to appreciate. Here, I argue that whereas retinogeniculate coupling is strong, what occurs in the LGN is judicious pruning of a retinal drive by nonretinal inputs. These nonretinal inputs reshape a receptive field that under the right conditions departs significantly from its retinal drive, even if transiently. I first review design features of the LGN and follow with evidence for 10 putative functions. Only two of these tend to surface in textbooks: parsing retinal axons by eye and functional group and gating by state. Among the remaining putative functions, implementation of the principle of graceful degradation and temporal decorrelation are at least as interesting but much less promoted. The retina solves formidable problems imposed by physics to yield multiple efficient and sensitive representations of the world. The LGN applies context, increasing content, and gates several of these representations. Even if the basic concentric receptive field remains, information transmitted for each LGN spike relative to each retinal spike is measurably increased.


2006 ◽  
Vol 23 (5) ◽  
pp. 795-805 ◽  
Author(s):  
DANIEL L. ADAMS ◽  
JONATHAN C. HORTON

During development, the projection from the lateral geniculate nucleus to striate cortex becomes segregated into monocular regions called ocular dominance columns. Prior studies in cats have suggested that experimental strabismus or alternating monocular occlusion increases the width and segregation of columns. In the squirrel monkey, strabismus has been reported to induce the formation of ocular dominance columns. However, these studies are difficult to interpret because no animal can serve as its own control and the degree of inter-individual variability among normal subjects is considerable. We have re-examined the effect of strabismus on ocular dominance columns in a large group of strabismic and normal squirrel monkeys. Five animals rendered strabismic at age one week had well-developed, widely spaced columns. Among 16 control animals, a wide spectrum of column morphology was encountered. Some control animals lacked ocular dominance columns, whereas others had columns similar to those observed in strabismic animals. Natural variation in column expression in normal squirrel monkeys, and potential uncontrolled genetic influences, made it impossible to determine if strabismus affects ocular dominance columns. It was evident however, that strabismus does not affect the binocular projection from the lateral geniculate nucleus to each CO patch in the upper layers. In strabismic monkeys, just as in normal animals, each patch received input from geniculate afferents serving both the left eye and the right eye. In addition, in strabismic monkeys, as in normal animals, patches were not aligned with ocular dominance columns.


2007 ◽  
Vol 24 (6) ◽  
pp. 775-785 ◽  
Author(s):  
MATTHEW R. KUTCHER ◽  
KEVIN R. DUFFY

Monocular deprivation during early development causes rearrangement of neural connections within the visual cortex that produces a shift in ocular dominance favoring the non-deprived eye. This alteration is manifested anatomically within deprived layers of the lateral geniculate nucleus (LGN) where neurons have smaller somata and reduced geniculocortical terminal fields compared to non-deprived counterparts. Experiments using monocular deprivation have demonstrated a spatial correlation between cytoskeleton alteration and morphological change within the cat LGN, raising the possibility that subcellular events mediating deprivation-related structural rearrangement include modification to the neuronal cytoskeleton. In the current study we compared the spatial and temporal relationships between cytoskeleton alteration and morphological change in the cat LGN. Cross-sectional soma area and neurofilament labeling were examined in the LGN of kittens monocularly deprived at the peak of the critical period for durations that ranged from 1 day to 7 months. After 4 days of deprivation, neuron somata within deprived layers of the LGN were significantly smaller than those within non-deprived layers. This structural change was accompanied by a spatially coincident reduction in neurofilament immunopositive neurons that was likewise significant after 4 days of deprivation. Both anatomical effects reached close to their maximum by 10 days of deprivation. Results from this study demonstrate that alteration to the neuronal cytoskeleton is both spatially and temporally linked to the gross structural changes induced by monocular deprivation.


1993 ◽  
Vol 69 (6) ◽  
pp. 2258-2260 ◽  
Author(s):  
T. G. Weyand ◽  
J. G. Malpeli

1. We tested the effects of eye position on the visual excitability of 88 neurons in the primary visual cortex of awake cats trained in oculomotor tasks. For most cells, we examined responses evoked by retinotopically identical stimuli for centered gaze, 8 degrees to the left of center, and 8 degrees to the right of center. 2. An effect of eye position was observed for 40% of the cells. For 13%, responsiveness varied by a factor of 2 or more. Most commonly, response was maximal with gaze shifted to one side, minimal when shifted to the opposite side, and intermediate for centered fixation. The exceptions were four cells for which excitability varied symmetrically with fixations to either side of center. 3. Variability in excitability associated with eye position is a wide-spread phenomenon, having been observed in the lateral geniculate nucleus, V1, and extrastriate cortex. These results are consistent with the belief that such variability is utilized in constructing a head-centered frame of reference from a retinotopic input.


2007 ◽  
Vol 84 (1) ◽  
pp. 176-184 ◽  
Author(s):  
Neeru Gupta ◽  
Tina Ly ◽  
Qiang Zhang ◽  
Paul L. Kaufman ◽  
Robert N. Weinreb ◽  
...  

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