Human Vision and Eye Anatomy

short to long, 400-700

Light bounces off the object and reflect into the eye through the cornea, the pupil, and his the lens, the lens either stretches or contract, and reaches the fovea and goes into retina, to optic nerve and into brain

focus

bend light so we are able to focus it or point it into fovea

center of vision and has highest visual acuity due to highest concentration of cones

the colored portion of the eye which is a muscle to contract and expand the pupil

to increase/decrease size of pupil to allow more or less light to hit the lens

The lens can stretch itself to become more flat or push itself together to bend light even which is underlined by ciliary muscles

because we have a blindspot in both of our eyes due to the optic nerve, our brain fills in missing information

going from a lot to a little

how much the ciliary muscles are pulling on the lens to focus on image.

far away

aka myopia, cant see far due to issues with lensciliary muscles

aka hyperopia

misshapen cornea

lens are clouded

blockage of drainage mechanisms within eye and filled with aqueous humor and vitreous humor

most common cause of age related blindness, disgusting of region around the eye due to protein occlusion which kills of photoreceptors

always leaking NT

light sensing cells in back of reign that takes a photo and turns it into electrical signal to create vision

proteins that are responsive to light

glutamate

turn off constant depolarization and receive less NT

shaped spirally to allow for more opsin receptor to allow for increased sensitivity to low levels of light, opsin regenerates slowly

shaped like a comb and has high acuity for color, needs more intense stimuli to activate, very little convergence,opsin regenerates fast

high sensitivity to light but low acuity

color, high acuity but low sensitivity

intensity into rods/cones

our central visual field favors photopic, peripheral visual field for scotopic vision

a machine that measures the amount of light thats bouncing off an object

chemical inside opsin called il cis retinal turns into il trans retinal in response to light.

The conversion of il cis retinal to il trans retinal

Movement of the eye

constant jiggle of the eye

Left or right movement of the eye.

Wouldn't be able to see anything because photoreceptors would be exhausted as long as you're looking at a constant image.

our eyes perceive exaggerated edges.

They serve as early processing units for the retina

each pixel of your retina not only activates itself but inhibits its neighbors

result of the identification of our three different photoreceptor cones

Peak response to 420nm, blue

Peak response to 525nm green

Peak response to 570nm red

dysfunction or absence of cones

dysfunction of medium or long cones

missing short cone

short, medium, long cones are not independent of each other, they activate and inhibit each other

Looking at short cone, it will send excitation to own ganglion cell and inhibit ganglion cells associated with medium and long cones

ganglion cells are performing comparisons between the types of cones

cells that are bundled together and send their axons out of the eye via optic nerve aka the blind spot

once a stimulus is received, goes to retina, to lateral geniculate nucleus of the thalamus, to v1 aka striate/calcarine cortex

contains the superior colliculus for vision and inferior colliculus for hearing

Orient us to a sudden visual stimulus aka reflex
Where is most of the visual cortex located? Mostly in the medial portion of the occipital lobe

important for clinical applications because it can give us a clue on what's happening in the brain. Lesions at different points in this pathway cause very different deficits

scotoma
What happens if there is a lesion in V1 for a temporary condition? Visual auras are due to a blind sport due to a higher level of deactivation in the visual pathway and impacts center of vision

where the brain fills in the gap that made by the scotoma

brain fills in gap with patterns, colors, flashes and stay in same part of the visual field

receptive fields

donut

they have surround and a center, like a donut, that interact together

strong output if stimulus is in center, by increasing the response to center stimulus but decrease responding to neighbor stimulus

strong output if nothing is in center, by decreasing the response to center stimulus but increase response to neighboring stimulus

Hypolarization of the cone where glutamate is decreased, stop inhibitory bipolar cell and the on center cell will depolarize and send more glutamate where the ganglion cell sends action potentials to the brain

long cone recieves excitation from flong wavelength cones and recieve inhibition from medium wavelength cones saying something red and something not green

response in medium and long wavelength cones and inhibited by short wavelength

excitation recieve by medium wavelength cones and inhibited by long wavelength cones

excitation of short wavelength cone and inhibited by both long and medium cones

4, damage of the optic nerve results in no visual field

3, damage of optic chiasm results in loss of function in fibers that cross aka loss of peripheral vision

2, damage after optic chiasm will result in losing right visual field

5, damage of a part of optic radiation (whiter matter tract that radiates from the thalamus to primary visual cortex, lose everything from upper right visual field

damage that results in loss of entire pathway but has something containing fovea sparing because some info from left hemisphereis going to cross over toward the back to make up for fovea

activation of surround will lead to hyperpolarization, and slower ap response

activation of surround will lead to depolarization and increased ap response

depolarize and lead to increase in ap response

on

off

hyperpolarize because surrounding regions dont have any stimulation via horizoantal cells which will reduce ap response

stimualtion of my on portion of the receptive field would increase membrane potential of the bipolar cell and decrease firing of ganglion cell of an oncenter/off surround, light stimulus in surround will hyperpolarize causing the bipolar cell to reduce firing firing frequency

stimulation of my off position of the receptive field would hyperpolarize the bipolar cell and depolarize on the onsurround which will cancel itself out resulting in no change in bipolar cell in membrane potential or no change in ap frequency

no change/detection due to everything being covered

no change/detection due to everything being covered

cell c will changfe firing rate to 2 hz because there is a stimulus in the off surround but no stimulus in on center

cell d will icnrease firing rate to 10 hz since all off center is stimulated and most of on surround is stimulated

WILL RESPOND WHEN A LINE OF RGCS RECIEVES AN ON SIGNAL THAT IS SURROUNDED BY 2 LINES OF RHCS THAT RECIEVE AN OFF SIGNAL WHICH GIVES A BAR/EDGE

shining a bar onto retina will lead to increase in activity

shine a bar of light below receptiv3e field then no increase inac tivity but has rebound effects

shining a bar of light horizontalling so its activating someof off and on cells will cancel so no activation

shine al ight so its only on the off section and on the on sections, cancels out and no stimulus

increasing in response

increasing in response

increasing in response

no activation

we seee something because theres an implied outline

the ability to see an object as the same color despite changes in lighting

idea that regardless of actula wavelength of light hitting your eye,m we percieve a color as constant for a particular object

seprates dorsal and ventral occiptal lobe

detects pattern and texture by comparing neighboring sort of pixels from v1 to determine what kinds of pattenrs are in those neighboring pixels

percieve color not actual wavelength by recieving info from blobs

achromatopsia. lack of color vision usually in one side of vision

percieves motion

akinetopsia, cant see constant fluid motion and cannot see the world when your eyes move

proceeds from occipital lobe up into parietal lobe. brain regions that are associated with body awareness, shape of object in terms of brightness/darkness, how deep/far away something is and how something is moving

can identify most objects but cant locate them in space or interact with them

path from v1 to temporal cortex associated with identifying objects by lining up shape with semantic memory

cant tell what object is until they pick it up

damage to a part of their visual pathway after it reaches the cortex that may lead to a lack of awareness

unable tos ay we know something

impairment of fusiform gyrus resulting in an inability in facial recognition

tendency to percieve faces in non face objects

apart of thinking about an object or tool is thinking "how will I interact with that?" and they cannot do that