visual masking ch.5 pp.164-185 the retino-cortical dynamics (recod) model
TRANSCRIPT
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 : 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.