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Poster

Retinotopic activation of macaque area V2 without input from primary visual cortex

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons84190

Schmid,  M
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons83787

Augath,  M
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons84063

Logothetis,  NK
Department Physiology of Cognitive Processes, Max Planck Institute for Biological Cybernetics, Max Planck Society;

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Zitation

Schmid, M., Augath, M., Logothetis, N., & Smirnakis, S. (2007). Retinotopic activation of macaque area V2 without input from primary visual cortex. Poster presented at 31st Göttingen Neurobiology Conference, Göttingen, Germany.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0013-CE41-0
Zusammenfassung
The presence of focal lesions in primary visual cortex (V1) provides the opportunity to study the role of extra-geniculo-striate pathways for activating extra-striate visual cortex. Previous studies in the macaque have shown that cells in area V2 stop firing after reversibly cooling V1 (Girard and Bullier, 1989; Schiller et al., 1974). However no studies on long term recovery after V1 lesions have been reported in the macaque. Here we use fMRI of the macaque monkey brain to study the organization of V2 from baseline levels up to 16 months post-lesioning. We find that BOLD responses in the lesion projection zone (LPZ) of area V2 are reduced by 80 compared to pre-lesion levels. Surprisingly the retinotopic organization inside the area V2 LPZ is similar before and after inducing the V1 lesion, suggesting that V2 activation is not the result of input arising from nearby non-lesioned V1 cortex. Monitoring of the activity over time after the lesion did not reveal systematic changes in signal amplitude near the LPZ border. We conclude that visually driven activation of extra-striate area V2 as revealed by the BOLD signal is 1) significantly reduced, but still present after depriving it of V1 input, 2) the area V2 LPZ largely retains its original retinotopic organization, and 3) the strength of visual modulation inside the LPZ does not seem to increase significantly up to 16 months post-lesioning. We discuss our findings in the context of parallel pathways in the brain which can activate V2 in the absence of V1 input and may contribute to the behavioral phenomenon of blindsight.