Lookup NU author(s): Professor Alexander Thiele
Full text for this publication is not currently held within this repository. Alternative links are provided below where available.
Recent in vitro studies have shown that acetylcholine (ACh) selectively reduces the efficacy of lateral cortical connections via a muscarinic mechanism, while boosting the efficacy of thalamocortical/feed-forward connections via a nicotinic mechanism. This suggests that high levels of ACh should reduce center-surround interactions of neurons in primary visual cortex, making cells more reliant on feed-forward information. In line with this hypothesis, we show that local iontophoretic application of ACh in primate primary visual cortex reduced the extent of spatial integration, assessed by recording a neurons' length tuning. When ACh was externally applied, neurons' preferred length shifted toward shorter bars, showing reduced impact of the extra-classical receptive field. We fitted a difference and a ratio of Gaussian model to these data to determine the underlying mechanisms of this dynamic change of spatial integration. These models assume overlapping summation and suppression areas with different widths and gains to be responsible for spatial integration and size tuning. ACh significantly reduced the extent of the summation area, but had no significant effect on the extent of the suppression area. In line with previous studies, we also show that applying ACh enhanced the response in the majority of cells, especially in the later (sustained) part of the response. These findings are similar to effects of attention on neuronal activity. The natural release of ACh is strongly linked with states of arousal and attention. Our results may therefore be relevant to the neurobiological mechanism of attention. Copyright © 2005 The American Physiological Society.
Author(s): Roberts MJ, Zinke W, Guo K, Robertson R, McDonald JS, Thiele A
Publication type: Article
Publication status: Published
Journal: Journal of Neurophysiology
Print publication date: 01/04/2005
ISSN (print): 0022-3077
ISSN (electronic): 1522-1598
Publisher: American Physiological Society
PubMed id: 15548624
Altmetrics provided by Altmetric