Alterations of retinal inputs following striate cortex removal in adult monkey

Dineen, John T.; Hendrickson, Anita E.; Keating, E. Gregory

doi:10.1007/bf00239362

Cited by 52 publications

(35 citation statements)

References 35 publications

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“…Even any P channel-derived inputs to hMTϩ are likely to be subject to summation and hence will likely saturate at a lower contrast than in V1. The fibers of the P pathway in particular undergo retrograde degeneration after damage to V1 (Dineen et al, 1982;Cowey et al, 1989). Surviving geniculate neurons are sparse and interspersed throughout the LGN with a mean diameter between M and P cell averages (Yukie and Iwai, 1981).…”

Section: The Relationship Between Fmri and Neurophysiology In Contrasmentioning

confidence: 99%

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

et al. 2015

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When the human primary visual cortex (V1) is damaged, the dominant geniculo-striate pathway can no longer convey visual information to the occipital cortex. However, many patients with such damage retain some residual visual function that must rely on an alternative pathway directly to extrastriate occipital regions. This residual vision is most robust for moving stimuli, suggesting a role for motion area hMTϩ. However, residual vision also requires high-contrast stimuli, which is inconsistent with hMTϩ sensitivity to contrast in which even low-contrast levels elicit near-maximal neural activation. We sought to investigate this discrepancy by measuring behavioral and neural responses to increasing contrast in patients with V1 damage. Eight patients underwent behavioral testing and functional magnetic resonance imaging to record contrast sensitivity in hMTϩ of their damaged hemisphere, using Gabor stimuli with a spatial frequency of 1 cycle/°. The responses from hMTϩ of the blind hemisphere were compared with hMTϩ and V1 responses in the sighted hemisphere of patients and a group of age-matched controls. Unlike hMTϩ, neural responses in V1 tend to increase linearly with increasing contrast, likely reflecting a dominant parvocellular channel input. Across all patients, the responses in hMTϩ of the blind hemisphere no longer showed early saturation but increased linearly with contrast. Given the spatiotemporal parameters used in this study and the known direct subcortical projections from the koniocellular layers of the lateral geniculate nucleus to hMTϩ, we propose that this altered contrast sensitivity in hMTϩ could be consistent with input from the koniocellular pathway.

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Section: The Relationship Between Fmri and Neurophysiology In Contrasmentioning

confidence: 99%

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

et al. 2015

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“…Earlier studies have employed surgical striate cortex lesions in adult cats and monkeys to investigate area 17/18 interactions (Donaldson and Nash, 1973), cortical blindness (Keating, 1977), visual capacity ('blind sight') remaining after the lesion (Weiskrantz and Cowey, 1970;Weiskrantz, 1978), intracortical axonal degeneration (Creutzfeldt et al, 1977), retinal degeneration (Dineen and Hendrickson, 1981), hypertrophy of dorsal lateral geniculate nucleus (dLGN) and alterations of retinal input after striate cortex lesions Dineen et al, 1982), projection patterns of surviving neurons in the dLGN (Cowey and Stoerig, 1989), and deactivation of area MT (Kaas and Krubitzer, 1992), as well as small excitotoxic striate cortex lesions to study the effects on eye movements (Newsome et al, 1985). In an earlier study we have used small acute heat lesions in the striate cortex to disclose the effects of lateral signal processing on cat single visual cortex cells (Eysel et al, 1987).…”

Section: Lesions Of the Striate Cortexmentioning

confidence: 99%

Increased Receptive Field Size in the Surround of Chronic Lesions in the Adult Cat Visual Cortex

1999

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Visual cortical lesions destroy the target cells for geniculocortical fibers from a certain retinotopic region. This leads to a cortical scotoma. We have investigated the receptive fields of cells in the visual cortex before, 2 days and 2 months after focal ibotenic acid lesions in the adult cat visual cortex and have found signs of receptive field plasticity in the surroundings of the chronic but not the acute and subacute excitotoxic lesions. In the subacute state (first two days post lesion) receptive field sizes of cells at the border of the lesion were reduced in size or remained unchanged. Remapping of cortical receptive fields 2 months later revealed a number of cells with multifold enlarged receptive fields at the border of the lesion. The cells with enlarged receptive fields displayed orientation and direction selectivity like normal cells. The size increase appeared not specifically directed towards the scotoma; however, the enlarged receptive fields can reduce the extent of a cortical scotoma, since previously unresponsive regions of the visual field activate cortical cells at the border of the lesion. This late receptive field plasticity could serve as a mechanism for the filling-in of cortical scotomata observed in patients with visual cortex lesions.

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“…While anatomical (1,(12)(13)(14) and physiological (15)(16)(17) studies in monkeys have helped elucidate the neural mechanisms of the vision surviving striate cortex damage, it is still unclear to what extent the phenomenology of the residual vision in monkeys parallels that of human blindsight. Cowey and Stoerig (18) recently reported that although monkeys with striate lesions could reach for stimuli presented in the affected hemifield, they failed to distinguish between stimulus trials and blank trials in a signal-detection task.…”

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confidence: 99%

Localization of visual stimuli after striate cortex damage in monkeys: parallels with human blindsight.

Moore

Rodman

Repp

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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Blindsight is a phenomenon in which human patients with damage to striate cortex deny any visual sensation in the resultant visual field defect but can nonetheless detect and localize stimuli when persuaded to guess. Although monkeys with striate lesions have also been shown to exhibit some residual vision, it is not yet clear to what extent the residual capacities in monkeys parallel the phenomenon of human blindsight. To clarify this issue, we trained two monkeys with unilateral lesions of striate cortex to make saccadic eye movements to visual targets in both hemifields under two conditions. In the condition analogous to clinical perimetry, they failed to initiate saccades to targets presented in the contralateral hemifield and thus appeared "blind." Only in the condition where the fixation point was turned off simultaneously with the onset of the target-signaling the animal to respond at the appropriate time-were monkeys able to localize targets contralateral to the striate lesion. These results indicate that the conditions under which residual vision is demonstrable are similar for monkeys with striate cortex damage and humans with blindsight.

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Alterations of retinal inputs following striate cortex removal in adult monkey

Cited by 52 publications

References 35 publications

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

Abnormal Contrast Responses in the Extrastriate Cortex of Blindsight Patients

Increased Receptive Field Size in the Surround of Chronic Lesions in the Adult Cat Visual Cortex

Localization of visual stimuli after striate cortex damage in monkeys: parallels with human blindsight.

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