OPTO30007 MST 1 Visual Neuroscience PDF

**[OPTO30007: Visual Neuroscience]** ***MST 1*** ***Three layers of the wall of the eye*** +-----------------+-----------------+-----------------+-----------------+ | | **Outer coat** | **Middle coat** | **Inner coat** | +-----------------+-----------------+-----------------+---...

**[OPTO30007: Visual Neuroscience]** ***MST 1*** ***Three layers of the wall of the eye*** +-----------------+-----------------+-----------------+-----------------+ | | **Outer coat** | **Middle coat** | **Inner coat** | +-----------------+-----------------+-----------------+-----------------+ | *Structures* | Cornea | Ciliary body, | Retina; | | | (transparent) | iris and | includes optic | | | and sclera | choroid | nerve, macula | | | (white) | | (and fovea), | | | | | posterior pole | | | | | and ora serrata | | | | | (junction | | | | | between the | | | | | retina and | | | | | ciliary body) | +-----------------+-----------------+-----------------+-----------------+ | *Function* | **Transparency* | **Aqueous | Generate | | | * | humour | electrical | | | (cornea): | production** | signals from | | | collagen | (ciliary body): | light stimulus | | | fibrils grouped | aqueous humour | to produce | | | into packets of | secreted by | visual | | | fibres | ciliary | perception | | | organised in | epithelial | | | | parallel; each | cells and | | | | packet is | provides | | | | oriented at a | nutrients (e.g. | | | | different angle | glucose and | | | | | amino acids) | | | | **Strength** | and O~2~ to | | | | (sclera): | cornea and lens | | | | collagen | (avascular | | | | fibrils are | zones) and | | | | organised in | maintain shape | | | | whirls | and intraocular | | | | | pressure (IOP) | | | | | of the eye; | | | | | aqueous humour | | | | | is secreted | | | | | near the iris | | | | | and enters the | | | | | anterior | | | | | chamber, where | | | | | it is | | | | | eventually | | | | | drained by the | | | | | trabecular | | | | | meshwork | | | | | | | | | | **Accommodation | | | | | ** | | | | | (ciliary body): | | | | | changes the | | | | | shape of the | | | | | lens to | | | | | accommodate | | | | | near vision; | | | | | | | | | | - When | | | | | viewing | | | | | **far** | | | | | objects, | | | | | ciliary | | | | | muscle is | | | | | relaxed and | | | | | ligaments | | | | | are taut, | | | | | causing | | | | | lens to | | | | | thin | | | | | | | | | | - when | | | | | viewing | | | | | **close** | | | | | objects, | | | | | ciliary | | | | | muscle | | | | | contracts | | | | | and | | | | | ligaments | | | | | are slack, | | | | | causing | | | | | lens to | | | | | bulge; | | | | | allows more | | | | | refraction | | | | | to focus | | | | | object | | +-----------------+-----------------+-----------------+-----------------+ +-----------------------------------+-----------------------------------+ | ***Optical factors limiting |  | | visual acuity*** | | | | ***Central vision*** | | - **Pupil size**: smaller pupil | | | allows better vision | Visual acuity is highest in the | | | fovea due to: | | - **Clarity of optical media**: | | | vision limited by | - Highest density of cones is | | abnormalities impeding | at fovea | | passage of light, e.g. | | | cataract or corneal opacity | - Non-photoreceptor cells are | | | pushed aside in the fovea | | - **Refractive errors**: | (RGCS and BCs); this limits | | abnormal eye size causes | the interference with the | | light to focus before/after | passage of light to cones | | retina, e.g. | | | | - Fovea is an avascular zone; | | | no blood vessels are present | | | here to limit the | | - Myopia: eye is too long so | interference with the passage | | light focuses BEFORE retina | of light | | short sightedness | | | | - Only red and green cones are | | - Hypermetropia: eye is too | present in the fovea | | short so light focuses AFTER | | | retina long sightedness | ***Optic nerve*** | | | | | - Astigmatism | The optic nerve must pass the | | | sclera to exit the retina; at the | | ***Neural components of the | optic nerve head (i.e. the site | | retina*** | where axons of RGCs exit the | | | retina) the sclera forms a | | **Through pathway**: | mesh-like structure for the optic | | | nerve fibres to pass called the | | - Photoreceptors (PRs) | **lamina cribrosa** \-- the | | | central retinal artery and | | - Bipolar cells (BCs) | central retinal vein, which run | | | through the centre of the optic | | - Retinal ganglion cells (RGCs) | nerve, also exit through the | | | lamina cribrosa | | **Lateral interactions**: | | | | ***Photopigment*** | | - Horizontal cells (HCs): | | | synapse between | The outer segment contains stacks | | photoreceptors | of outer segment discs; these are | | | membranous discs that have | | - Amacrine cells (Acs): synapse | photopigments embedded in their | | between bipolar cells and | membrane. The photopigments | | retinal ganglion cells (RGCs) | comprise a G-protein coupled | | | receptor (opsin, e.g. rhodopsin | | ***Layers of the retina*** | or cone-opsin) bound to a | | | chromophore (i.e. 11-cis | | - Nerve fibre layer: axons of | retinal/vitamin A). | | RGCs | | | | ***Phototransduction*** | | - Ganglion cell layer: contains | | | cell bodies of RGCs | Photoreceptors are hyperpolarised | | | by light and signal by graded | | - Inner plexiform layer: | changes in membrane potential | | synaptic layer between RGCs | which lead to graded changes in | | and BCs | glutamate release (same for | | | bipolar cells); degree of | | - Inner nuclear layer: contains | hyperpolarisation increases with | | cell bodies of BCs (and HCs | intensity of light source. | | and Acs) | | | | **In the dark**, | | - Outer plexiform layer: | | | synaptic layer between BCs | 1. intracellular cGMP is high | | and PRs | | | | 2. cGMP-gated Na^+^ channels in | | - Outer nuclear layer: contains | the outer segment are kept | | cell bodies of PRs | open by cGMP | | | | | ***Photoreceptors*** | 3. Continuous influx of Na^+^ | | | ions through cGMP-gated | | Photoreceptors are either | channel causes depolarisation | | **rods** or **cones** | | | | 4. High levels of glutamate | | - **Rods** are responsible for | release | | night vision (i.e. scotopic) | | | | **In the light**, | | | | | | 1. Light causes 11-cis retinal | | - Very sensitive: can respond | to straighten and become | | to low light levels | all-trans retinal causing the | | | opsin protein to change | | - One type | conformation | | | | | - 95% of PR | 2. G-protein (transducin) is | | | activated by conformational | | - Cannot discriminate colour | change in opsin | | | | | - Absent from fovea and densest | 3. Phosphodiesterase is | | at 15⁰ from fovea | activated by transducin which | | | breaks down cGMP into GMP | | | | | | 4. cGMP-gated Na^+^ channels | | - **Cones** are responsible for | close | | day vision (i.e. photopic) | | | | 5. Influx of Na^+^ stops causing | | | photoreceptor to become | | | hyperpolarised | | - Less sensitive to light | | | | 6. Less glutamate is released | | - Three types (L-, M- and | | | S-cones) | ***Calcium regulation of | | | photoreceptor recovery*** | | - 5% of PR | | | | **In the dark**, Ca^2+^ enters | | - Can discriminate colour | photoreceptor via open cGMP-gated | | | channels and voltage-gated Ca^2+^ | | - Densest at fovea and drop off | channels (VGCC) | | rapidly in periphery (poor | | | visual acuity in periphery) | **In the light**, cGMP-gated | | \-- cone density determines | channels are closed and VGCC are | | visual acuity | closed so Ca^2+^ influx is | | | reduced | | Photoreceptors are comprised of: | | | | - Guanylate cyclase is | | - Outer segment: contains outer | inhibited by Ca^2+^; | | segment discs that have | therefore, guanylate cyclase | | photopigment embedded in | activity is upregulated in | | their membrane, site of | the light (due to low Ca^2+^) | | phototransduction | | | | - Rhodopsin kinase is also | | - Inner segment: contains | inhibited by Ca^2+^, | | mitochondria, ribosomes and | therefore more arrestin can | | Golgi apparatus | bind rhodopsin in light | | | | | - Cell body: contains the | - Ca^2+^ decreases the affinity | | nucleus of the photoreceptor | of cGMP for cGMP-gated | | | channels so cGMP binds | | - Synaptic terminal: site of | channels more strongly in | | neurotransmitter release, | light | | photoreceptors contact BCs | | | and HCs | ***Colour vision*** | | | | | ***Evidence for glutamate release | Each type of cone responds to | | from photoreceptors*** | each wavelength of light | | | differently to create different | | [Synthesis]: | patterns of activation for each | | | wavelength which correspond to a | | - Photoreceptors express | colour; the type of cone is | | enzymes for glutamate | determined by the amino acid | | synthesis | sequence of the cone opsin (as | | | they all have the same structure) | | - Glutamate labelling shows | | | glutamate in photoreceptor | - S (blue) cone opsin: | | terminals | rhodopsin and blue cone opsin | | | have very different sequence; | | [Release] | encoded on different | | | chromosomes | | [Receptor | | | activation]: | - M (green) cone opsin: blue | | | and green cone opsin have | | - Glutamate receptors | very different sequence; | | identified on bipolar cells | encoded on different | | | chromosomes | | [Degradation]: | | | | - L (red) cone opsin: green and | | - Muller glia cells at | red cone opsin have **very | | photoreceptor-bipolar cell | similar sequences**; encoded | | synapse | by the same chromosomal | | | region | | ***Photoreceptor recovery*** | | | | Red cones ≈ green cones \>\> blue | | Must recover 11-cis retinal | cones | | rapidly to allow photoreceptor to | | | respond to next flicker of light | *Note*: rod BCs are ON bipolar | | (perform phototransduction in | cells, whereas cone BCs can be ON | | reverse): | or OFF bipolar cells | | | | | - [Restore cGMP | ***Ganglion cells*** | | levels]: cGMP is | | | constitutively produced by | Types of ganglion cells: | | **guanylate cyclase** (GC) | | | | - [M (parasol or magnocellular) | | - [Restore rhodopsin to | ganglion cells]: | | inactive state]: | large dendritic | | activated rhodopsin is | trees/receptive fields; | | rapidly phosphorylated by | provide motion detection, | | **rhodopsin kinase** leading | flicker and analysis of gross | | to binding of **arrestin** | features | | which prevents rhodopsin from | | | activating transducin | - [P (midget or parvocellular) | | | ganglion cells]: | | - [Restore 11-cis | small dendritic | | retinal]: | trees/receptive fields; | | all-trans retinal is recycled | provide colour vision and | | in the retinal pigment | visual acuity | | epithelium (RPE) in the | | | **retinoid cycle** | | | | | | 1. All-trans retinal transported | - P ganglion cells \> M | | out of photoreceptor and | ganglion cells | | converted to all-trans | | | retinol | | | | | | 2. All-trans retinol transported | - [OFF-centre ganglion | | into RPE by IRBP | cells]: | | | **hyperpolarised by light on | | 3. All-trans retinol converted | centre** and synapse w. OFF | | back to 11-cis retinal by | BCs, express iGluRs | | several isomerases | | | | - [ON-centre ganglion | | 4. 11-cis retinal transported | cells]: | | back into photoreceptor by | **depolarised by light on | | IRBP to bind opsin protein | centre** and synapse w. ON | | | BCs; express iGluRs | |  | | | | - [Intrinsically photosensitive | | ***Bipolar cells*** | ganglion cell]: | | | respond to light without | | There are 10 different types of | through pathway | | bipolar cells (1 rod BC and 9 | | | cone BCs); each has a different | ***Centre-surround receptive | | morphology, therefore different | fields*** | | function. | | | | Ganglion cell receptive fields | | [OFF bipolar cells] | are organised so the response in | | are **hyperpolarised by light** | the centre is opposite to the | | and terminate in the upper region | response in the periphery | | of the inner plexiform layer | | | (IPL). OFF BCs express | - [Central | | **ionotropic glutamate | response] is | | receptors** (iGluRs): | determined by **through | | | pathway**, i.e. input from | | - Either AMPA, kainite or NMDA | PRs to BCs to GCs | | | | | - In the dark, PRs release lots | | | of glutamate causing OFF BCs | | | to depolarise as many | - ON BCs input to ON GCs | | channels are open | | | | - OFF BCs input to OFF GCs | | - In the light, PRs release | | | little glutamate causing OFF |  | | BCs to hyperpolarise as few | | | channels are open | - [Surround | | | response] is | | [ON bipolar cells] | determined by **input from | | are **depolarised by light** and | horizontal cells** | | terminate in the lower region of | | | the IPL. ON BCs express | | | **metabotropic glutamate | | | receptors** (mGluR6): | - HCs express iGluRs and | | | release GABA | | - Glutamate binding to mGluR6 | | | initiates a second messenger | 1. In the light, PRs release | | cascade which leads to | less glutamate onto HCs | | closure of **TRPM1 channels** | causing HCs to be | | (a cation channel) | hyperpolarised | | | | | - In the dark, PRs release lots | 2. HCs release less GABA onto | | of glutamate causing ON BCs | central photoreceptors | | to hyperpolarise as many | causing them to depolarise | | TRPM1 channels are closed | and increase glutamate | | | release | | - In the light, PRs release | | | little glutamate causing ON | 3. In ON pathway, mGluR6 is | | BCs to depolarise as few | activated more causing | | TRPM1 channels are closed | hyperpolarisation of ON BCs | | | | | [TRPM1 deficiency]: | 4. In OFF pathway, iGluRs are | | | activated more causing | | - Appaloosa horses have reduced | depolarisation of OFF BCs | | TRPM1 expression, i.e. | | | reduced ON bipolar cell | Centre-surround organisation | | activity | allows ganglion cells to respond | | | optimally to edges; ganglion cell | | | will fire differently depending | | | on where borders fall on the | | - No b-wave in | receptive field | | electroretinogram | | | (corresponds to ON BC | [Rod through | | activity) | pathway]: | | | | | - Night blindness |  | | | | | - Spotty coats | ooDSGCs target three primary | | | pathways: | | ***Amacrine cells*** | | | | - **Lateral geniculate | | Amacrine cells primarily release | nucleus** for conscious | | inhibitory neurotransmitters onto | visual perception | | BCs and GCs to modify the | | | ganglion cell output. | - **Superior colliculus** for | | | reflexive eye movements | | There are approximately 22 types | | | of amacrine cells which contain | - **Accessory optic nucleus** | | EITHER glycine or GABA, and can | for nystagmus | | contain other NTs, e.g. ACh, | | | dopamine or neuropeptides. Each | ***Ganglion cell function*** | | type has a different morphology, | | | therefore different function. | Size of ganglion cell dendritic | | These are axonless cells | field (i.e. receptive field) is | | | smallest in fovea and increases | | [AII amacrine cells]: | with distance from fovea | | mediate rod through pathway as it | | | 'piggy backs' onto cone through | [Visual acuity**:**] | | pathway as night vision is recent | | | evolutionary adaptation | - **In the fovea**, there is a | | | 1:1 connection between cones | | - Rod photoreceptors synapse | and P ganglion cells, i.e. | | with a **rod bipolar cell** | **one cone** synapses with | | which expresses **mGluR6**, | **one ON (or OFF) bipolar | | i.e. rod BCs are ON bipolar | cell** which synapses with | | cells because they are | one ON (or OFF) P ganglion | | **depolarised by light** | cell \-- each P ganglion cell | | | can encode a single piece of | | - Rod bipolar cells DO NOT | information from cone | | synapse with ganglion cells, | photoreceptors to produce | | only synapse with **AII | maximal visual acuity | | amacrine cells** which | | | express **iGluRs** and | - **In the periphery**, there | | **release glycine** to | is a many:one connection | | communicate with ON and OFF | between cones and P ganglion | | cone bipolar cells to | cells, i.e. **several cones** | | transmit signals | synapse with several ON (or | | | OFF) bipolar cells which | | - AII amacrine cells form | synapse with **one ON (or | | synaptic connections w. OFF | off) P ganglion cell** \-- | | cone BCs and form gap | each P ganglion cell encodes | | junctions w. ON cone BCs | information from several | | | cones and cannot discriminate | | **In the light**, | this information to produce | | | poorer visual acuity | | 1. Rod BCs are depolarised to | | | release more glutamate onto | - With increasing distance from | | AII amacrine cells | the fovea, the ratio of | | | cone:P ganglion cell | | 2. AII amacrine cells release | increases | | more glycine onto OFF cone | | | BCs OFF cone BCs are | | | hyperpolarised by light | | | falling on rod PRs | | | | | | 3. AII amacrine cells are | | | depolarised so positive ions | | | flow passively into ON cone | | | BCs ON cone BCs are | | | depolarised by light falling | | | on rod PRs | | | | | | [Starburst amacrine cells | | | (SBACs)]: produce | | | direction selectivity; ablating | | | SBACs causes DSGCs to have same | | | response to stimuli moving in all | | | directions, i.e. direction | | | selectivity is lost | | | | | | - SBACs primarily release GABA, | | | can also release ACh | | | | | | - SBACs are found in retina of | | | primates and lower | | | vertebrates | | | | | | **ON-OFF direction selective | | | ganglion cells** (ooDSGCs): | | | respond maximally to a bar of | | | light moving in preferred | | | direction and no response when | | | bar of light moves in null | | | (opposite) direction, this is | | | determined by SBAC activity | | | | | | - SBACs activity can be | | | measured by intracellular | | | Ca^2+^ levels (more Ca^2+^ = | | | more GABA release) | | | | | | - SBACs respond maximally to | | | stimuli moving from **soma to | | | dendrite** and responds | | | minimally to stimuli moving | | | from dendrite to soma, i.e. | | | respond maximally to the null | | | direction of its postsynaptic | | | ooDSGC | | | | | | - **In the preferred | | | direction**, light moves from | | | dendrite to soma of SBACs | | | causing little GABA release | | | ooDSGCs receive little | | | inhibition and fire rapidly | | | | | | - **In the null direction**, | | | light moves from soma to | | | dendrite of SBACs causing | | | lots of GABA release ooDSGCs | | | receive lots of inhibition to | | | reduce their firing rate | | +===================================+===================================+ | [Colour | Evidence for the activity of | | discrimination]: | ipGCs | | | | | 1. **Wavelength detection**: | - Inducing expression of | | Each type of cone responds | melanopsin in HEK293 (kidney) | | differently to each | cells causes membrane | | wavelength of light; | potential to change in | | combination of cone responses | response to light stimulus | | encodes a particular | | | wavelength in the visible | - In blind rd1 mice which have | | spectrum | severe degeneration of | | | photoreceptors, activity | | 2. **Colour discrimination**: P | could still be observed in | | ganglion cells have colour | ganglion cells | | opponent centre-surround | | | receptive fields; depolarised | Targets of ipGCs include: | | by one colour on centre and | | | hyperpolarised by opponent | - **Suprachiasmatic nucleus** | | colour on surround | of the hypothalamus: controls | | | the circadian rhythm | | - Red-green opponency | | | | - **Lateral habenula**: light | | - Blue-yellow opponency | regulation of mood | | | | | Central response is | - **Posterior nucleus of the | | determined by type of cone PR | thalamus**: involved in | | in through pathway (to ON BCs | allodynia (perceiving | | and GCs) and surround | non-painful stimuli as | | response is determined by | painful), i.e. photophobia | | opponent cone PR feeding into | | | horizontal cells (similar to | - **Superior colliculus**: | | ON/OFF-centre ganglion cells) | coordinates eye movements | | | | | [Non-image forming | - **Optical pretectal nucleus** | | functions]: | (optical pretectum in the | | | midbrain); light directed to | | Intrinsically photosensitive | one eye causes dilation in | | ganglion cells (ipGCs) express | both eyes (consensual | | melanopsin \-- melanopsin is a | response) | | G-protein coupled receptor | | | associated w. a G~q~ protein: | | | | | | 1. Light causes G~q~ protein to | - Axons of ipGCs synapse with | | dissociate and activates | neurons in the ipsilateral | | phospholipase C | pretectal nucleus before | | | reaching the LGN | | 2. Second messenger cascade | | | opens TRPC channel to allow | - Pretectal neurons send | | cation influx | excitatory inputs to | | | parasympathetic nerves in the | | 3. ipGC is **depolarised by | Edinger-Westphal nucleus on | | light** | the ipsilateral and | | | contralateral side | | ipGCs have larger dendritic | | | fields than M and P ganglion | - Parasympathetic nerves | | cells and are much sparser in the | innervate sphincter pupillae | | retina | muscles, causing them to | | | contract | |  | | | | ***Dark adaptation*** | | ***Visual adaptation*** | | | | Adaptation following transition | | Must be able to detect small | from light to dark luminance | | changes in light intensity, | levels (e.g. entering a movie | | colour and position (for moving | theatre on a bright summer day) | | stimuli). Therefore, visual | | | system must adjust its operating | - Slower process (approx. 40 | | range to a billion-fold intensity | minutes): can be detrimental | | range to maintain sensitivity to | to survival | | light; mostly done by | | | photoreceptors as pupils only | - | | account for 10-fold change. | | | | [Weber's law and dark | | At low intensities, there is a | adaptation]: with | | trade off in the scotopic (rod) | increasing time in the dark, the | | and photopic (cone) systems; | threshold required to detect a | | spatial and temporal resolution | light stimulus decreases | | are reduced, however the visual | | | system is maximally sensitive and | - Cones are more sensitive | | can respond to individual photons | initially when presenting | | | brighter stimuli | | The ideal visual system for | | | adaptation would have **high | - Rods are more sensitive later | | sensitivity at low light levels** | when presenting dimmer | | AND **would not saturate** (i.e. | stimuli | | stop being able to detect light) | | | **at high light levels**. | - Red light can be used to more | | | quickly dark adapt as rods | | - **Rods** have high | are relatively insensitive to | | sensitivity at low light | long (red) wavelengths (and | | levels, but saturate at high | will not saturate) | | light levels | | | | ***Light adaptation*** | | | | | | Adaptation following transition | | - Rods detect single photons | from dark to light luminance | | but have slow response | levels (e.g. after leaving the | | kinetics and a short | cinema on a bright summer day) | | operating range | | | | - Fast process (seconds): | | | beneficial to survival | | | | | - **Cones** do not saturate at | [Weber's | | high light levels, but have | law and light | | poorer sensitivity | adaptation]: the | | | threshold required to detect a | | | light stimulus increases with | | | background illuminance | | - Cones are less sensitive but | | | have fast response kinetics | - Rods are more sensitive | | and a wide operating range | initially at lower background | | | illuminance | | Therefore, rods and cones | | | function together to optimise the | - Cones are more sensitive | | visual response to a wide range | later at higher background | | of luminance | illuminances | | | | | [Weber's | ***Molecular basis of light | | Law]: the threshold | adaptation*** | | for detecting a change in a | | | stimulus is in a constant ratio | Mechanisms that contribute to | | with the background intensity, | light adaptation are related to | | i.e. more noise = harder to | mechanisms of photoreceptor | | detect stimulus | recovery | | | | | ***Rod adaptation*** | [Ca^2+^-independent | | | processes]: | | Without adaptation, rods would be | | | expected to saturate rapidly and | - **Pigment depletion** (in | | be unable to respond to | cones): recovery of | | incremental stimuli. | photopigment by PDE | | | | | - Rods are able to recover and | - **Activation of | | respond to subsequent stimuli | phosphodiesterase** (in rods | | at very low intensities, | and cones): in the light, | | however this occurs over a | cGMP turnover is much faster | | **restricted range of | due to increased PDE activity | | intensity** (1-2 log units) | \-- causes cone response to | | | incremental stimuli in | | - Recovery of rods is more | background illumination to be | | pronounced in higher light | reduced (i.e. | | intensities | desensitisation) | | | | | - Rod saturation at very low | [Ca^2+^-dependent | | light levels can be induced | processes]: | | by reducing cytoplasmic | | | Ca^2+^ | Responsible for majority of light | | | adaptation response via a | | ***Cone adaptation*** | negative feedback loop \-- | | | cytoplasmic Ca^2+^ decreases in | | Cones | response to light to cause | | respond to subsequent light | photoreceptor recovery (and avoid | | flashes with high fidelity and | saturation) via **Ca^2+^ | | increase their response as | unbinding from**: | | intensity of the stimulus | | | increases, due to their ability | - **Guanylate cyclase | | to light adapt quickly | activating proteins** | | | (GCAPs): GCAP activates | | - Cones **recover much more | guanylate cyclase to increase | | rapidly** and can adapt over | cytoplasmic levels of cGMP | | a wide range of light | causing cGMP-gated channels | | intensities without becoming | to open and PR able to | | saturated | respond to new stimulus | | | | | - Cones can adapt even when | | | background illumination is | | | present, however their | - 1 unit of Ca^2+^ change = 12 | | response to incremental | units of cGMP channel opening | | stimuli is reduced | | | | | | - Cones use Ca^2+^-dependent | | | and Ca^2+^-independent | - **Recoverin**: recoverin | | mechanism of light adaptation | inhibits rhodopsin kinase | | \-- mouse models w. no GCAP, | activity at high Ca^2+^ | | recoverin or cones can still | levels, therefore unbinding | | light adapt and lowering | of Ca^2+^ from recoverin | | cytoplasmic Ca^2+^ still | causes phosphorylation of | | allows light adaptation to | activated rhodopsin (R^\*^) | | occur (albeit, slower) | \-- lifetime of R^\*^ is | | | reduced (faster turnover) and | | - Cones **do not saturate** | PR can respond to new | | because: | stimulus | | | | | | - **Calmodulin** | | | (rods)**/Ca^2+^-sensitive CNG | | - Cones have 20-fold shorter | channel regulator** (cones; | | time constants than rods so | unknown type): Unbinding of | | can recover rapidly | Ca^2+^ from calmodulin (and | | | its cone analogue) causes | | - cGMP binds cone cGMP-gated | cGMP to bind cGMP-gated | | channels more tightly in low | channels more tightly -- same | | Ca^2+^ concentration | concentration of cGMP will | | | open more cGMP-gated channels | | ***Rod vs. cone adaptation*** | | | | ***Inheritance patterns of | | Cones require 240X more intense | IRDs*** | | stimulus to saturate than rods | | | | *[Autosomal | | - Rods and cones express the | recessive]*: | | **same GCAP and recoverin** | individual must have **two | | protein | copies** of the disease variant | | | to cause disease | | - Rods and cones have | | | **different cGMP-gated | - Mechanism: **loss of | | channel proteins** (encoded | function** mutation; | | by different genes | insufficient protein to | | | perform normal function | | - Response kinetics in **rods | | | is much slower** than cones | - Inheritance: carriers have | | (PDE activation and R^\*^ | one copy of genetic variant | | much longer) | but usually show no symptoms | | | | | - **Cones receive recycled | - Example: ABCA4-related IRDs | | 11-cis retinal** from the | -- ABCA4 gene encodes | | **RPE and Muller glia cells** | ATP-binding cassette | | vs. rods receive recycles | transporter 4 located in | | 11-cis retinal ONLY from RPE | photoreceptor outer segment | | | involved in retinoid cycle by | | ***Inherited retinal diseases | preventing build-up of toxic | | (IRD)*** | vitamin A derivates in the | | | RPE; mutations in ABCA4 gene | | IRD are **rare** genetic | cause RPE breakdown | | mutations in genes that encode | | | proteins required for | | | **photoreceptor survival and | | | function** (includes 300+ genes) | - Associated diseases include | | | Stargardt disease, rod-cone | | - Different genes can produce | dystrophy (e.g. retinitis | | same disease phenotype (if | pigmentosa) or cone-rod | | mutation is in protein that | dystrophy | | mediates same function) | | | | *[Autosomal | | - Mutations in the same gene | dominant]*: | | can produce different disease | individual only needs **one | | phenotypes | copy** of the disease variant to | | | cause disease | | - Genetic mutations can be | | | caused by environmental | - Mechanism: **loss of | | factors (e.g. chemical or | function** mutation; one copy | | radiation damage from UV | of the gene is insufficient | | light) or genetic factors | to maintain normal function | | (errors in DNA replication or | OR **dominant | | recombination) | negative****N75**: initial | so cannot recover as well | | negative deflection generated | | | by activity in **LGN** | Mice HCN1 mutants have poor | | | temporal resolution; cannot track | | - **P100**: positive deflection | high frequency information and | | generated by activity in | show similar responses to short | | **visual cortex** | and fast flashes of light | | | | | - Late waveforms: generated by | | | activity in association areas | | | or other conscious processing | | | areas of brain | | | | | | *[Clinical application of | | | VEP]*: | | | | | | - Albinism: optic nerve does | | | not cross at optic chiasm \-- | | | produces bilateral | | | contralateral predominance in | | | VEP so strongest signal is in | | | contralateral hemisphere to | | | the eye being stimulated vs. | | | normal VEP shows symmetrical | | | distribution of VEP signal | | | (largest signal in central | | | electrode, smaller signals in | | | flanking electrodes) | | | | | |  | | | | | | - Visual acuity in children: | | | alternate checkerboard | | | pattern with decreasing size | | | of checks and measure VEP | | | amplitude until no signal is | | | produced -- indicates maximum | | | visual acuity | | | | | | - Amblyopia | | | | | | - Measure function of visual | | | pathway in conditions that | | | degrade neurons, e.g. MS or | | | stroke \-- seen as delayed | | | P100 | | +-----------------------------------+-----------------------------------+ **\ ** ***MST 2*** +-----------------------------------+-----------------------------------+ | ***Layers of the LGN*** | ***Contrast sensitivity*** | | | | | [Magnocellular | Contrast can be calculated as: | | layer]: | | | | [\$Micehlson\\ contrast = \\ | | - receives input from **parasol | \\frac{(L\_{\\max} - | | RGCs** | L\_{\\min})}{(L\_{\\max} + | | | L\_{\\min})}\$]{.math.inline} | | - comprises LGN **layers 1 and | | | 2** | OR | | | | | [Parvocellular | \ | | layer:] | [\$\$Contrast = \\ | | | \\frac{\\mathrm{\\Delta}L}{L\_{\\ | | - receives input from **midget | text{average}}}\$\$]{.math | | RGCs** |.display}\ | | | | | - comprises **LGN layers 3 -- | The lowest contrast at which a | | 6** | grating can be *detected* is the | | | **contrast threshold**. The | | [Koniocellular | reciprocal of contrast threshold | | layer:] | is **contrast sensitivity**, e.g. | | | if a patient detects a grating | | - receives input from **small | with 1% contrast, the contrast | | bistratified cells** | sensitivity for that spatial | | | frequency is 100 (1/0.1). | | - located between the 6 layers | Therefore, the higher the | | | contrast sensitivity, the lower | | Layers **1, 4 and 6** receive | the contrast level needed to | | input from the **contralateral | detect the grating. This is | | eye**, whereas layers **2, 3 and | usually measured with sine wave | | 5** receive input from the | gratings that differ in their | | **ipsilateral eye** | spatial frequency | | | | |  | The **spatial contrast | | | sensitivity function** (spatial | | ***Response to contrast*** | CSF) plots the contrast | | | sensitivity for a number of | | **ON-centre cells** respond to | spatial frequencies -- this | | **positive contrast** (centre is | reveals that contrast sensitivity | | brighter than surround) and | is highest for gratings of medium | | **OFF-centre cells** respond to | spatial frequency (4 -- 6 | | **negative contrast** (centre is | cycles/degree). This is because | | darker than surround). This is an | medium spatial frequency gratings | | adaptive mechanism that | have one half of the grating | | **increases the range of | falling on the centre of the | | stimuli** that we can respond to | receptive field and the other | | and **reduces the metabolic | half falls on the surround, | | cost** of these neurons; having | producing maximal activity in the | | two separate cells to respond to | centre and surround, whereas the | | each end of the spectrum of | other types of gratings produce | | contrast means baseline firing | equal stimulation of the centre | | rates can be kept close to zero | and surround, which cancel each | | (which requires minimal energy to | other out. | | maintain) and that each type of | | | cell can encode many responses to |  | | one type of contrast (compared to | | | a cell that has baseline firing | This curve is similar for humans | | at medium levels and | and macaque monkeys. | | increases/reduces firing in | | | response to positive/negative | ***Koniocellular pathway*** | | contrast, which would require | | | more energy and have a shorter | Small bistratified cells are a | | range. | type of RGC that carry signals | | | from short wavelength sensitive | | ***Properties of LGN cells*** | (blue) cones to koniocellular | | | layers of the LGN. Koniocellular | | Single cell recordings of cells | cells are located in between the | | in the LGN can reveal their | M and P layers and form 'konio | | contrast sensitivity by recording | bridges' that pass through P | | their spike response to gratings | layers. | | of different contrast. | | | | ***Response properties of LGN | | - Magnocellular cells are | cells*** | | **more sensitive to | | | contrast** than parvocellular | - [Magnocellular | | cells (response rate is | cells] respond | | higher in magnocellular cells | optimally to achromatic | | at lower contrasts). | stimuli (black and white | | Therefore, low contrast | gratings with different | | vision is mediated by | contrast) | | magnocellular cells. | | | | - [Parvocellular | | - Magnoce | cells] respond | | llular | optimally to isoluminant\* | | cells are **colourblind**; | red/green gratings | | they show similar responses | | | to all colours, whereas | \-- these cells will show | | parvocellular cells show | poor response to isoluminant | | **chromatic selectivity** | blue/yellow stimulus because | | (i.e. different responses to | yellow correspond to equal | | different colours | red and green input | | | | | | - [Koniocellular | | | cells] respond | | - Magnocellular cells are | optimally to isoluminant | | **sensitive to motion**; they | blue/yellow gratings | | show much better responses to | | | gratings moving at different | \*Isoluminant means that colour | | temporal frequencies | is the only difference, not | | | difference in luminance | |  | (brightness) | +-----------------------------------+-----------------------------------+ +-----------------------------------+-----------------------------------+ | **Magnocellular cells** | **Parvocellular cells** | +-----------------------------------+-----------------------------------+ | Large receptive fields (low | Small receptive cells (high | | spatial resolution) | spatial resolution) | | | | | High contrast sensitivity | Lower contrast sensitivity | | | | | Poor isoluminant response | Chromatic selectivity | | | | | Good motion sensitivity (high | Poor motion sensitivity (low | | temporal resolution) | temporal frequency) | | | | | Fast conduction velocity (larger | Slow conduction velocity | | axons) | | | | Sustained response (respond for | | Transient response (respond to | entire duration of stimulus | | onset of stimulus) | onset) | | | | | Drive motion perception | Drive red/green colour vision | +-----------------------------------+-----------------------------------+ +-----------------------------------+-----------------------------------+ | ***Balance*** | ***Optokinetic response (OKR)*** | | | | | Sense of balance is necessary to | The OKR is the reflex that | | inform the nervous system where | stabilises the image of a moving | | our head and body are in space. | visual scene on the retina, which | | Information about balance is used | can be caused by: | | without any conscious effort to | | | control muscular contractions | - **Self-motion** (our own | | for: | movement through the world); | | | this is *most common source* | | - allowing us to stand upright | of movement of the visual | | | world | | - adjusting for disturbances in | | | body position (e.g. if | - A **moving environment** (the | | someone pushes us over) | world moves around us) | | | | | - positioning our bodies in | The OKR is **more important in | | space | animals with lateral eyes** as | | | this causes the world to stream | | - directing our eyes to where | past the eyes, whereas in animals | | they should be to maximise | with frontally placed eyes (e.g., | | the stability of the retinal | primates) the visual scene tends | | image as our heads move | to loom closer to the eyes when | | around | moving around. | | | | | The primary sources of | ***Optokinetic nystagmus (OKN)*** | | information for determining body | | | orientation in space are: | In the modern world, humans are | | | exposed to scenarios where the | | 1. Visual: can be high level | visual world itself is moving | | (i.e. known orientation of | (e.g. on a train). In this | | the scene) or low level (bulk | situation, OKN is elicited, which | | motion of a scene) | involves two phases: | | | | | 2. Proprioceptive/kinaesthetic: | 1. A slow eye movement that | | knowledge about joint | follows the moving stimulus, | | position and muscle force | followed by | | | | | 3. Vestibular: detects | 2. A fast saccade in the | | accelerations of the head | opposite direction to reset | | | the gaze | | ***Accessory Optic System*** | | | | The cells that produce OKN have | | The OKR first evolved in the | large receptive fields, so do not | | primitive **accessory optic | respond to fine detail (only low | | system** (AOS) which bypasses the | grade texture). | | geniculocortical pathway. In | | | fish, there is full decussation | Experimental tests of OKN can be | | of retinal fibres (i.e. each AOS | a test of vision in non-verbal | | receives input from the | subjects. These require large, | | contralateral eye ONLY) which | full-field stimuli which elicit | | project directly to the pretectal | robust OKN (vs. small hand-held | | area (APT) of the AOS which have | devices that elicit smooth | | direct projections to the ocular | pursuit via cortical inputs) | | motor nuclei which control | | | movement of extraocular muscles | ***Vestibulo-ocular reflex | | to initiate compensatory eye | (VOR)*** | | movements. | | | | The VOR is critical in primates | | In mammals, the AOS still | and describes the compensatory | | receives direct projections from | eye movements (in the opposite | | the retina, however the AOS also | direction) that are produced | | receives projections from the | during head movements to | | geniculocortical pathway to | stabilise the image of the visual | | modulate activity of the AOS \-- | scene on the retina. | | these inputs are driven by the | | | smooth pursuit system to allow us | The vestibular system, located in | | to track particular features in a | the **inner ear**, activates the | | visual scene, rather than the | VOR in response to **head | | whole scene (as the primitive AOS | motion**, which can be of two | | system does). The contribution of | types: | | inputs to the AOS varies between | | | animals, e.g. | - World-fixed: trying to fixate | | | a static object while you are | | - In fish, retinal (R) input | moving; this will **enhance | | only | the VOR** | | | | | - In cats, R and cortical (C) | - Head-fixed: trying to fixate | | input available but retina | an object that is moving | | dominates | exactly with you; this will | | | **suppress the VOR** | | - In monkeys, R & C inputs | | | available but cortex | The vestibular system functions | | dominates | to (1) maintain balance by | | | detecting linear acceleration and | | - In humans, R & C input | (2) maintain gaze fixation during | | available but almost entirely | head movement by detecting | | cortical | rotational head movements. It | | | uses inputs from other sensory | | However, the relative inputs can | systems to drive the VOR. | | vary based on stimulus type. | | | | The vestibular system detects: | | ***Vestibular and optokinetic | | | systems interaction*** | - **Translational** (head) | | | **motion**: movement along | | The vestibular system receives | axes (up/down, left/right and | | input from the optokinetic | forward/backwards); these are | | pathway, which can alter the | also called linear | | response of the vestibular | accelerations and are more | | system. Movement of the whole | difficult to study in a | | visual scene can produce the | laboratory setting | | sensation of self-motion | | | (circularvection or | - **Rotational** (head) | | linearvection) by activating the | **motion**: movement around | | optokinetic system which feeds | these axes; these are most | | into the vestibular system -- | relevant to eye movements | | this is likely because these | | | systems evolved in synchrony to | ***Rotational motion*** | | stabilise the gaze; we expect if | | | the world is moving, the body is | Head rotations are detected by | | moving through the world. It is | the semicircular canals (SCC); | | evolutionarily unlikely that body | there are three SCC that sense | | movement does not accompany world | rotations along three planes that | | movement. Therefore, conflict | form (almost) right angles | | between these systems (only one | (left/right, up/down and | | type of movement) can produce | side-to-side) | | motion sickness. | | | | When moving the head along one | | ***Translational motion (linear | plane: | | acceleration)*** | | | | 1. The endolymph lags behind the | | Translational motion is detected | movement of the head due to | | by the otolith organs and | inertia | | comprises the **utricule** (which | | | detects horizontal motion, i.e. | 2. This produces a force against | | left/right and forward/backwards) | the capula that surrounds the | | and the **saccule** (which | sensory hair cells \-- the | | detects vertical motion, i.e. | capula bridges the width of | | up/down). Each of these | the ampulla (base of the SCC) | | structures has hair cells | which forms a barrier to the | | covering all possible direction | movement of endolymph | | in the relevant plane to ensure | | | all types of linear motion can be | 3. The capula distends in the | | detected. | opposite direction of head | | | movement | | These structures contain a layer | | | of hair cells with their | 4. This bends the hair cells | | stereocilia embedded in a | either towards the kinocilium | | gelatinous membrane which is | (tallest cilium) which | | covered by a layer of CaCO~3~ | produces depolarisation of | | crystals (i.e. otoliths) lining | the hair cell or away from | | the top. These CaCO~3~ crystals | the kinocilium which produces | | are heavy and become displaced in | hyperpolarisation | | response to linear accelerations, | | | which causes the cilia to bend | 5. Hair cells respond with | | and produce graded potentials to | graded potentials and input | | change the rate of firing in the | to bipolar cell neurons which | | vestibulo-cochlear nerve (CN | fire action potentials | | VIII). | through their axons which | | | comprise part of cranial | |  | nerve VIII | | | (vestibulo-cochlear nerve) | | ***VOR dysfunction*** | | | | 6. When the head is rotated at a | | Head rotation is sensed by the | constant velocity, the | | relative difference in the firing | endolymph catches up and the | | rate from the two canals (one | capula straightens and firing | | excited, one inhibited). | through CNVIII returns to | | Therefore, damage to one SCC or | baseline levels \-- i.e. this | | CN VIII on one side would produce | system detects | | a difference in the firing rate | **acceleration** | | between the two sides which would | | | be perceived as due to rotation |  | | which generates a compensatory | | | eye movement followed by a | ***VOR reflex arc*** | | saccade to bring the gaze back to | | | fixation, which repeats as the | The SCC has opposing responses on | | brain still senses a rotation due | each side of the head \-- | | to the imbalance of firing, i.e. | excitation in one is accompanied | | **vestibular nystagmus**. This | by inhibition in the other. | | can produce feelings of dizziness | Excitation occurs in the SCC on | | and oscillopsia (oscillation of | the same side as the direction of | | the visual world). | head movement (e.g. left head | | | turn excites left SCC). This | | The **head thrust** test can be | activates a 'three-neuron arc' | | used to assess the VOR \-- the | which is a rapid reflex arc | | clinician holds the patient's | (\100ms) processing can be | - Similarity: objects with | | modulated by higher cortical | shared features are grouped | | areas | | | | - Closure: objects with shared | | 2. V2: perceives **borders** and | features that form a boundary | | illusory contours and | in space will be perceived as | | performs figure-ground | one | | segregation; these neurons | | | can infer contours where one | - Connection: objects arranged | | does not visually exist or | on a line will be linked | | those behind an occluder | together | | | | | 3. V4: integrates stimulus | - Common fate: objects moving | | features into a **global | in the same direction will be | | shape**; these neurons | grouped together | | respond to a particular | | | curvature and have large RF | ***Visual agnosia*** | | that show position invariance | | | (i.e. respond to preferred | Damage to the ventral stream can | | stimulus at any location in | cause visual agnosia (i.e. | | their RF) and can | inability to recognise objects), | | discriminate between real | which include; | | object borders and those | | | created by occlusion | - Apperceptive agnosia: caused | | | by damage to earlier visual | | 4. Lateral occipital cortex | area, patients are unable to | | (LOC): responds selectively | integrate stimulus features | | to objects (including real | into a global percept | | objects, abstract objects and | | | familiar/unfamiliar objects); | - Associative agnosia: caused | | these neurons have large RF | by damage to higher visual | | and show size invariance | areas (e.g. categorisation | | (i.e. respond to objects of | areas), patients can | | any size in their RF) and | integrate features into a | | form-cue invariance (i.e. | single object but cannot | | respond to real objects and | recognise that object | | images of objects the same); | | | object representations are | - Prosopagnosia: caused by | | organised into categories, | damage to fusiform face area | | e.g. faces and animals, | (FFA) in area IT, patients | | houses and landscapes, tools | are selectively unable to | | and word shapes; AND/OR | recognise faces based on | | | visual input (but can still | | 5. Area IT (inferior temporal): | recognise individual facial | | respond selectively to faces | features, but can't integrate | | in normal representation | into a unified percept. | | (response to faces with | | | scrambled or occluded | ***Direction selectivity*** | | features reduced the | | | response); these neurons | Some V1 cells are direction | | respond to individual facial | selective (DS), and these cells | | features and their spatial | are distributed throughout the | | configurations and show | different layers of the cortex in | | position and size invariance | different proportions (densest in | | | layer 4a and 4b). | | Alternatively, the predictive | | | coding model suggests that the | Direction selectivity arises from | | brain predicts the expected | the input of many presynaptic | | visual input and compares this | orientation selective cells to a | | with the incoming sensory | single direction selective cell. | | information. Neurons at one layer | These presynaptic cells have | | of the hierarchy send feedback to | different response latencies; | | the layer below about the | presynaptic neurons at the start | | predicted input and compares this | of the RF have longer latencies | | to the incoming sensory input; | than neurons at the end of the | | the mismatch between these | RF. Therefore, when a stimulus | | signals (i.e. **prediction | moves in the preferred direction, | | error** signal) is sent to the | the presynaptic neurons with | | layer above. | longer latencies are activated | | | first meaning their inputs arrive | | ***Motion perception*** | at the postsynaptic neuron at the | | | same time as the presynaptic | | Motion is detected by an object | neurons with shorter response | | changing position over time; this | latencies that are at the end of | | allows us to detect real motion | the RF, causing temporal | | and apparent motion (stationary | summation of their inputs at the | | objects are presented in rapid | postsynaptic cell to reach | | succession). Types of motion | threshold. However, when the | | include: | stimulus moves in the | | | non-preferred direction, neurons | | - Simple smooth motion | with shorter response latencies | | | are activated first, meaning | | - Optic flow | these inputs arrive at the | | | postsynaptic cell at different | | - Complex biological motion | times, so do not reach threshold. | | | | | Motion perception is a critical | ***Akinetopsia*** | | function for navigation, hazard | | | avoidance and segmentation of | Bilateral damage to area MT or | | objects | MST causes motion blindness; | | | patients with this condition | | ***Dorsal visual stream*** | cannot perceive fluid motion, | | | rather objects seem to appear and | | The hierarchical model of motion | disappear. | | perception proposes that inputs | | | are sent from V1 → area MT | ***Blindsight*** | | (middle temporal)/V5 → area MST | | | (medial superior temporal) → | Patients with damage to V1 cannot | | posterior parietal cortex (PPC). | consciously perceive visual | | Input from V1 → area MT can be | stimuli within the affected area, | | direct or indirect via V2 or V3. | but can still respond to visual | | | stimuli, e.g. can navigate an | | 1. V1: direction selective cells | obstacle course despite not being | | encode the **direction of | able to consciously perceive the | | stimulus movement** | obstacles | | | | | 2. Area MT: performs **global | ***Alternative motion processing | | motion integration**; these | pathways*** | | cells have large RF and | | | respond to coherence of | There are motion processing | | motion (i.e. proportion of | pathways that bypass V1 in their | | stimuli moving in the same | projection to area MT. These | | direction) | areas are responsible for | | | producing blindsight in | | - Lesions in MT increase | cortically blind individuals. | | coherence threshold for | | | detecting motion from 1-2% to | - **Geniculo-extrastriate | | 10-20% | pathway**: retina → | | | koniocellular cells of LGN → | | - Microelectrode stimulation of | area MT; responsible for | | a cell with a preferred | motion detection in | | direction of motion increases | blindsight | | the likelihood of detecting | | | motion in the preferred | - **Colliculi-cortical | | direction | pathway**: retina → superior | | | colliculus/pulvinar → area | | These neurons show motion | MT; responsible for residual | | adaptation -- prolonged | vision in blindsight | | exposure to a stimulus moving | | | in a preferred direction |  | | causes the activity of the | | | corresponding cells to | ***Depth perception*** | | reduce; if motion is encoded | | | as the relative difference in | Animals with **frontal eyes** | | firing of DS neurons, when | receive overlapping images on the | | redirecting gaze to a | retina (with varying offsets), | | stationary stimulus, the | therefore **stereopsis** | | relative activity of cells | dominates depth perception. | | sensitive to the opposite | | | direction will be higher and | Animals with **side eyes** do not | | motion in this direction is | receive overlapping images on the | | falsely perceived (seen in | retina which produces better | | **motion aftereffects**) | peripheral vision but rely on | | | **monocular cues** for depth | | 3. Area MST: sensitive to | perception. | | **complex motion**; these | | | neurons have larger RF than | ***Monocular cues to depth*** | | area MT and are more | | | sensitive to various types of | Depth cues that can be perceived | | complex motion | with a single eye; these cues | | | encode the **absolute distance** | | ***Stereopsis*** | of objects. These cues typically | | | rely on past experience which can | | The image projected to each | produce illusions of depth. The | | retina has slight positional | monocular cues to depth include: | | differences due to the offset of | | | eyes in our head. Comparison of | - **Relative size**: objects | | the disparity between retinal | that are known to have the | | image allows us to perceive the | same size but appear to have | | **relative distance** between | different sizes, this is | | objects in space | interpreted as these objects | | | being at different distances | | - Corresponding points: objects | (e.g. smaller object is | | on the fovea will be | further away) | | represented at the same point | | | on the retina | - **Linear perspective**: | | | parallel lines that recede | | - Non-corresponding points: | into the distance appear to | | objects in front of or behind | converge; objects of the same | | the fovea project to | size placed along these lines | | different points on each | will be perceived as larger | | retina (i.e. have non-zero | or smaller based on their | | disparity) | perceived depth | | | | | - Horopter: plane of points | - **Aerial perspective**: light | | that fall on corresponding | scattering by dust causes | | points of the retina (i.e. | more distant objects to | | have zero disparity) | decrease in contrast and | | | colour saturation, appear | | | blurrier and have cooler | | | tones | | - Objects before the horopter | | | project to temporal points of | - **Occlusion**: an object that | | the fovea in each eye | is occluded by another is | | | perceived as farther away | | - Objects behind the horopter | | | project to nasal points of | - **Texture**: objects with | | the fovea in each eye | more detailed texture appear | | | closer | | There are disparity selective | | | cells along the dorsal stream | - **Cast shadows**: objects | | which have a preferred disparity, | with a larger shadow appear | | and can be excitatory or | to be further away from the | | inhibitory: | background | | | | | - Near disparity cell: responds | - **Motion parallax**: objects | | maximally to stimuli | that are closer appear to | | presented before the horopter | move faster than objects that | | | are further away | | - Far disparity cell: responds | | | maximally to stimuli | Information about the vergence | | presented behind the horopter | angle of the eyes can also | | | provide information about depth. | | - Zero disparity cell: responds | | | maximally to stimuli along | ***Visual search experiments*** | | the horopter | | | | [Parallel search | | The proportion of disparity | tasks]: participants | | sensitive cells increases at each | must identify a target with a | | layer of the dorsal stream: | unique feature from all | | | distractors (e.g. colour or | | - V1/V2: 40% of cells; mostly | orientation); the target | | near-zero disparity cells | 'pops-out', therefore this | | | process engages **exogenous | | - V3: 80% of cells | attention** | | | | | - Area MT: 70% of cells | - Reaction time (RT) stays | | | constant as the number of | | - Area MST: 93% of cells; | distractors increases | | mostly non-zero disparity | | | cells | [Serial search | | | tasks]: participants | | ***Selective attention*** | identify a target based on the | | | conjunction of two features (e.g. | | [Inattentional | colour AND orientation); a | | blindness]: inability | feature of the target is shared | | to perceive an unexpected | with the distractors so the | | stimulus due to attentional | visual field must be analysed in | | allocation elsewhere, e.g. the | succession, therefore this | | invisible gorilla or the long arm | process engages **endogenous | | task. | attention**. This processing can | | | be explained by 'feature | |  | integration theory' (FIT) -- | | | overt attention directs the gaze | | [Change blindness]: | to a particular location in the | | inability to perceive changes in | visual field and the attentional | | a visual stimulus due to lack of | spotlight (covert attention) | | attention at these locations, | processes stimuli around this | | e.g. The Door Study (50% of | area, which repeats until the | | participants did not notice the | target is found. | | person they were giving | | | directions changed). | - RT increases as the number of | | | distractors increases | | [Attentional blink]: | | | inability to perceive a second | fMRI studies support the | | target stimulus presented within | existence of an attentional | | a 500ms interval of the first | spotlight. The pattern of | | target stimulus (unless the | activation in V1 when a stimulus | | second target immediately follows | is presented at *successive | | the first target, i.e. lag 1 | locations* in the retina on a | | sparing), e.g. RSVP task | blank background is the same as | | | the pattern of activation when | | ***Types of attention*** | participants are asked to attend | | | single locations on a *constant | | [Exogenous | background* | | attention]: bottom-up | | | process; involuntary engagement |  | | of attention, driven by the | | | saliency of stimulus | ***Mechanism of attentional | | | spotlight*** | | [Endogenous | | | attention]: top-down | 1. Magnocellular input (fast | | process; voluntary engagement of | signal) arrives in \