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The Effects of Short-Term Synaptic Depression at Thalamocortical Synapses on Orientation Tuning in Cat V1

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  • Aylin Cimenser
  • Kenneth D Miller

Abstract

We examine the effects of short-term synaptic depression on the orientation tuning of the LGN input to simple cells in cat primary visual cortex (V1). The total LGN input has an untuned component as well as a tuned component, both of which grow with stimulus contrast. The untuned component is not visible in the firing rate responses of the simple cells. The suppression of the contribution of the untuned input component to firing rate responses is key to establishing orientation selectivity and its invariance with stimulus contrast. It has been argued that synaptic depression of LGN inputs could contribute to the selective suppression of the untuned component and thus contribute to the tuning observed in simple cells. We examine this using a model fit to the depression observed at thalamocortical synapses in-vivo, and compare this to an earlier model fit based on in-vitro observations. We examine the tuning of both the conductance and the firing rate induced in simple cells by the net LGN input. We find that depression causes minimal suppression of the untuned component. The primary effect of depression is to cause the contrast response curve to saturate at lower contrasts without differentially affecting the tuned vs. untuned components. This effect is slightly weaker for in-vivo vs. in-vitro parameters. Thus, synaptic depression of LGN inputs does not appreciably contribute to the orientation tuning of V1 simple cells.

Suggested Citation

  • Aylin Cimenser & Kenneth D Miller, 2014. "The Effects of Short-Term Synaptic Depression at Thalamocortical Synapses on Orientation Tuning in Cat V1," PLOS ONE, Public Library of Science, vol. 9(8), pages 1-18, August.
  • Handle: RePEc:plo:pone00:0106046
    DOI: 10.1371/journal.pone.0106046
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    Cited by:

    1. Tristan G. Heintz & Antonio J. Hinojosa & Sina E. Dominiak & Leon Lagnado, 2022. "Opposite forms of adaptation in mouse visual cortex are controlled by distinct inhibitory microcircuits," Nature Communications, Nature, vol. 13(1), pages 1-14, December.

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