12-week lecture series on "the neural basis of consciousness" by Prof Nao Tsuchiya.
Given to 3rd year undergraduate level. No prerequisites.
Contents:
1) What are the neural correlates of consciousness (NCC)?
2) What are positive and negative evidence for V1 as the NCC?
3) What are the properties of neurons in higher visual areas?
2. Recap of Wk 5
Argument in support for color vision at the periphery:
Brief presentation (no eye movement) still induces vivid
color sensation.
Neurons at the far eccentricity have bigger RFs.
This convergence effect accumulates over the hierarchy.
Uniform colored surfaces can be the optimal stimulus for
such RFs.
3. Recap of Wk 5
Arguments against for color vision at the periphery:
Cone “density” degrades rapidly off the fovea.
In V1, the fovea is over represented at the expense of the
periphery.
This cortical magnification implies poor vision (not only for
color) at the periphery.
4. Recap of Wk 5
Neural mechanisms underlying blindsight
~90% of visual input from the retina goes through LGN to
V1
~10% goes through superior colliculus and pulvinar to the
cortex
The latter can mediate eye movements and localization in
a nonconscious manner in blindsight
5. Recap of Wk 5
Important concepts/features of neurons in the visual system.
RF and visual hierarchy
Complexication of RF properties
Bigger size of RF
(but, temporal latency may not respect hierarchy)
Columnar organization & layer structure
Multiple visual pathways
6. In Wk 6,
We will address the questions of:
What is the link between neurons and phenomenology?
What is the role of V1 for conscious vision?
What are the properties of the visual cortex beyond V1?
7. Learning Objectives
To be able to answer the following questions:
● What are the neural correlates of consciousness (NCC)?
● What are positive and negative evidence for V1 as the
NCC?
● What are the properties of neurons in higher visual areas?
QFC Chapter 5, 6, 7, 8 (Optional: Frith 1999)
8. In Week 5, we encountered …
... the following fundamental questions:
● Why do we not see images upside down?
● Why do we not see images in a distorted way?
● What is the relationship between the outside world,
our experience and neurons in the brain?
What is the NCC?
9. Are we stuck with these questions?
1990~: An empirical scientific research program
Search for the neural correlates of consciousness
“It seems probable, however, that at any one moment some
active neuronal processes correlate with consciousness,
while others do not. What are the differences between them?
… Where in the brain are the neural correlates of
consciousness?”
What is the NCC?
10. The NCC
QFC Glossary:
“The minimal set of neuronal mechanisms or events jointly
sufficient for a specific conscious percept or experience
(Figure 1.1 and Chapter 5). This is what this book is about”
What is the NCC?
11. Further refinement of the NCC
Full neural correlates of consciousness:
The neural substrate supporting experience in general,
irrespective of its specific content.
Content-specific neural correlates of consciousness:
The neural substrate supporting a particular content of
experience (for example, faces) whether seen, dreamt or
imagined. Koch 2016 Nat Rev Neuro
What is the NCC?
12. How can we find the NCC? -> Final project
Frith 1999 Trends Cogn Sci
What is the NCC?
Neural Correlates of Sensory
stimulation
Neural Correlates of Behaviors
Fix two while varying only one.
Fix one and examine the relations of
the two.
19. What is the NCC?
Summary
Searching the NCC is an empirical research program that has
made a huge advance since 1990.
There are many empirical approaches, some of which can be
great inspiration for your final research proposal (Assessment
4 & 5)!
20.
21. Where is the NCC?
Based on blindsight discussion, it seems the first candidate
area for the NCC is V1.
Blindsight : loss of phenomenology due to V1 damage
Let’s see the evidence for and against it!
Does V1 qualify as the NCC?
22. A psychologists’ “microelectrode”: Adaptation
QFC Glossary: Aftereffect: Prolonged exposure to a stimulus
attribute causes a short lived deficit in the ability to detect that
attribute (as in the orientation-dependent aftereffect; Section 6.2).
In some cases, the opposite attribute is seen, as in the motion
aftereffect where the observer sees upward motion after being
habituated to downward motion (also known as the waterfall illusion;
Section 8.3) or in color afterimages.
Aftereffects are thought to be caused by a recalibration or
adaptation of the underlying neurons.
Does V1 qualify as the NCC?
23. A psychologists’ “microelectrode”: Adaptation
Aftereffects are thought to be caused by a recalibration or
adaptation of the underlying neurons.
○ Adaptation can cause vivid alteration of conscious
phenomenology without changing the stimulus (>>> fixed
NCS with varied NCC)
○ If the adaptation is caused by specific neurons, it can be
used to infer WHERE in the brain the adaptation is
happening.
○ Adaptation can be combined with independent manipulation
of consciousness (or visibility) and “attention”.Does V1 qualify as the NCC?
26. Combination of afterimage, Troxler fading and
attentional modulation?
https://michaelbach.de/ot/
Lilac Chaser
https://michaelbach.de/ot/col-lilacChaser/index.html
Does V1 qualify as the NCC?
31. Orientation-dependent adaptation as a probe
Considered to occur in V1 (and beyond).
Why?
Neurons in the retina and LGN RF do not have selectivity
to the line orientation
Do we need to consciously see the adaptor during
adaptation?
Does V1 qualify as the NCC?
36. Dissociating “adaptation” from “visibility” with “crowding”
Does V1 qualify as the NCC?
Crowded / invisible
orientation still evoke
strong threshold
elevation (= strong
adaptation)
He 1996 Nature
37. Other evidence in favor of V1 as not the NCC
Does V1 qualify as the NCC?
QFC Ch 6
Dreaming vs V1 (during REM, V1 is suppressed)
V1 neurons’ properties do not follow properties of
consciousness
Eye of origin information is not consciously accessible
V1 cells are affected by blinks and eye movements
38. Crick & Koch 1995 V1 Hypothesis
NCC is not in the V1
V1 has no direct projection to the
prefrontal and premotor cortical areas
Does V1 qualify as the NCC?
39. Summary
Crick & Koch’s V1 hypothesis promoted various empirical
research since 1995
V1’s involvement for “reported/reportable” percepts are
unlikely based on various perceptual and neuronal findings.
However, in terms of its involvement for consciousness per
se, it is still unclear.
What about the other areas beyond V1?
Does V1 qualify as the NCC?
43. Neurons in V2 strongly responds to illusory line
Beyond V1
44. Crowded illusory line also generates adaptation
Beyond V1Montaser-Kouhsari 2008 Vision Research
45. Crowded illusory line also generates adaptation
Beyond V1Montaser-Kouhsari 2008 Vision Research
46. … Does nonconscious adaptation requires attention?
Beyond V1Montaser-Kouhsari 2008 Vision Research
47. Summary
Neurons in V2 responds to illusory lines.
Illusory lines can generate adaptation even they are not
visible.
However, this nonconscious adaptation requires attentional
amplification.
Does this pose a question about “sufficiency” of attention for
conscious perception? -> Next week
Beyond V1
48.
49. Visual motion and Middle Temporal (MT/V5) area
(Don’t confuse
MT with MTL -
Medial
Temporal Lobe
- containing
hippocampus
and amygdala)
Beyond V1
MT/V5
MTL
50. Motion after effects and consciousness
Motion aftereffects (Requires visibility & attention)
https://michaelbach.de/ot/mot-adapt/index.html
Beyond V1
51. Adaptation to visible vs. invisible simple and
complex motion
Beyond V1
Initial 68s
adaptation,
then top up
2s
Kaunitz 2011 J of Vision
52. Adaptation to simple and complex motion
Simple motion : evokes sizable MAE without consciousness
and without attention
Beyond V1Kaunitz 2011 J of Vision
53. Adaptation to simple and complex motion
Visible complex motion evokes MAE. Invisible complex
motion evokes very weak MEA.
Beyond V1Kaunitz 2011 J of Vision
56. Phenomenological reports of bilateral MT patients
QFC Glossary: Akinetopsia: A specific deficit in the perception
of visual motion due to a cortical lesion in and around area
MT (Section 8.3).
Fiction, but it looks quite compelling
https://www.youtube.com/watch?v=B47Js1MtT4w
Motion perception deficit in monkey (Newsome 1988 JNS)
Beyond V1
61. Summary
MT’s causal role for visual motion qualia is strongly implicated
by phenomenology, psychophysics, fMRI, lesion,
neurophysiology and microstimulation.
Bilateral lesion abolishes motion qualia (but not others)
Microstimulation causally interfere with the motion
judgement.
Beyond V1
62. Summary
Why does MT generate motion qualia?
What is special about MT? Input? Output? Biophysics? Local
neural circuitry?
This is another form of the Hard Problem...
Beyond V1