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Blindsight depends on the lateral geniculate nucleus

Author

Listed:
  • Michael C. Schmid

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • Sylwia W. Mrowka

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • Janita Turchi

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • Richard C. Saunders

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • Melanie Wilke

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • Andrew J. Peters

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • Frank Q. Ye

    (Neurophysiology Imaging Facility, NIMH, National Institute of Neurological Disorders and Stroke (NINDS), National Eye Institute (NEI), 49 Convent Drive, Bethesda, Maryland 20892, USA)

  • David A. Leopold

    (Laboratory of Neuropsychology, National Institute of Mental Health (NIMH), 49 Convent Drive, Bethesda, Maryland 20892, USA
    Neurophysiology Imaging Facility, NIMH, National Institute of Neurological Disorders and Stroke (NINDS), National Eye Institute (NEI), 49 Convent Drive, Bethesda, Maryland 20892, USA)

Abstract

The blindsight pathway The primary visual cortex (V1) is crucial for vision, but nearly 40 years ago it was noted that, intriguingly, human patients with V1 injuries can still point to or avoid visual stimuli despite having no conscious perception of them. It has long been thought that this 'blindsight' relies on visual pathways that bypass the usual route from the lateral geniculate nucleus (LGN) to the V1. Using a combination of permanent and reversible lesions, along with behavioural testing and functional magnetic resonance imaging (fMRI) of multiple visual areas in macaques, Schmid et al. show that the LGN itself is a vital link in the 'alternate pathway'. In V1-lesioned animals, LGN inactivation abolishes both visual detection and fMRI activation in higher visual areas, implicating direct LGN projections not only in blindsight, but also as a viable secondary pathway for fast detection during normal vision.

Suggested Citation

  • Michael C. Schmid & Sylwia W. Mrowka & Janita Turchi & Richard C. Saunders & Melanie Wilke & Andrew J. Peters & Frank Q. Ye & David A. Leopold, 2010. "Blindsight depends on the lateral geniculate nucleus," Nature, Nature, vol. 466(7304), pages 373-377, July.
    • Handle: RePEc:nat:nature:v:466:y:2010:i:7304:d:10.1038_nature09179
    DOI: 10.1038/nature09179
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    Cited by:

    1. Laura Biagi & Sofia Allegra Crespi & Michela Tosetti & Maria Concetta Morrone, 2015. "BOLD Response Selective to Flow-Motion in Very Young Infants," PLOS Biology, Public Library of Science, vol. 13(9), pages 1-22, September.
    2. Antoine Barbot & Anasuya Das & Michael D. Melnick & Matthew R. Cavanaugh & Elisha P. Merriam & David J. Heeger & Krystel R. Huxlin, 2021. "Spared perilesional V1 activity underlies training-induced recovery of luminance detection sensitivity in cortically-blind patients," Nature Communications, Nature, vol. 12(1), pages 1-18, December.

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