Effects of monocular deprivation on the lateral geniculate nucleus in a primate.

Sesma, Michael A.; Irvin, Gregg E.; Kuyk, Thomas; Norton, Thomas T.; Casagrande, Vivien A.

doi:10.1073/pnas.81.7.2255

Cited by 12 publications

(5 citation statements)

References 40 publications

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“…There might conceivably be subtle effects of deprivation in the monkey on the numbers of Y cells, on their responsiveness (as Derrington & Hawken, 1981, found in the cat), on their spatial properties, or on their structure-function relations, but our data are inadequate to permit us to comment on these possibilities. Recently Sesma, Irvin, Kuyk, Norton & Casagrande (1984) reported the effects (or rather lack of effects) of monocular deprivation on the l.g.n. of a New-World primate, the bush baby, Galago.…”

Section: Discussionmentioning

confidence: 99%

Effects of visual deprivation on the development of the monkey's lateral geniculate nucleus.

Blakemore¹,

Vital‐Durand²

1986

The Journal of Physiology

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SUMMARY1. We have studied the physiological properties of cells in the deprived layers of the lateral geniculate nucleus (l.g.n.) in monkeys monocularly deprived from birth for up to 27 weeks, and compared them with results from the non-deprived layers in the same animals and in a series of normal animals.2. Despite the relative shrinkage of cell bodies in the deprived layers, units were easily isolated, were visually responsive and could readily be classified as linear (X) or non-linear (Y) by means of tests of spatial summation. The laminar distribution of cell types and the proportion of Y cells did not seem to be affected by deprivation.3. The patterns and latencies of discharge produced by contrast-reversing gratings did not differ grossly between deprived and non-deprived cells. The peak firing frequencies for drifting gratings were also similar. The degree of surround antagonism (though very variable from cell to cell) seemed unaffected by deprivation.4. Most surprising of all, there was little or no deficit in the spatial resolution of the receptive fields of deprived cells. Recordings were always taken ipsilateral to the deprived eye, and neural 'acuity' tended to be slightly lower in the deprived laminae than the non-deprived. However, this nasal/temporal asymmetry in spatial resolution was not obviously more pronounced than in normal animals.5. Neural 'acuity' was not abnormally low in either contralateral or ipsilateral layers in the l.g.n. of an animal binocularly deprived from birth until a year of age.6. We have not examined chromatic properties or temporal characteristics adequately to say whether they are affected by deprivation.7. Paradoxically, although the post-natal maturation of visual acuity in normal monkeys seems to be mainly limited by peripheral factors, deprivation (which causes a profound defect of behavioural acuity) does not seem to interfere substantially with physiological development of the retina or the geniculate nucleus.

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Section: Discussionmentioning

confidence: 99%

Effects of visual deprivation on the development of the monkey's lateral geniculate nucleus.

Blakemore¹,

Vital‐Durand²

1986

The Journal of Physiology

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“…To date, there have been no studies of the maturation of individual primate axon arbors in the striate cortex. The galago is a particularly appropriate primate model for such a study since a broad data base exists on the normal adult morphology and on the physiology of the geniculostriate system (Carey et al, 1979;Casagrande & Skeen, 1980;Casagrande et al, 1986;Conley et al, 1985;Diamond etal., 1985;Florence & Casagrande, 1987;Glendenning et al, 1976;Irvin et al, 1986;Kaas et al, 1978;Norton et al, 1988;Norton & Casagrande, 1982;Sesma et al, 1984; for reviews, see Casagrande & DeBruyn, 1982;Weller & Kaas, 1982). More importantly, we can directly com-pare the normal development of geniculocortical axons with the normal development of retinogeniculate axons and the effects of monocular deprivation on the retinogeniculate and geniculocortical axons in galagos (Lachica et al, 1989(Lachica et al, , 1990.…”

Section: Introductionmentioning

confidence: 99%

Development of geniculocortical axon arbors in a primate

Florence

Casagrande

1990

Vis Neurosci

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The main objective of the present study was to describe the postnatal development of magnocellular and parvocellular LGN axons within the primate striate cortex. For this purpose, we bulk labeled axons in neonatal prosimians (galagos) in vivo or in vitro at regular intervals from birth (PO) to 12 weeks after birth by injecting horseradish peroxidase (HRP) into white matter anterior to the striate cortex. Filled axons within layer IV were reconstructed, quantitatively analyzed, and compared to a population of adult axons described previously (Florence & Casagrande, 1987).Our results show that although axons are morphologically immature at birth, they are restricted to the upper (IVa) and lower (IV/3) tiers of layer IV of the striate cortex as in adults. In adults, we referred to the presumed magnocellular LGN axons terminating in IVa as type I and the presumed parvocellular axons terminating in IV0 as type II. We used the same convention for developing axons.From birth to 3 weeks postnatal, type I and II axon classes are more variable in appearance than adult counterparts, and are not morphologically class distinct. As axons mature, parent axon shafts increase in caliber, arbors become smaller and more radial, and other immature features (e.g. spikes, protrusions, growth cones) are less evident. Both arbor classes mature slowly and some still exhibit immature features (e.g. growth cones) as late as 12 weeks postnatally. Although arbors do not show class-distinctive features until late in development, each class does show some unique maturational trends. Type I arbors are only slightly larger than adult counterparts at birth, whereas type II arbors are dramatically larger. Type I arbors increase in branch complexity with age, whereas type II arbors simply show a shift in complexity toward the center of the arbor with decreasing size over time. These growth trends suggest that magnocellular and parvocellular pathways to cortex could be differentially vulnerable to the manipulation of postnatal visual experience.

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“…Even outside the LPZ, a shrinkage of neurons was observed in the LGN layers for the treated eye. The type of cell shrinkage perhaps resulted from blurred vision during early development due to the diffuser lens, similar to the shrinkage of LGN neurons in lid‐sutured animals (Casagrande, Guillery, & Harting, ; Sesma, Irvin, Kuyk, Norton, & Casagrande, ; Wiesel & Hubel, ). Therefore, a shrinkage of the LGN neurons outside of the LPZ in these monkeys appears to reflect abnormal developmental alterations in their V1 circuitry.…”

Section: Discussionmentioning

confidence: 82%

Long‐term histological changes in the macaque primary visual cortex and the lateral geniculate nucleus after monocular deprivation produced by early restricted retinal lesions and diffuser induced form deprivation

Takahata

Patel

Balaram

et al. 2018

J of Comparative Neurology

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Ocular dominance (OD) plasticity has been extensively studied in various mammalian species. While robust OD shifts are typically observed after monocular eyelid suture, relatively poor OD plasticity is observed for early eye removal or after tetrodotoxin (TTX) injections in mice. Hence, abnormal binocular signal interactions in the visual cortex may play a critical role in eliciting OD plasticity. Here, we examined the histochemical changes in the lateral geniculate nucleus (LGN) and the striate cortex (V1) in macaque monkeys that experienced two different monocular sensory deprivations in the same eye beginning at 3 weeks of age: restricted laser lesions in macular or peripheral retina and form deprivation induced by wearing a diffuser lens during the critical period. The monkeys were subsequently reared for 5 years under a normal visual environment. In the LGN, atrophy of neurons and a dramatic increase of GFAP expression were observed in the lesion projection zones (LPZs). In V1, although no obvious shift of the LPZ border was found, the ocular dominance columns (ODCs) for the lesioned eye shrunk and those for the intact eye expanded over the entirety of V1. This ODC size change was larger in the area outside the LPZ and in the region inside the LPZ near the border compared to that in the LPZ center. These developmental changes may reflect abnormal binocular interactions in V1 during early infancy. Our observations provide insights into the nature of degenerative and plastic changes in the LGN and V1 following early chronic monocular sensory deprivations.

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Effects of monocular deprivation on the lateral geniculate nucleus in a primate.

Cited by 12 publications

References 40 publications

Effects of visual deprivation on the development of the monkey's lateral geniculate nucleus.

Effects of visual deprivation on the development of the monkey's lateral geniculate nucleus.

Development of geniculocortical axon arbors in a primate

Long‐term histological changes in the macaque primary visual cortex and the lateral geniculate nucleus after monocular deprivation produced by early restricted retinal lesions and diffuser induced form deprivation

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