Bypassing V1: a direct geniculate input to area MT.

Beckman Vision Center, University of California, 10 Koret Way, San Francisco, California 94143, USA. <>
Nature Neuroscience (Impact Factor: 14.98). 11/2004; 7(10):1123-8. DOI: 10.1038/nn1318
Source: PubMed

ABSTRACT Thalamic nuclei are thought to funnel sensory information to the brain's primary cortical areas, which in turn transmit signals afresh to higher cortical areas. Here we describe a direct projection in the macaque monkey from the lateral geniculate nucleus (LGN) to the motion-selective middle temporal area (MTor V5), a cortical area not previously considered 'primary'. The constituent neurons are mostly koniocellular, send virtually no collateral axons to primary visual cortex (V1) and equal about 10% of the V1 population innervating MT. This pathway could explain the persistence of motion sensitivity in subjects following injury to V1, suggesting more generally that residual perception after damage in a primary area may arise from sparse thalamic input to 'secondary' cortical areas.

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    ABSTRACT: Area V5 of the visual brain, first identified anatomically in 1969 as a separate visual area, is critical for the perception of visual motion. As one of the most intensively studied parts of the visual brain, it has yielded many insights into how the visual brain operates. Among these are: the diversity of signals that determine the functional capacities of a visual area; the relationship between single cell activity in a specialized visual area and perception of, and preference for, attributes of a visual stimulus; the multiple asynchronous inputs into, and outputs from, an area as well as the multiple operations that it undertakes asynchronously; the relationship between activity at given, specialized, areas of the visual brain and conscious awareness; and the mechanisms used to " bind " signals from one area with those from another, with a different specialization, to give us our unitary perception of the visual world. Hence V5 is, in a sense, a microcosm of the visual world and its study gives important insights into how the whole visual brain is organized—anatomically, functionally and perceptually.
    Frontiers in Integrative Neuroscience 05/2015; 9. DOI:10.3389/fnint.2015.00021
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    ABSTRACT: Patients with striate cortex lesions experience visual perception loss in the contralateral visual field. In few patients, however, stimuli within the blind field can lead to unconscious (blindsight) or even conscious perception when the stimuli are moving (Riddoch syndrome). Using functional magnetic resonance imaging (fMRI), we investigated the neural responses elicited by motion stimulation in the sighted and blind visual fields of eight patients with lesions of the striate cortex. Importantly, repeated testing ensured that none of the patients exhibited blindsight or a Riddoch syndrome. Three patients had additional lesions in the ipsilesional pulvinar. For blind visual field stimulation, great care was given that the moving stimulus was precisely presented within the borders of the scotoma. In six of eight patients, the stimulation within the scotoma elicited hemodynamic activity in area human middle temporal (hMT) while no activity was observed within the ipsilateral lesioned area of the striate cortex. One of the two patients in whom no ipsilesional activity was observed had an extensive lesion including massive subcortical damage. The other patient had an additional focal lesion within the lateral inferior pulvinar. Fiber-tracking based on anatomical and functional markers (hMT and Pulvinar) on individual diffusion tensor imaging (DTI) data from each patient revealed the structural integrity of subcortical pathways in all but the patient with the extensive subcortical lesion. These results provide clear evidence for the robustness of direct subcortical pathways from the pulvinar to area hMT in patients with striate cortex lesions and demonstrate that ipsilesional activity in area hMT is completely independent of conscious perception. Hum Brain Mapp, 2014. © 2014 Wiley Periodicals, Inc.
    Human Brain Mapping 12/2014; 36(4). DOI:10.1002/hbm.22725 · 6.92 Impact Factor
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    ABSTRACT: Motion area V5/MT+ shows a variety of characteristic visual responses, often linked to perception, which are heavily influenced by its rich connectivity with the primary visual cortex (V1). This human motion area also receives a number of inputs from other visual regions, including direct subcortical connections and callosal connections with the contralateral hemisphere. Little is currently known about such alternative inputs to V5/MT+ and how they may drive and influence its activity. Using functional magnetic resonance imaging, the response of human V5/MT+ to increasing the proportion of coherent motion was measured in seven patients with unilateral V1 damage acquired during adulthood, and a group of healthy age-matched controls. When V1 was damaged, the typical V5/MT+ response to increasing coherence was lost. Rather, V5/MT+ in patients showed a negative trend with coherence that was similar to coherence-related activity in V1 of healthy control subjects. This shift to a response-pattern more typical of early visual cortex suggests that in the absence of V1, V5/MT+ activity may be shaped by similar direct subcortical input. This is likely to reflect intact residual pathways rather than a change in connectivity, and has important implications for blindsight function. It also confirms predictions that V1 is critically involved in normal V5/MT+ global motion processing, consistent with a convergent model of V1 input to V5/MT+. Historically, most attempts to model cortical visual responses do not consider the contribution of direct subcortical inputs that may bypass striate cortex, such as input to V5/MT+. We have shown that the signal change driven by these non-striate pathways can be measured, and suggest that models of the intact visual system may benefit from considering their contribution. © The Author (2014). Published by Oxford University Press on behalf of the Guarantors of Brain.
    Brain 11/2014; 138(1). DOI:10.1093/brain/awu328 · 10.23 Impact Factor


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