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J Neurophysiol (June 13, 2007). doi:10.1152/jn.00433.2007
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Submitted on April 17, 2007
Accepted on May 26, 2007

Complex cells increase their phase-sensitivity at low contrasts and following adaptation

Nathan A Crowder1, Joshua Van Kleef1, Bogdan Dreher2, and Michael R. Ibbotson3*

1 Visual Sciences, Research School of Biological Sciences, Australian National University, Canberra, Australian Capital Territory, Australia
2 School of Medical Sciences & Institute for Biomedical Research, University of Sydney, Sydney, Australian Capital Territory, Australia
3 Australia; Visual Sciences, Research School of Biological Sciences, Australian National University, Canberra, Australian Capital Territory, Australia

* To whom correspondence should be addressed. E-mail: ibbotson{at}rsbs.anu.edu.au.

One of the best-known dichotomies in neuroscience is the division of neurons in the mammalian primary visual cortex into simple and complex cells. Simple cells have receptive fields with separate ON and OFF subregions and give phase-sensitive responses to moving gratings, while complex cells have uniform receptive fields and are phase-invariant. The phase-sensitivity of a cell is calculated as the ratio of the first Fourier co-efficient (F1) to the mean time-average (F0) of the response to moving sinusoidal gratings at 100% contrast. Cells are then classified as simple (F1/F0>1) or complex (F1/F0<1). We manipulated cell responses by changing the stimulus contrast or through adaptation. The F1/F0 ratios of cells defined as complex at 100% contrast increased at low contrasts and following adaptation. Conversely, the F1/F0 ratios remained constant for cells defined as simple at 100% contrast. The latter cell type was primarily located in thalamorecipient layers 4 and 6. Many cells initially classified as complex exhibit F1/F0>1 at low contrasts and after adaptation (particularly in layer 4). The results are consistent with the spike-threshold hypothesis, which suggests that the division of cells into two types arises from the non-linear interaction of spike threshold with membrane potential responses.




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