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Systems neuroscience
Sensory systems:
Energy → action potentials
Motor systems:
Action potentials → energy
In CNS, all membrane potentials (graded + action)
Sensory coding
We can only sense those aspects of the world for which we have receptors → specialised neurons that transduce energy into action potentials
Perceiving the world
Distal stimulus: external world
Proximal stimulus: pattern of light on the retina
Only info we have
based on energy we can detect
Stimulus: properties of visible light
electromagnetic radiation
travels in photons
each photon has a wavelength (390-700nm)
all photons of the same wavelength are identical
Visible light
Visible light spectrum neatly aligns with transmission through water
A photon can be
Reflected (blue reflects off blue)
absorbed (red absorbs green)
transmitted (red passes through red)
Two conditions of light
Low intensity/scotopic (different wavelength, low intensity → nighttime)
High intensity/photopic (different wavelength, high intensity → daytime)
Scotopic vision
Intensity of photons is the same (low), no sense of hue or change in brightness
490nm is brightest
640nm is dimmest
Change in brightness w/o change in intensity??
Photopic vision
Intensity of photons in the same (high), can see hue
540nm brightest
420/640nm dimmest
Combining coloured light
540nm (Gr. Yellow) + 640nm (red) = yellow (identical to 580nm)
490nm (blue) + 580nm (yellow) = white
Therefore 490nm + 540nm + 640nm = white
Any given wavelength simulated by superimposing diff. wavelengths
Additive colour mixing
Adding photons to create colour (light-based)
Overlap = white
Subtractive colour mixing
Pigments rely on absorption + reflection of light
Overlap = black
Colour vision anomalies
Protanopia/maly
Deuteranopia/maly
Tritanopia/maly
Monochromacy (occurs after brain injury)
Achromatopsia
Basic colour theory
Additive colour mixing: blue, red, green
Ewald Hering: Blue, Red, Yellow, Green
→ opponent afterimages
Negative afterimages
Gradual adaptation to image
Changes zero point so white looks different
Look at yellow → system leans more blue to stop responding to yellow
When look at white again, see blue
Foveal pit
One region where vision is least distorted → small patch of acute vision + saccades to create a whole image
Optic nerve
Creates blind spot in vision
Rods
120 million in each retina
Distributed all over retina except fovea
Contain rhodopsin → bleaches when exposed to light, hyperpolarises photoreceptor → depolarised bipolar cell → stimulates ganglion cell
Respond to very low light levels
Respond differentially to wavelength
Rod Physiology
Dark current → Na+ channels opened, rod is partially depolarised → releases glutamate into synaptic cleft (excitatory during darkness)
Light transduction → Na+ channels close, rod becomes hyperpolarised → glu release terminates (inhibitory AP generated)
Rod response to light
Similar peak as in scotopic vision (peak around 500nm).
Why do low intensity lights vary in brightness?
Rhodopsin absorption varies in wavelength (peaking at 500nm) → peak efficiency at this wavelength therefore relatively blind to other wavelengths
Frequency coding
The intensity of a stimulus is often coded by the frequency of firing (action potentials) in cells that respond to that stimulus (MORE not LARGER)
Principle of Univariance
A given receptor can be excited by multiple attributes (wavelength AND intensity), but its output (firing rates) varies in only one dimension (i.e., univariate) → so it can only code a single dimension and cannot distinguish between stimulus attributes
Cone responses (trichromats)
Three cone types
Short
Medium
Long
Not just generated via AP → distinguish light based on ratio of activity in each cone
Coarse coding
Neurons respond to a broad range of stimuli, with a GRADED response depending on the match to a preferred stimulus → short cones respond most to blue, less to green, least to red
Population coding
Integrating the responses from a number of differently tuned neurons enables precise coding → e.g. large response from all cones = white light, no response from any cones = dark
Protanopia
No L cones
Deuteranopia
No M cones
Tritanopia
No S cones
Opponent-process theory of colour vision
Hering noted colours seemed to form opponent pairs (red/green), (blue/yellow)
Hurvich and Jameson proposed that neurons beyond the photoreceptors could implement opponent processing
Cell can only code either red/green but not both, same from blue/yellow
Nonopponent RGC
Excitatory input from L and M cones
No understanding of hue
Greyscale
L+M- opponent RGC
Excited by short wavelength (L cone peaks slightly)
Inhibited by medium wavelength (M cone peaks)
Excited by long wavelength (L cone peaks)
S+ (L&M) -
Excited by short wavelength (coded by s cone)
inhibited by medium and long wavelength (shows as yellow)
Opponent processing
Many neurons that encode some dimension do so in an opponent fashion, so that excitation and inhibition of the neuron have opposite interpretations in the nervous system
Colour coding in RGC
L+M+, L+M-, S+(L&M)- combine to create visual light rainbow spectrum
appearance of each monochromatic light (hue and brightness) can be understood in terms of the responses across these RGC types
Opponent RGC responses define a colour space like that proposed by hering and hurvich & jamison
Retina to Cortex
Optic nerve (RGC axons)
Optic chiasm (crossover of axons from nasal hemiretina)
Optic tract (still RGC axons)
Lateral geniculate nucleus (optic radiations)
Striate cortex (LGN projects to here)
Retinal Ganglion Cells (RGCs)
Transmit action potentials from retina to brain.
Parasol (M-projecting) → 10% of retina, large dendrites, large axons, magnocellular level (1&2) of LGN
Midget (P-projecting) → 80% of retina, small axons, level parvocellular level (3-6) of LGN
Receptive fields
Coarse coding of visual space
parasol cells in periphery, less overlap = low visual acuity
midget cells in centre, closely packed = high visual acuity
Multiple cone signals converge into one RGC →
Centre-surround opponency
Found in midget RGCs → stimulus in centre of RF can excite or inhibit
On-centre
Off centre
Colour opponent → m-cones opposed by L cones, s cones opposed by l and m cones
On-centre
Stimulus in the periphery inhibits the cell
Off-centre
A stimulus in the periphery excites the cell
Mach bands
Uniform grey bands appear to have a gradient from left (brighter) to right (dimmer)
Uniform stimulation in RF = minimal response
More stimulation in centre = cell is excited
More stimulation in surround = cell is inhibited
RGC images
Emphasise boundaries between objects
creates outlines
respond to areas of changing stimulation instead of uniform
tracing areas of VF that change stimulation
LGN response latency
Parvocellular: Tonic response
Stimulation continues in order to get a good look → cell still responding to stimulus after intial showing
Magnocellular: Phasic response
Large receptors → quick AP, detecting change → lose interest once things stay stable
LGN Physiology
Magnocellular (1-2) → Large RF, fast latency, phasic (responsive only to change), L+M+, L-M- (non-opponent, greyscale)
Parvocellular (3-6) → small RF, slow latency, tonic (detail-oriented, even when stimuli is stable), L+M-, L-M+, S+(L&M)- (opponent RGC, centre surround)
Parallel processing
Different populations of neurons perform different functions. Complex problems broken up into relatively simpler ones (colour, motion, form)
Visual cortex electrophysiology
Cat thing where theres the crackling and the line with the x’s
Simple cells
LGN layer 4C → midget cells combine to a larger simple cell (forms a line)
Cytochrome oxidase blobs
Staining sample of PVC (V1) with cytochrome oxidase = blobs
Neurons in the blobs are more active (dark areas) than interblobs (lighter between dark areas)
dark areas more metabolically active