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Chromatic sensitivity of neurones in area MT of the anaesthetised macaque monkey compared to human motion perception

Lookup NU author(s): Professor Alexander Thiele

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Abstract

We recorded activity from neurones in cortical motion-processing areas, middle temporal area (MT) and middle posterior superior temporal sulcus (MST), of anaesthetised and paralysed macaque monkeys in response to moving sinewave gratings modulated in luminance and chrominance. The activity of MT and MST neurones was highly dependent on luminance contrast. In three of four animals isoluminant chromatic modulations failed to activate MT/MST neurones significantly. At low luminance contrast a systematic dependence on chromaticity was revealed, attributable mostly to residual activity of the magnocellular pathway. Additionally, we found indications for a weak S-cone input, but rod intrusion could also have made a contribution. In contrast to the activity of MT and MST neurones, speed judgments and onset amplitude of evoked optokinetic eye movements in human subjects confronted with equivalent visual stimuli were largely independent of luminance modulation. Motion of every grating (including isoluminant) was readily visible for all but one observer. Similarity with the activity of MT/MST cells was found only for motion-nulling equivalent luminance contrast judgments at isoluminance. Our results suggest that areas MT and MST may not be involved in the processing of chromatic motion, but effects of central anaesthesia and/or the existence of intra- and inter-species differences must also be considered. © Springer-Verlag 2005.


Publication metadata

Author(s): Riecansky I, Thiele A, Distler C, Hoffmann K-P

Publication type: Article

Publication status: Published

Journal: Experimental Brain Research

Year: 2005

Volume: 167

Issue: 4

Pages: 504-525

Print publication date: 01/12/2005

ISSN (print): 0014-4819

ISSN (electronic): 1432-1106

Publisher: Springer

URL: http://dx.doi.org/10.1007/s00221-005-0058-2

DOI: 10.1007/s00221-005-0058-2

PubMed id: 16170529


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