Visual MaskingCh.5 pp.164-185

The retino-cortical dynamics (RECOD) model

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)

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

Breitmeyer and Ganz’s sustained transient dual-channel model (1976).

Main assumptions :

1. Both target and mask activate long-latency sustained as well as short-latency transient channels.

2. Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition.

3. Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition.

4. 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).

l Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

Breitmeyer and Ganz’s sustained transient dual-channel model (1976).

Main assumptions :

1. Both target and mask activate long-latency sustained as well as short-latency transient channels.

2. Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition.

3. Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition.

4. 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).

l Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

Breitmeyer and Ganz’s sustained transient dual-channel model (1976).

Main assumptions :

1. Both target and mask activate long-latency sustained as well as short-latency transient channels.

2. Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition.

3. Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition.

4. 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).

l Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

Breitmeyer and Ganz’s sustained transient dual-channel model (1976).

Main assumptions :

1. Both target and mask activate long-latency sustained as well as short-latency transient channels.

2. Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition.

3. Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition.

4. 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).

l Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

Breitmeyer and Ganz’s sustained transient dual-channel model (1976).

Main assumptions :

1. Both target and mask activate long-latency sustained as well as short-latency transient channels.

2. Within a channel, inhibition is realized via the center-surround antagonism of receptive-field. This is intra-channel inhibition.

3. Between the two channels there exists mutual and reciprocal inhibition, the inter-channel inhibition.

4. 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).

l Transient channels signal the location, presence, rapid changes over time; sustained channels signal patterns (Brightness, contrast and contour of slowly moving stimulus)

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

inhibitionBreimeyer and Ganz (1976)

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

Purushothaman et al. (1998)

The retino-cortical dynamics (RECOD) model

A solution: temporal mutiplexing.

The dynamics of visual processes unfolds in 3 phases.

1. A feedforward-dominant phase. Strong afferent signals travel to cortical areas allowing read-out of input.

2. A feeback-dominant phase. Afferent signal decays and feedback signal establishes perceptual synthesis.

3. A reset phase is initiated when inputs change. A fast transient inhibition of the feedback signal allows dominance of the new input.

Purushothaman et al. (1998)

The retino-cortical dynamics (RECOD) model

A solution: temporal mutiplexing.

The dynamics of visual processes unfolds in 3 phases.

1. A feedforward-dominant phase. Strong afferent signals travel to cortical areas allowing read-out of input.

2. A feeback-dominant phase. Afferent signal decays and feedback signal establishes perceptual synthesis.

3. A reset phase is initiated when inputs change. A fast transient inhibition of the feedback signal allows dominance of the new input.

Purushothaman et al. (1998)

The retino-cortical dynamics (RECOD) model

A solution: temporal mutiplexing.

The dynamics of visual processes unfolds in 3 phases.

1. A feedforward-dominant phase. Strong afferent signals travel to cortical areas allowing read-out of input.

2. A feeback-dominant phase. Afferent signal decays and feedback signal establishes perceptual synthesis.

3. A reset phase is initiated when inputs change. A fast transient inhibition of the feedback signal allows dominance of the new input.

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

p is the activity variable for the cortical P cells.

The first term ensures the exponential decay of the signal.

RECOD model : the mathematical basis

p

RECOD model : the mathematical basis

p The first excitatory term is

the feedback signal.

p2 for small p and is linear for greater values.

RECOD model : the mathematical basis

p The second excitatory term

is the afferent parvocellular signal.

is the delay between magno- and parvocellular pathways.

RECOD model : the mathematical basis

p Feedback inhibition

RECOD model : the mathematical basis

p Afferent parvocellular

inhibition

RECOD model : the mathematical basis

p Inter-channel transient-on-

sustained inhibition

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

RECOD model : contour and surface

Metacontrast

SOA of optimal suppression is shorter for contour visibility than for brightness visibility.

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.

RECOD model : contour and surface

Paracontrast

Maximal facilitatory effects on contour visibility are found at larger SOA than for brightness.

Explanatory scope of RECOD model : localization and visibility

Dissociation between target visibility and target localization in metacontrast

Next week...

We will look closer at the explanatory scope of the RECOD model.

We will compare model simulations with results of psychophysical experiments.