Abstract
A central transformation that occurs within mammalian visual cortex is the change from linear, polarity-sensitive responses to nonlinear, polarity-insensitive responses. These neurons are classically labelled as either simple or complex, respectively, on the basis of their response linearity (Skottun et al., 1991). While the difference between cell classes is clear when the stimulus strength is high, reducing stimulus strength diminishes the differences between the cell types and causes some complex cells to respond as simple cells (Crowder et al., 2007; van Kleef et al., 2010; Hietanen et al., 2013). To understand the synaptic basis for this shift in behaviour we used in vivo whole cell recordings while systematically shifting stimulus contrast. We find systematic shifts in the degree of complex cell responses in mouse primary visual cortex (V1) at the subthreshold level, demonstrating that synaptic inputs change in concert with the shifts in response linearity and that the change in response linearity is not simply due to the threshold nonlinearity. These shifts are consistent with a visual cortex model in which the recurrent amplification acts as a critical component in the generation of complex cell responses (Chance et al., 1999).
Significance statement The discovery of simple and complex cells in the primary visual cortex (V1) has been fundamental to our understanding of visual processing. While both cell types are orientation selective, simple cells are spatial phase sensitive while complex cells are phase-invariant. Extracellular recordings have shown that the responses of complex cells become phase sensitive at lower stimulus contrasts, suggesting more flexibility in processing mechanisms than previously thought. The mechanism by which this flexibility arises is not understood. Using in vivo whole cell recordings, we demonstrated that the flexibility in phase sensitivity is also apparent in the subthreshold responses of mouse V1 cells, suggesting that the effect arises from active cortical recurrent network activity and not from passive spiking threshold mechanisms.
Footnotes
The authors report no conflict of interest.
This work was supported by the Australian Research Council Centre of Excellence for Integrative Brain Function (CE140100007), the National Health and Medical Research Council (GNT0525459), the L.E.W. Carty Charitable Fund & Lions Foundation of Victoria and the National Health Institutes (EY-020592).
This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.
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