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Contribution of inhibitory mechanisms to direction selectivity and response normalization in macaque middle temporal area

Lookup NU author(s): Professor Alexander Thiele

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Abstract

Inhibitory mechanisms contribute to directional tuning in primary visual cortex, and it has been suggested that, in the primate brain, the middle temporal area (MT) inherits most of its directional information from primary visual cortex (V1). To test the validity of this hierarchical scheme, we investigated whether directional tuning in MT was present upon blockade of local γ-aminobutyratergic (GABAergic) inhibitory mechanisms. Direction selectivity during the initial 50 ms after response onset was abolished in many MT cells when the local inhibitory network was inactivated whereas direction selectivity in later response periods was largely unaffected. Thus, direction selectivity during early response periods is often generated autonomously within MT whereas direction selectivity during later response periods is either inherited from other visual areas or locally mediated by mechanisms other than γ-aminobutyric acid type A receptor (GABAA) inhibition. GABAergic inhibition may also mediate contrast normalization. Our data suggest that GABAA inhibition implements a local direction-selective static nonlinearity, rather than a full normalization in MT. These findings put constraints on strict hierarchical models according to which MT performs more complex computations based on local motion measurements provided by earlier areas, arguing for more distributed and independent information processing.


Publication metadata

Author(s): Thiele A, Distler C, Korbmacher H, Hoffmann K-P

Publication type: Article

Publication status: Published

Journal: Proceedings of the National Academy of Sciences of the United States of America

Year: 2004

Volume: 101

Issue: 26

Pages: 9810-9815

ISSN (print): 0027-8424

ISSN (electronic): 1091-6490

Publisher: National Academy of Sciences

URL: http://dx.doi.org/10.1073/pnas.0307754101

DOI: 10.1073/pnas.0307754101

PubMed id: 15210975


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