Vision Flashcards
(26 cards)
Draw (think of) a diagram showing the 3 main streams of vision.
Receptors in retina detect light. RGCs fire.
Ventral stream: ‘what’ pathway for form, colour
* midget cells to parvocellular cells to layers 3-6 of LGN
* Layer 4Cβ of V1 (input)
* Layers 2/3 interblobs and blobs to V2, V4 and eventually IT
Dorsal stream: ‘where’ pathway for movement
* Parasol cells to magnocellular cells to layers 1-2 LGN
* Layers 4C α of V1 to interblobs to V3, V5
Collicular Pathway:
* Retina to SC to caudal pulvinar to POR
* POR relies on SC activity
* Feeds into V5
Can regions identified in collicular pathway of mice be translated to humans?
Several areas suggested as equivalents:
* Lateromedial areas ~ V2
* POR ~ PHC in humans BUT POR anatomical region, PHC functional region
However:
* Mice have very different brain structure (cortical percentage)
* Less reliant on vision (more olfactory and auditory)
* POR has stong A1 connection in mice - is this the same in humans?
Which techniques were used to show that POR receives its input from the SC not LGN/V1?
V1 input not necessary for POR function
* Activity of POR maintained despite silencing of V1
* ChR2 in inhibitory neurons used
Anatomical tracing:
* Few input neurons originated in LGN - retrograte cholera toxin B injected into POR
* Most neurons originate in caudal pulvinar which themselves come from SC - anterograde tracing
Where does Pulvinar get its input from? How does V1 affect activity?
Pulvinar is heterogeneous:
* Caudal: input from SC
* Rostral: input from V1
* Shown using anatomical tracing
V1 silencing largely silences pulvinar, suggesting rostral is dominant (which hides heterogeneity).
Provide an example where anatomical evidence supports functional specialisation
Structure/anatomy does not infer function. However, it can highlight areas of interest to support functional hypotheses.
Blobs and interblobs:
* So called due to different staining patterns (blobs stain darker with cytochrome oxidase)
* Because they contain more metabolically expensive cells, so more mitochondria so darker staining
What are the input and output layers of V1? How was this established?
Input = layer IVβ. Output layer 2/3
* Electrode tracks record through many layers of cortex
* Activity on visual stimulation in layer IV
* Blobs more active on colour image seen
How did electrophysiology assist in the model of cortical modules in V1?
- Understanding of input (IV) and output (2/3) layers
- Orientation columns
- Retinotopic mapping
What is the Jennifer Anniston cell hypothesis?
Idea that cells can be so selective they only respond to one specific face (e.g. Jennifer Anniston).
* Evidence for - some cells (in FCPs) are highly selective.
* Evidence against - death of one cell does not cause loss of only that face recognition (Kabatake et al)
What evidence is there that the dorsal stream may still be necessary for form processing?
Janssen et al 2018 - dorsal areas active during still image viewing
* fMRI BOLD study shows ventral and dorsal areas active with difference in time for activation too short for relay communication.
* When viewing 3D still image
What evidence is there for plasticity of cell selectivity in V1? What are the consequences on this discovery?
Bachatene et al 2015: cells in particular orientation columns can be ‘reprogrammed’ to change their selectivity
* Recording active neurons in orientation column when presenting a non-optimal stimulus.
* Cells shift their peak sensitivity slightly towards (attractive) or away (repulsive) - known previously
* Interestingly, neighbouring columns also seem to shift their orientation despite not being stimulated (reactive)
* To maintain uniform organisation (i.e. 16.5˚for each 0.09mm)
Consequences:
* Does this plasticity exist in higher levels of visual system?
* This experiment is in an anaestetised animal (is that representative?)
* Does this explain some inter-personal variation seen?
What is the purpose of V1?
V1 provides ‘conditions to allow awareness to arise’ for concious visual perception (Mazzi et al)
Organises visual inputs by position (retinotopic map) and type (colour, temporal propoerties…).
What is the major evidence that the two-stream hypothesis (mediated through V1) is incomplete?
Blindsight - i.e. isual ability without concious perception.
* Patients have no concious sight but somehow manage to navigate around objects, dodge objects etc with astonishing accuracy
* Can even show response to different facial expressions (amygdala activity) - Diano et al 2017
* Possible explanation: V1 damaged but collicular pathway intact
What are the pros and cons of human lesion studies when investigating blndsight?
Pros:
* Representative of humans (real!)
* Showed the phenomenon of blindsight
Cons:
* Not repeatable
* No temporal or spatial control (not a clean lesion, so other areas may be damaged)
Why is it better to excite inhibitory cells rather than inhibit excitatory cells when silencing?
Exciting inhibitory cells (e.g. ChR2 into GABAergic cells) less damaging than inhibiting excitatory cells (halorhodopsin):
* Halorhodopsin needs sustained light exposure, more likely to cause damage
How can the heterogeneity of the pulvinar be seen anatomically?
Anterograde tracer (AAV1) linked to GFP injected into SC and Tdtomato injected into V1.
Shows green caudal and red rostral pulvinar split.
Provide evidence that the collicular pathway is responsive to motion.
Gets input through SC:
* SC known to provide input to cerebellum for balance etc
* Presentation of a linearly moving dot (vs. random dots) stimulates much greater activity in SC (compared to V1 where activity the same)
* Sensitivity of SC higher (threshold lower for movement detection)
* Can differentiate between self and object movement
Why is there a trade off between resolution and sensitivity?
Sensitivity requires larger receptive field but resolution requires smaller receptive fields.
Large convergence of receptors increases the change that enough cells in receptive field will be active to stimulate RGC activation, but increases RF size.
What are the outputs of the POR? How is it organised?
Outputs to V1, links to V5 (movement discrimination which bypasses V1) and amygdala
Wang et al 2007 showed that POR has retinotopic organisation. This is important for integration with other areas (e.g. for spatial navigation).
* Shown using retrograde tracing
Why have experiments on the collicular pathway been difficult to repeat in primates (as opposed to mice)?
Similar pathway expected (e.g. given blindsight) but differences:
* POR vs. PHC (anatomically vs. functionally defined)
* Mice less reliant on complex vision (therefore more on collicular?)
Optogenetic techniques used in mice very difficult to replicate in primates:
* Thicker cortex reduces light penetration (1000x more intense for each mm) - ability to increase intensity limited due to photodamage
What are the different regions of V2?
Ventral stream:
* Blobs → thin stripes V2 → V4
* Interblobs → interstripes V2 → V4
Dorsal stream:
* V1 layer 4Ca (M pathway) → thick stripes V2 → middle temporal area (V5)
What is the parallel processing hypothesis?
Different visual characteristics (e.g. colour, form, orientation, movement) are processed simultaneously. Perception achieved by concurrent activation.
What is scotoma?
Inability to report presence of stimuli in a portion of visual field (i.e. a blindspot)
What are the general visual pathways involving the SC?
- Collicular – Pulvinar – MT pathway
- Collicular – Pulvinar – Amygdala pathway
- Collicular – Geniculate – MT pathway (K layers of LGN project (sparsely) to V5 (MT) bypassing V1)
What is ‘visual perception’?
May be considered as the ‘brains ability to interpret visual information’.
There are specialised network for particular facets of vision (ventral, dorsal streams).
