Visual and Auditory Systems Flashcards
What makes the aqueous humor in the eye?
Ciliary body
Where is aqueous humour drained?
-trabecular meshwork into Schlemm’s canal at the limbus (the joining point of the cornea and sclera)
What does the iris control?
how much light enters via pupil size
enough for brightness, not too much for clarity
The layers of the eye are: fibrous, vascular and neural. What are the 4 layers of the neural retina?
- RPE (part of the non-neural retina)
- Photoreceptor layer
- inner nuclear layer (interneurones)
- Ganglion cells
- (Vitrious)
Why do you have course vision at peripheral retina?
- before light reaches cones it passes through many translucent layers, light gets scattered
- cones are large, widely spaced and converge to 1 GC
How is vision much clearer in the central retina?
- foveal pit has no overlying layers (no scattering)
- red and green cones detect detailed vision
- cones are slender, packed close, + no convergence
Damage infront of the chiasm leads to…
different deficits in both eyes
vs behind chiasm would be matching
What is involved in constriction of the pupil?
- SHORT ciliary nerves innervate sphicter pupilae
- CNIII, Ach.
What is involved in dilation of the pupil?
- LONG ciliary nerves to dilator pupilae
- NA, occurs due to a strong emotional drive
What happens in accomodation?
Normally the ciliary muscle is relaxed (suspensory ligaments taut on lens) so lens is flat, poor refractive power…….
Accomodation..Ach on short ciliary nerves causes ciliary muscles to contract (suspensory ligaments lax)
-lens bulges, more refractive power to see close
What is myopia? (-)
- optics too strong, focus infront of retina
- ‘short sightedness’
What is presbyopia?
Middle age, lens becomes stiff, proteins degenerate
Focus becomes fixed
What is the anatomical axis of the eyes?
- divides orbital pyramid in half
- but 45/2 is 22.5 degrees from midline
In the visual axis, (eyes forward-22 degrees adducted) what actions does contraction of the superior oblique have?
- moves eye down and out
- intorsion
In the abducted eye (by medial rectus) what action does the superior oblique have? (what role does SR have now?)
Pure depressor (SR will intort eye ball)
The outer part of the photoreceptor contains phospholipid membrane bound stacks for…?
What is the RMP? how?
- they hold chemicals/protiens needed for the transduction of stimuli
- RMP -40mV as Na+ can leak in meaning theres a small default glutamate released
What happens to the outer segment/RMP when the photoreceptor is illuminated?
- The leak Na+ channels close, cell hyperpolarises
- The glutamate release stops
What happens to the outer segment/RMP when illumination of a photoreceptor decreases?
- More leak Na+ channels open, cell depolarises
- More glutamate release
What apparatus is involved in the membrane discs of photoreceptors to transduce a light signal?
-the photopigment (opsin bound to 11-cis retinal)
Upon a photon hitting the photopigment, -the 11-cis bond breaks, now all bonds are trans…what does this trigger?
- triggers activated photopigment which amplifies a biochemical cascade resulting in decreased c.GMP conc
- c.GMP ususally holds open the Na+ leak channels so now some Na+ close -> hyperpolarisation
How is the activated photopigment response terminated?
- trans retinal is converted back to 11-cis retinal in the RPE and opsin is inactivated, more c.GMP and
- c.GMP is replenished by an enzyme, Na+ open again
How do photoreceptors adapt to constant levels of illumination?
- as illumination causes hyperpolarisation
- also with constant levels of illumination this becomes the new normal, it adapts
Photoreceptors outer segment have a high RMR and need a rapid O2/nutrient supply..where is this from?
-the photoreceptors lie just under the RPE - which is surrounded by the choroid plexus
What happens in retinal detachment?
- Retina is held to the RPE as RPE cells suck fluid out the gaps
- with a retinal tear the retina pulls away from the RPE
Name 3 functions of the RPE
- blood-retina barrier with TJs controlling flow
- phagocytic cells -> outersegments replaced often
- absorbs stray light via pigment granules
What causes damage to the outersegment of photoreceptors?
-retinoids and photoxidation
With age what clogs the basement membrane of the RPE? How can they decrease vision/macular degeneration?
Lipofusin. Attracts cholesterol and immune cells -> drusen plaques that block supply/kill photoreceptors
What do parvocellular ganglion cells do?
- high resolution & colour of a stable image, which is in the centre of the receptive field
- cone activates inhibitory interneurones to inhibit surrounding cones via lateral inhibition
- they see CONTRAST/edges
What do magnocellular ganglion cells do?
- detect fast movements and broad outlines
- large receptive field, convergence of many rods/cones
- low resolution
What wavelength of light do the following cones respond to?
Red, Green, Blue
Red -> long wavelengths
Green -> medium
Blue -> short wavelengths
What are “off” and “on” Ganglion cells? We have 50/50 of each
- “off cells” excited by decreased illumination of their photoreceptors
- “on cells” are excited by increased illumination
What 2 things do the retina and LGN encode?
- contrast
- wavelength
What 3 things do the 1 visual cortical cells encode?
- edge orientation ( I or – ), -presence of corners
- direction of motion
- binocular disparity -> depth
Which colours do cones compare?
- Red to green
- Blue to yellow
How does binocular disparity work?
- the difference in the location of an object as seen through the 2 eyes
- in the cortex the input from the 2 eyes relating to same locations make synaptic contacts onto the SAME cortical cells, slight variations from each eye –> depth
What are the 2 pathways of visual cortex, what does each do?
- Inferoremporal ‘what’ pathway - meaning, shape, colour
- Parietal ‘where’ pathway - where, relations to surroundings, self movement control. The superior temporal areas encode movement and feed in here
Lesion in the Inferoremporal ‘what’ pathway leads to what?
Associated agnosia (cant say what an object/face is)
Lesion in the Parietal ‘where’ pathway leads to what?
Cant see whole image, bump into things, cant reach accurately
What is the pathway involved in a Reflexive Saccade?
Retina - Superior Colliculus - Gaze centres - EO muscles
so eyes move towards visual stimulus (this is a reflex-no cortex involved)
What CN nuclei do the following activate
- horizontal gaze centres
- vertical gaze centres
Horizontal -> CNIII and CN VI
Vertical -> CNIII and CNIV
What is the pathway involved in a Exploratory Saccade?
e.g. explore fine detail in image
Retina - V1 - Parietal Cortex- Superior Colliculus - Gaze centres - EO muscles
Scanning to find important features&recognise them
What is the pathway involved in a Voluntary Saccade?
e.g. looking at a clock
Frontal Cortex - Superior Colliculus - Gaze centres - EO muscles
What is smooth pursuit coordinated by?
What 2 things drive it?
Pontine nuclei via cerebellum to vestibular nuclei -> EO
- frontal eye fields (voluntary decision to follow x)
- superior temporal areas (movement sensitive)
Convergence is a disconjugate eye movement.
The cortex projects to the pretectal nucleus, activates CNIII on both sides to MR, at same time what happens?
pretectal nucleus -> edingher westpal -> short cililary nerve -> parasympathetic -> pupil constriction and lens bulges, more refractive power
What part of the ear is the bony labryrinth? What 3 things does it include? What is it filled with?
- wall of inner ear
- vestibule, semicircular canals and cochlear
- Na+ rich periperilymph
Inside the bony labyrinth is the smaller membranous labyrinth, which is filled with what?
And its components are..
K+ rich endolymph
..utricle, saccule, the lateral, superior and posterior semicircular ducts.
The cochlear has 3 chambers, what are they? And what fills them? What membranes separate them?
- scala vestibuli - perilymph, vestibular membrane
- cochlear duct -endo, basilar membrane
- scala tympani - peri
What sits on the basilar membrane in the cochlear duct? What attached to this?
The spiral organ/of Corti, here auditory cells project up
Tectorial membrane overs and attaches to spiral organ
What is the difference between inner and outer stereocilia, structurally and functionally?
- inner are closer to origin of tectorial membrane
- inner do discriminitive hearing at varying pitches
- outer amplify sensitivity of system upon depolarisation
What are tiplinks? What do they do?
Glycoproteins. They transduce sound wave to electrical signals
What is the function of the ossicles in the middle ear?
Capture the vibrations/waves of pressure, allow them to be converted to waves in the fluid (stirrup) & amplify the sound
What causes the hair cells to depolarise?
- vibration of basilar membrane as taller stereocilia are pulled away from their shorter neighbours
- tugging on the tip links
What is the ears RMP?
- 40mV partially depolarised
- tonic glutamate release
How does sound cause an AP? Sound, vibrating basilar membrane, tugs on tip links…..
..tug pulls open some mechanically gated K+ channels on the ADJACENT stereocilia
-K+ influx through the K+ rich endolymph -> big increase in glutamate release and burst of AP
When does the stereocilia tug on the tip link?
Every time they tilt in the direction of the taller pair, they tug on the tip link
The hair cells are sitting in intracellular fluid (high in K+, low in Na+). The top (sterocilia) project up into the endolymph (high K+, low Na+) so how does opening of K+ channel cause depolarisation?
The endolymph is +80mV (ion pumps that generate the endolymph pump more + charge into cochlear duct than they remove)
The intracellular part is -40mV so K+ goes down the electrical gradient
What is responsible for making the endolymph in the coclear duct?
The stria vascularis (exchanges ions from blood to endolymph-making the high K+, positive fluid)
Pathology relating to endolymph production/reabsorption imbalance? Commonly in what disease?
- endolymphatic hydrops (high pressure)
- Ménière disease -> vertigo, tinnitis, gradual hearing loss
Name 2 things that cause ototoxicity to sterocilia.
- aminoglycoside antibiotics (gentamyacin)
- platinum based anti-cancer drugs (cisplatin)
How do we percieve louder sounds? If too loud what happens?
Loud=larger vibrations so cause bigger receptor potentials, more APs and more NT released
-damage stereocilia, kill hair cells, excitotoxic damage
Low frequency sounds-each wave causes sterocilia to tilt, AP.. at the Hz of sound, what happens with high frequency sounds?
-continuous depolarisation as they cant depolarise, hyperpolrise etc that fast
Where are high and low frequency sounds detected?
- high (20kHz) at base of cochlear basilar membrane and at the back of the A1 cortex
- low (20Hz) at apex resonates and at the front of A1
Where is the 1ry Auditory Pathway-for discriminative hearing?
Inner hair cells -> dorsal cochlear nuclei –> INF colliculus –> MGN –> 1 Auditory Cortex
What happens if you wipe out a primary auditory cortex?
If you wipe out both?
- still good hearing through other auditory cortex
- damaged discriminative hearing but not deafness (due to some bypass routes)
What is Presbycusis?
Loss of ss/tt sound hearing in speech (high frequency), decreases understanding, especially in elderly
Where is complex speech comprehension done?
Wernicke’s area
How is high frequency located?
- (L)ateral superior olivary nuclei comparing the (L)oudness of high frequency sounds in the 2 ears
- as high frequency sounds are absorbed in the head
How is low frequency sound located?
- the medial superior olivary nuclei compares the timing of low frequency sounds in the 2 ears
- they pass straight through head, are not absorbed
What is the pathway involved in sound localisation?
VENTRAL cochlear nucleus -> S.O.N (medial/lateral) –> Inf colliculus –> MGN –> A1
Which cochlear nucleus does discrimination
DORSAL
Cochlear has to exit through the inner ear encased in bone. What can happen here and what part?
The vestibular part of CNVIII tends to produce an acoustic neuroma’s via out of control replication of schwann cells. Ringing in ears, crushes auditory afferents…
What makes up the otolith system. Which acceleration does each part do? (As well as gravity sensing)
The Utricle - horizontal movement
Saccule - Vertical movements
What makes up the vestibular apparatus? With the 5 sets of patches of hair cells.
- the vestibule (utricle and saccule)
- the semicircular canals (semicircular ducts with the 3 ampullae where they attach to the utricle)
What is the purpose of the otoconia?
crystals that provide mass and inertia (resistance to change). This lies on top of the otolith (gelatinous membrane on top of sterocilia)
If head moves in a linear horizontal direction what happens on each side of head? (Utricle responsible)
- the otolith lags behind, head movement, sterocilia tilt
- in the ear that the stereocilia tilts towards the tallest sterocillium, channels open, more active afferent
- in other ear, that they tilt towards shortest one, channels close, hyperpolarise, less glutamate.
What is the main output of the vestibular system for? Via what? Which muscles?
Postural control via vestibulospinal tract
Targets anti-gravity muscles of legs and trunk
The 3 ampullae of the semicircular ducts are responsible for rotation of the head. Explain the arrangement.
Stereocilia sit in ampullae crest, projecting into endolymph with a gelatinous material, the cupula.
The upper surface of cells is at interface between the endolymph and normal ECF
What happens in the left semicircular canal when head rotates left? (Push-pull system)
- On left, fluid lags behind rotation movement, presses on cupula, tilts sterocilia, all sterocillia point in same direction so are all depolarised and send afferent signal
- On right they are all silenced by hyperpolarisation
What EO muscles do the left and right horizontal canals project to?
Medial and lateral rectus muscles that do horizontal eye movements
What is the semicircular canals main output, via? e.g. compensate for externally induced movements..
-head stability, visually guided movements
-via medial vestibulospinal tract
-bilaterally neck and shoulder muscles
+Vestibulo-ocular reflexes
The vestibular nuclei brings together what? To do what?
Integrate Vestibular info and Visual info
- to move the eyes to follow the visual stimulus
- while compensating for the movements of the head
Why is the vestibulo-ocular reflex vulnerable to damage eg. from MS?
- they are heavily myelinated to be so fast
- MLF-medial longitudinal fasiculus links the EO motor nuclei, a plaque here disrupts this coordination
Where does the vestibular nucleus receive input from where for pursuit?
-parietal cortex to eye fields project to the pontine nucleus which goes to the vestibular nucleus via the floculo-nodular lobe cerebellum
What are 2 key roles of the cerebellum?
- controlling and correcting fine delicate movements e.g. smooth pursuit
- improves performance in motor learning
Where do the cerebellum Purkinje cells project to? What do they do here? And if due to a pathology the eye moving pathways are weaker…?
To the vestibular nuclei and inhibits it
Inhibition is weaker/stops if a correction to the fine movement is needed
-in a pathology, the purkinje cells will adapt/re-calibrate the level of inhibition they send
Name 2 vestibular system dysfunctions.
- Nystagmus
- Vertigo
- nausea and vomiting
What would happen if you have a dysfunctional left horizontal canal?
- You will have the sensation of your head turning right
- Your eyes will turn to the left and back again
- Diziness and nystagmus and nausea
What 3 areas involved in the vestibular system can cause Nausea and Vomiting with lesions?
- vestibular apparatus lesions
- vestibular pathway lesions
- cerebellar lesions
What 4 things can cause motion sickness?
- actual motion (boat)
- zero gravity
- extreme vestibular stimulation (roller-coasters)
- illusion of motion (VR, cinema)
Name 3 things that can cause the vestibular nuclei to increase signalling to the NTS to induce Nausea/Vomiting.
- vestibular/cerebellar dysfunction -> abnormal input
- overstimulation -> abnormal input to vestibular organs
- sensory conflict between visual system and vestibular organs -> abnormal output. Brain thinks am I poisoned..
