Visual Masking Ch.5 pp.164-185

1. Visual MaskingCh.5 pp.164-185 The retino-cortical dynamics (RECOD) model

2. Models of visual masking • Neural-network models • Hartline-Ratliff inhibitory network (Bridgeman) • Rashevski-Landahl two-factor network (Weissstein) • RECOD (Breitmeyer and Ögmen) • Perceptual Retouch (Bachmann) • Boundary Contour System (Francis) • Evidence for Transient-Sustained channel approach • Transient channel (coarse spatial scales, information about temporal change in the stimulus) • Sustained-channel (fine spatial scales, information on stimulus form)

3. Outline • Breitmeyer and Ganz’s sustained-transient dual-channel model • The RECOD model • Theoretical rationale • Temporal multiplexing • Basic architecture • The mathematical basis • Unlumping: contour and surface • Localization and visibility • Next week: Explanatory scope of the RECOD model

4. Breitmeyer and Ganz’s sustained transient dual-channel model (1976). • Main assumptions : • Both target and mask activate long-latency sustained as well as short-latency transient channels. • Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition. • Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition. • Masking occurs in three ways: • Via intra-channel inhibition (particularly in the sustained channel) • Via inter-channel inhibition (partic. transient-on-sustained inhibition) • Via sharing of sustained or transient pathways by the neural activity generated by target and mask when they are spatially overlapping (intra-channel integration). • Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

5. Breitmeyer and Ganz’s sustained transient dual-channel model (1976). • Main assumptions : • Both target and mask activate long-latency sustained as well as short-latency transient channels. • Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition. • Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition. • Masking occurs in three ways: • Via intra-channel inhibition (particularly in the sustained channel) • Via inter-channel inhibition (partic. transient-on-sustained inhibition) • Via sharing of sustained or transient pathways by the neural activity generated by target and mask when they are spatially overlapping (intra-channel integration). • Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

6. Breitmeyer and Ganz’s sustained transient dual-channel model (1976). • Main assumptions : • Both target and mask activate long-latency sustained as well as short-latency transient channels. • Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition. • Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition. • Masking occurs in three ways: • Via intra-channel inhibition (particularly in the sustained channel) • Via inter-channel inhibition (partic. transient-on-sustained inhibition) • Via sharing of sustained or transient pathways by the neural activity generated by target and mask when they are spatially overlapping (intra-channel integration). • Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

7. Breitmeyer and Ganz’s sustained transient dual-channel model (1976). • Main assumptions : • Both target and mask activate long-latency sustained as well as short-latency transient channels. • Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition. • Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition. • Masking occurs in three ways: • Via intra-channel inhibition (particularly in the sustained channel) • Via inter-channel inhibition (partic. transient-on-sustained inhibition) • Via sharing of sustained or transient pathways by the neural activity generated by target and mask when they are spatially overlapping (intra-channel integration). • Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

8. Breitmeyer and Ganz’s sustained transient dual-channel model (1976). • Main assumptions : • Both target and mask activate long-latency sustained as well as short-latency transient channels. • Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition. • Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition. • Masking occurs in three ways: • Via intra-channel inhibition (particularly in the sustained channel) • Via inter-channel inhibition (partic. transient-on-sustained inhibition) • Via sharing of sustained or transient pathways by the neural activity generated by target and mask when they are spatially overlapping (intra-channel integration). • Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

9. Breitmeyer and Ganz’s sustained-transient dual-channel model (1976) • Forward masking • Inter-channel inhibition • Intra-channel integration (structure, noise) and inhibition (paracontrast) • Near synchrony • Intra-channel integration and inhibition (as before) • Backward masking • Inter-channel inhibition • Intra-channel integration and inhibition Breimeyer and Ganz (1976)

10. The retino-cortical dynamics (RECOD) model (Ögmen 1993) • How to deal with feedback processes: theoretical rationale behind the model • Mathematical perspective: need to avoid unstable behaviour • Trade-off between stimulus read-out and perceptual synthesis in a feedback system

11. Purushothaman et al. (1998) The retino-cortical dynamics (RECOD) model • A solution: temporal mutiplexing. • The dynamics of visual processes unfolds in 3 phases. • A feedforward-dominant phase. Strong afferent signals travel to cortical areas allowing read-out of input. • A feeback-dominant phase. Afferent signal decays and feedback signal establishes perceptual synthesis. • A reset phase is initiated when inputs change. A fast transient inhibition of the feedback signal allows dominance of the new input.

12. Purushothaman et al. (1998) The retino-cortical dynamics (RECOD) model • A solution: temporal mutiplexing. • The dynamics of visual processes unfolds in 3 phases. • A feedforward-dominant phase. Strong afferent signals travel to cortical areas allowing read-out of input. • A feeback-dominant phase. Afferent signal decays and feedback signal establishes perceptual synthesis. • A reset phase is initiated when inputs change. A fast transient inhibition of the feedback signal allows dominance of the new input.

13. Purushothaman et al. (1998) The retino-cortical dynamics (RECOD) model • A solution: temporal mutiplexing. • The dynamics of visual processes unfolds in 3 phases. • A feedforward-dominant phase. Strong afferent signals travel to cortical areas allowing read-out of input. • A feeback-dominant phase. Afferent signal decays and feedback signal establishes perceptual synthesis. • A reset phase is initiated when inputs change. A fast transient inhibition of the feedback signal allows dominance of the new input.

14. RECOD model : the basic architecture • The magnocellular / parvocellular pathways are identified with the transient/sustained channels. • Two layers: retinal ganglion cells and LGN+cortical cells • Two channels: fast-phasic M cells (left) and slower tonic P cells (right). • Each channel possesses both positive and negative connectivity patterns. • Intra-channel integration and inhibition for both M and P pathways • Inter-channel inhibition

15. p RECOD model : the mathematical basis • p is the activity variable for the cortical P cells. • The first term ensures the exponential decay of the signal.

16. p RECOD model : the mathematical basis • The first excitatory term is the feedback signal. • ~p2 for small p and is linear for greater values.

17. p RECOD model : the mathematical basis • The second excitatory term is the afferent parvocellular signal. •  is the delay between magno- and parvocellular pathways.

18. p RECOD model : the mathematical basis • Feedback inhibition

19. p RECOD model : the mathematical basis • Afferent parvocellular inhibition

20. p RECOD model : the mathematical basis • Inter-channel transient-on-sustained inhibition

21. RECOD model : contour and surface • Example of model unlumping: contour and surface dynamics • The P pathway post-retinal network is devided in two networks. • Contour processing • Surface processing • A subcortical network is added to account for facilitatory effects in paracontrast

22. RECOD model : contour and surface • Metacontrast • SOA of optimal suppression is shorter for contour visibility than for brightness visibility.

23. RECOD model : contour and surface • Example of model unlumping: contour and surface dynamics • The P pathway post-retinal network is devided in two networks. • Contour processing • Surface processing • A subcortical network is added to account for facilitatory effects in paracontrast.

24. RECOD model : contour and surface • Paracontrast • Maximal facilitatory effects on contour visibility are found at larger SOA than for brightness.

25. Explanatory scope of RECOD model : localization and visibility • Dissociation between target visibility and target localization in metacontrast

26. Next week... • We will look closer at the explanatory scope of the RECOD model. • We will compare model simulations with results of psychophysical experiments.