Lecture 6 + Assignment 5 Flashcards
On-center ganglion cells
Center and surround
fire most when bright center AND dark surround
Light center:
- center cone to hyperpolarize
- release less glutamate
- opens mGluR6 (metabotropic) Na channels
- causes depolarization of the on-center bipolar cell
= more APs fired
Dark surround:
- surround cones depolarize
- release more glutamate onto horizontal cells ionotropic receptors
- horizontal cells depolarize
- h cells release GABA onto the center cone
- hyperpolarizes center cone
like it got more light
Colour-opponency in retinal ganglion cells
the center and surround cones can be different types, causing colour opponency
Organization of primary visual cortex (V1)
Sulcus name
left visual field activates right visual cortex
(decussation)
- top and bottom flipped
- calcarine sulcus between them
macula = the middle
- much greater magnification closer to the fovea
- more neurons responding
Vision pathway + what causes contralaterality
left visual field / fixation point / right vf
temporal + nasal retinas
optic nerve
optic chiasm
optic tract
LGN (in thalamus)
optic radiation
striate cortex
contralaterality caused by decussation of the nasal retinal axons @ optic chiasm
optic nerve (CN II) = axons from one eye
optic tract = axons from both eyes
Key visual structures in the brain
- cerebral cortex
- pineal gland
- superior colliculus
- primary visual cortex
- hypothalamus
- pituitary
- optic chiasm
- suprachiasmatic nucleus
Primary visual cortex
Brodmans area
V1
- Brodmann area 17
- striate (striped) cortex
5 visual field deficits + damage location
Names basically say what they’re missing
- Right monocular blindness
- right optic nerve lesion - Bitemporal hemianopsia
- optic chiasm lesion - Left homonymous hemianopsia
- right optic tract nerve lesion - Left superior quadrantanopsia
- optic radiation lesion - Left homonymous hemianopsia with foveal sparing
- striate cortex lesion
Orientation-selective V1 receptive fields
- respond maximally to a certain orientation
- still respond slightly to other orientations
- all columns have the same orientation throughout their layers
V1 population vectors
- may be used to infer stimulus orientation
just do vector addition (tip-to-tail approach)
can do negative degrees too
Hubel and Wiesel - ice cube model
- 1981 nobel prize in physiology or medicine
- Characterised information processing in the visual system
- It illustrates how the cortex is divided, and at the same time, into two kinds of slabs, one set of ocular dominance (left and right) and one set for orientation
Layers in the LGN
- LGN gets input from both eyes and has 6 layers
- each layer only responds to one eye
individual neurons = monocular
entire LGN = binocular
Ocular dominance columns in the V1
when do they mix
- mix in superficial layer = past level 4
- neurons B/D/F respond to both eyes
Transneuronal labeling with radioactive amino acids
- used to see which eye connects to which LGN and cortical layers
- inject radioactively labelled amino acids into one eye
- undergo anterograde axonal transport
retina to thalamus to cortex
Thalamus
- transneuronal transport of label
Cortex
- terminally labeled
Binocular disparity and stereopsis
Stereopsis: the ability to perceive depth using binocular vision
- form of binocular disparity
Objects at different depths
- closer = more temporal point on retina
= disparity
OR
more temporal location on the retina gives the ILLUSION of depth
Objects at the same depth
no disparity
OR
more temporal location on the retina gives the ILLUSION of depth
Stereogram
give the illusion of 3D
Higher visual cortical areas
many complicated connection paths
“Where” pathway + lesion name
V1 to MT/V5 to parietal lobe
dorsal - spatial vision pathway
cerebral akinetopsia
“What” pathway + lesion name
V1 to V4 to temporal lobe
ventral - object recognition pathway
cerebral achromatopsia
Where pathway inferring movement
- each vector represents one neuron in MT
- each have a preferred motion direction
magnitude of the vector is the neurons firing rate
population vector = direction of motion
Waterfall illusion
- due to adaptation followed by inference
downward cells adapt during viewing of the stimulus
usually, stationary image activates all MT cells equally
when waterfall video stops, downward (adapted cells) will have lower firing rates than other cells
= appear to be moving upwards
Photo uncaging (with glutamate) - general
- bathe brain tissue with caged glutamate
- flash UV light to uncage/free glutamate through photolysis
- cage prevents glutamate from entering and binding to receptor
done in-vitro
Cortical column
- 2 mm thick in mammals
- similar receptive field
Pyramidal cell (cortex 2)
- projection neuron
- glutamatergic (excitatory)
- 70%
Stellate cell (cortex 4)
- non-pyramidal interneuron
- excitatory OR inhibitory
- 30%
Photo uncaging (with glutamate) - visual cortex
- take a coronal slice
- do whole-cell patch clamp recording
- of a neuron at pos 2/3
- look at what neurons can activate this neuron
- shine UV at other neurons around
AP at the location
EPSPs at surrounding
maybe some cause IPSPs
look at strength of connections between neurons
Electrical stimulation
- use electrode to inject current (similar)
- might accidentally activate axons too (no glutamate receptors)
Photo uncaging (with glutamate) - cerebellum
- pre-fill patch clamp with dye
- lights up neuron
(ex. Purkinje cell)
inject traces (downward peak = current instead of voltage)
Black squares grey intersections illusion
cell at crossroads fires fewer action potentials bc more of its surround is in the light
= brain infers darkness
look directly at it = smaller rf bc fovea = entire thing in the light
“Lines tilting up then horizontal lines appear to be tilting down” illusion
- tilt after-effect
- result of adaptation then inference
- tilted up cells get fatigued
= fire less - resulting population vector gets tilted downward
