wk 14, lec 2 Flashcards
bipolar cells in retina are for
visual info. processing
what is lateral inhibition and what cells help with it
bipolar cells
brain gets sharpened signals of contrasts in light and dark, enabling fine discrimination of edges and patterns
rod bipolar cells vs cone bipolar cells
which ones have on renters and which ones have off renters
which is scototopic (low light) and which is photooptic (bright light)
rods- scototopic and on centers
cones- photooptic and on and off centers
rod bipolar cells- how are on renters activated
- Scotopic vision (low light) and are “on-center” cells, meaning they’re activated when light falls on center of receptive field (center brighter than surround)
cone bipolar cells- how are on and off centres activated
- On-center: activated by light hitting center of receptive field, center brighter than surround
- Off-center: activated when light falls on surround of receptive field, surround is brighter than center
center- surround organization
on vs off centre activation
o On-center receptive fields stimulated when center brighter than surround
o Off-center receptive fields stimulated when surround brighter than center
oppositional regulation in on and off centres
what is the effect
o On and off center cells have opposite response to same stimulus (i.e. on stimulated and off inhibited)
o Enhances contrasts and edge detection, better visual acuity for brain
after activation, in the dark what needs to happen to rhodopsin for cells to respond again
needs to be regenerated
what happens to opsin when not working
bleached
retinal needs to be converted into which for to regenerate rhodopsin and where
trans to cis retinal into the pigment layer
what needs to combine to be ready to respond to light again
cis retinal and opsin
rods process of adaptation is slow; what is the effect of this
Rods not effective at adapting to rapid light changes
i.e. hard to adjust to bright after dark
go into dark room pupils dilate to let as much light as possible but photopigments that were bleached take time to regenerate
steps in the regeneration of rhodopsin
- After activation, in the dark, rhodopsin needs to be regenerated before cells can respond again
o Trans retinal separates from opsin (GPCR)
Opsin= bleach and inactive
Trans-retinal travels to pigment layer, converts back to cis-retinal which travels to rod to recombine with opsin = ready to respond to light again
what happens when you move into sunlight quickly after being in the dark
- activate photoreceptors, temporarily “blinded” by overstimulation, pupils constrict and you squint to reduce light
- rods becomes saturated (bleached) and cant respond to light
- cones regenerate faster than rods, so they don’t saturate and continue to respond and vision becomes mediated by cones
horizontal cells for
shapen contrast
amacrine cells for
o help detect changes in vision, i.e. movement and lights on/off
bipolar cells for
process visual signals at level of retina (i.e. different patterns of lights –> on and off center)
how do visual signals get to the brain
- visual signals from rods and cones are transmitted by ganglion cell axons to brain via optic nerve
steps from photoreceptors to get to brain
photoreceptor to bipolar cells via graded receptor potential
bipolar cells to ganglion cells via all or none action potential
go to brain via optic nerve
graded and action potentials in which cells
graded receptor potential in photoreceptor cells
action potential in bipolar cells
optic nerve is formed by
- formed by axons of ganglion cells
optic nerve exits back of eyeball to create
optic disc (blindspot)
crossing of optic nerve fibers
- 50% fibers cross at optic chiasm and join contralateral fibers
o Form optic tract
steps of optic nerve fibers to get to the brain
optic nerve fibers - 50% cross at optic chiasm and form optic tract
optic tract synapses in thalamus and leaves as optic radiations
optic radiations synapse in visual cortex (occipital lobe)
bilateral hemianopia
lose outer fields in both eyes
right homonymous hemianopia
o Lose right ½ of visual field in both eyes
scotoma
area with vision loss in an otherwise normal visual field
primary visual cortex for
register shape and colour and movement
secondary visual cortex
recognize shape and colour
primary somatosensory cortex
registers sensation
secondary somatosensory cortex
recognizes sensation
parieto-occipito-temporal association cortex
combines visual and tactile info to conclude the experience (I,e finger is burnt because touched hot stove)
which brain regions combined the sensations from somatosenosy cortex and the colour shape and movement from the visual cortex
parieto-occipito-temporal association cortex
what happens in the brain when there’s a visual defect in the eye
- Visual cortex ignores images from eye with visual defect (i.e. myopia, eye wanders)
amblyopia
vision in affected eye is worse than would be explained by visual defect alone
cortical blindness is a result of a lesion in the
primary visual cortex
lesions in the secondary visual cortex (responsible for shape and colour recognition) could result in 3 things
- movement agnosia
- visual agnosia
- colour agnosia
movement agnosia (from lesion in secondary visual cortex)
Object appears in another location, movement not noted
visual agnosia (from lesion in secondary visual cortex)
Inability to identify common objects as a “whole” and copy drawings
colour agnosia (from lesion in secondary visual cortex)
Grey scale
Cerebral achromatopsia: cannot recognize colour even though cones intact
Cerebral achromatopsia:
cannot recognize colour even though cones intact
EYE MUSCLE CHART
look at seperate slidedeck
medial rectus muscle
nerve innervation and action?
CN III (somatic)- oculomotor
adduction of eye (look to nose)
lateral rectus muscle
nerve innervation and action?
CN VI- abducens
abduction eye (look to ears)
inferior rectus muscel
nerve innervation and action?
CN III (somatic)
downward eye, extorsion
superior rectus muscle
nerve innervation and action?
CN III (somatic)
upward eye, intorsion
inferior oblique muscle
nerve innervation and action?
CN III (somatic)
elevate and abduct eye
superior oblique muscle
nerve innervation and action?
CN IV- trochlear
downward and abducted eye
levator palpebrae superioris muscle
nerve innervation and action?
CN III (somatic)
elevated upper eyelid
ciliary muscle
nerve innervation and action?
CN III (visceral: parasympathetic)
contraction leading to increased convexity of lens
pupillary sphincter muscle
nerve innervation and action?
CN III (visceral: parasympathetic)
miosis (pupillary constriction)
which 2 muscles are innervated by visceral parasympathetic CN III (oculomotor)
ciliary muscle and pupillary sphincter
I, II, III, IV
V, VI, VII, VIII
IX, X, XI, XII
I= nose (olfactory)
II= eye (retina)
III and IV = midbrain
V, VI, VII, VIII= pons
V (in all 3)
IX, X, XI, XII = medulla
2 nuclei in CN III (oculomotor)
- Oculomotor motor nucleus (somatic nucleus)
- Edinger- Westphal nucleus (EDW) (visceral motor)
- Oculomotor motor nucleus (somatic nucleus) in CN III for what function
o Motor innervation to all muscles that move eye ball except superior oblique (down and abduct) and lateral rectus (abduct)
o Motor innervation for levator palpebrae superioris (elevate upper eyelid)
what are the 2 muscles that the DOESNT the Oculomotor motor nucleus (somatic nucleus) in CN III innervate (does all others)
Motor innervation to all muscles that move eye ball except superior oblique (down and abduct) and lateral rectus (abduct)
- Edinger- Westphal nucleus (EDW) (visceral motor) of CN III is innovated by what system
PNS
2 functions and muscles in Edinger- Westphal nucleus (EDW) (visceral motor) of CN III
- pupillary sphincter (miosis- pupil constrict)
- ciliary muscle (accomodation- near vision)
if the oculomotor (CN III) somatic nucleus has a problem what is the pathology
o External ophthalmoplegia: weakness in 1+ eye muscles
Eye symptom: down and abducted
External ophthalmoplegia
weakness in 1+ eye muscles from CN III
Eye symptom: down and abducted
damage to visceral (EDW) of oculomotor CN III causes what
pupil dilated and non-reactive to light
ability to focus on near objects impaired (cant accommodate)
graded vs action potentials
Graded potentials via bipolar cells in response to light intensity
Action potential via ganglion cells
macular degeneration and sparing
- Macular degeneration= center of retina, so lose central vision
- Macular sparing= central vision is preserved
glaucoma
peripheral vision loss (tunnel vision)
amblyopia aka
lazy eye
fix amblyopia
o Fix with patching or blurring drops in stronger eye to make weaker eye work, contacts, surgery,
if someone has right primary cortex lesion what happens to vision
left homonymous hemianopsia (left side visual field is blind in both eyes)
oculomotor III damage causes
dilated pupil (mydriasis) and loss of accommodation
2 reflexes mediated by CN I and III
- accomodation reflex
- pupillary reflex
accomodation reflex (CN I and III)
o object moves closer, retinal image comes out of focus so accommodation reflex is activated to help focus on the image:
3 parts of accomodation reflex (CN I and III)
- convergence of eyes
- increased convexity of lens
- constriction of pupil
which muscle and part of CN III for convergence of the eyes in the accomodation reflex
muscle: medial rectus
CNIII: motor
which muscle and part of CN III for increased convexity of lens in the accomodation reflex
muscle: ciliary muscle
CNIII: EDW
which muscle and part of CN III for constriction of pupil in the accomodation reflex
Muscle: sphincter pupillae
CNIII: EDW
light in 1 eye causes constriction of both pupils via what CN
CN III EDW
both accomodation and pupillary reflexes use what nucleus
EDW nucleus from CN III
what area of brain does pupillary reflex involve and therefore damage to this area affects pupil ability to constrict
o Pupillary reflex involves pretectal area of midbrain (accommodation reflex doesn’t)
Damage to pretectal area affects pupil ability to constrict
- Can’t constrict to bright light
- Can still constrict to accommodate
where is trochlear IV nucleus
midbrain
what is trochlear IV innervated by
contralateral superior oblique
superior oblique for which motions
o Action: eye down and abduct
o Additional action: intorsion
which muscle does intorsion and which does extorsion and whats the purpose
superior oblique= intorsion
inferior oblique= extorsion
important for visual stability when head changes position
SIN is acronym for
superior oblique, intorsion, nose
if trochlear nucleus on right side is damaged and patient looks ahead then which eye is affected? what muscle compromised? what muscle takes over? causes extorsion of intorsion?
o Left eye affected
o Superior oblique muscle compromised, so inferior oblique muscle takes over
o Causes eyes to rotate to ear – extorsion
Creates double vision- diplopia
Patient will tilt head to left to compensate and have neck pain instead of blurry vision
when is the abducens VI nucleus
in the pons
muscle for abducens VI and function
- Muscle: lateral rectus
o Abduction
abducen mediates the lateral gaze how?
muscles?
coordinated by?
o Coordinated by the reticular formation in the pons (PPRF)
o Involves lateral rectus (CN VI) and medial rectus (CN III)
which tract connects CN III, IV, VI
- Medial longitudinal fasciculus (MLF) (tract) connects CN III, CN IV and CN VI (extra-occular nuclei)
what reflex does abducens VI mediate
vestibule-ocular reflex
what is vestibule-ocular reflex
o Eyes remain fixed to an object even when head moves
o Movement picked up by vestibular apparatus
Send signals to PPRF
Nerves to extra-ocular muscles are engaged by fibres running through MLF
hoe to keep straight gaze when head moves
- slide 49: head move to right; left eye use lateral rectus (CN VI) and right eye use medial rectus (CN III) to keep straight gaze
o via MLF
damage to abducens VI causes
- i.e. left eye damage causes them to look straight or deviate medially; cant abduct (bc lateral rectus compromised)
o right eye will look left from medial rectus
o causes: decreased depth perception, diplopia
