sight, taste and smell Flashcards

1
Q

what is the spectrum of visible light?

A

400 nm - 700 nm, blue at lower end, red at higher end

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2
Q

describe the gross anatomy of the eye

A

pupil - lets light in

iris - muscles controlling amount of light entering the eye

Cornea - transparent covering of pupil and iris, refracts light onto retina

Sclera - outer layer (minus cornea), tough and protective, maintains shape

Extraocular muscles, controlled by oculomotor nerve (CN III)

Optic nerve -carries axons from retina to brain (CN II)

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3
Q

what is the retina?

A

where light is refracted on to, has cones and rods, fovea has highest visual acuity and is surrounded by the macula (good but visual acuity due to fewer blood vessels in this area)

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4
Q

where are the blood vessels of the eye?

A

at the optic disk, the blind spot

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5
Q

what is the aqueous humor and the vitreous humor?

A

aqueous humor is behind the cornea and supports cells without the need for blood vessels which would interfere with refraction

vitreous humor is fluid filled main body of the eye and maintains the shape

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6
Q

how does the cornea refract light?

A

due to it having a significant difference in refractive index to air
refracts 80% of light in the eye

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7
Q

define focal length
why does the lens become thinner for distant objects?

A

focal length = distance from refractive surface to point of convergence of parallel light rays

light rays from far apart are closer to being parallel, which requires less refraction, which the accommodates for

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8
Q

to flatten and weaken the lens (far objects) what happens?

A

suspensory ligaments tighten and ciliary muscles relax

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9
Q

what is:
1) emmetropia
2) hyperopia
3) myopia and how are they fixed?

A

1) things are all working correctly
2) far-sight, close objects are harder to see because light converges behind the retina as eye is too short - use a convex lens to increase refraction
3) short sight, far objects are harder to see as light converges too early, before the retina, so use a concave lens to make light rays less parallel

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10
Q

the retina has laminar organisation
how does this not effect the photoreceptors of the fovea?

A

they bend out of the way

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11
Q

there are 7 layers in the organisation of the retina, what are they?

A

the ganglion cell layer, closest to the vitreous humor, outputs info from retina to brain

inner plexiform layer - synapses, between ganglion, amacrine and bipolar cells

inner nuclear layer - amacrine cells, horizontal cells involved in modulating info
and bipolar cell bodies

outer plexiform layer - closer to back of the eye - synapses, between bipolar and photoreceptor cells

outer nuclear layer - cell bodies of the photoreceptors

photoreceptor outer segments

pigmented epithelium - absorbs light the photoreceptors don’t to prevent reflection back to the retina, increasing visual acuity

*signal transduced at photoreceptors (GP), bipolar cells (GP) send signal onto ganglion cells (AP)

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12
Q

where are the light-sensitive pigments in photoreceptors?

A

membranous disks

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13
Q

compare rods and cones

A

Rods -
High sensitivity
More disks, with higher concentration of photopigments in each disks, so 1000x more sensitive than cones (so at night - only rods used, so no colour seen)
Low resolution - many receptors to one bipolar neuron
Cones -
High resolution/visual acuity (and colour)
Fewer disks and lower photopigment concentrations
Not as easily saturated (less sensitive) so better at continuous response to stimuli

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14
Q

where are rods and cones found?

A

fovea = only cones
blind spot = neither
either side of the fovea = lots of rods maybe a few cones
peripheral retina = mostly rods
central retina = more cones

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15
Q

why in the peripheral retina are there many bipolar neurons synapsing eith one ganglion cell?

A

allows for high sensitivity (light levels are lower0 but low acuity as it is unclear exactly where the light came from, seeing as there is multiple inputs

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16
Q

what photopigments are used and why? why are some relied on more at different times?

A

rhodopsin in rods, only ones used at night when we are most sensitive to 500 nm

S, M and L opsins in cones for short medium and long wavelengths, cones relied on more in the day when we are most sensitive to 560 nm

retinal ganglion cells have melanopsin which allows them to respond to huge changes in light, important in circadian rhythm, distinguishing between night and day

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17
Q

what makes photoreceptors so unusual (and how does it work)?

A

they are depolarised at rest and hyperpolarised when activated

ligand gated ion channel on the inside, ligand being cGMP

when it’s dark cGMP keeps these channels open allowing influx of cations (mostly Na+), keeping the cell depolarised (open K+ channels allow K+ to leave so as not to depolarise too far)

when its light cGMP levels drop, channels close, hyperpolarise the cell

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18
Q

explain the signalling cascade in photoreceptors

A

the opsin is a GPCR in the membranous discs
this GPCR has a small molecule - retinal - within
photons change the retinal from cis to trans, exchanging the GPCR’s GDP for GTP

alpha subunit activates phosphodiesterase, an enzyme that converts cGMP to GMP, meaning light causes low cGMP levels and the LGICs close

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19
Q

what occurs in saturation (rods vs cones)?

A

it’s when cGMP levels are so low you have closed all the ion channels you can and cannot hyperpolarise any further

rods are easily saturated, cones are able to maintain a longer response to high light intensities

rhodopsin gets bleached and time is required to reset retinal back to it’s cis state

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20
Q

how does light adaption work, specifically the role of calcium?

A

initial light = high hyperpolarisation
if it continues, photoreceptors gradually depolarise in order to make room for response if light intensity increases

the LGICs allow in calcium as it is a cation
calcium inhibits guanylyl cyclase, the enzyme making cGMP, so in the dark calcium comes in and prevents too much cGMP form overly depolarising the cell

in the light, when LGICs are closing, no calcium allows guanylyl cyclase to go crazy, opening those channels and allowing depolarisation even in the presence of light which initially causes hyperpolarisation

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21
Q

explain how on vs off bipolar cells work

A

photoreceptors - when dark = depolarised = more glutamate
when light = hyperpolarised = less glutamate

the name on or off is based on how they respond to light, which means how they respond to less glutamate

on bipolar cells are depolarised in light - so depolarised by less glutamate - so must use the inhibitory metabotropic GPCR

off bipolar cells become hyperpolarised in light so must use excitatory ionotropic glutamate receptor

22
Q

what is centre-surround organisation when referring to bipolar cells?

A

a bipolar cell has a receptive field centre where it synapses with several photoreceptors, and then a receptive filed surround where it receives info from the surrounding photoreceptors via a middle man - a horizontal cell

23
Q

what are the tests for visual acuity?

A

Snellen’s types and Landolt’s circles

24
Q

visual acuity test - what’s the formula?

A

visual acuity = distance of observer from chart/number of smallest type they can read

25
Q

equation for someone’s ‘distance apart two points on the retina must be to be distinguished’?

A

a =
(distance from optical centre to refracting system which is 15.5mm / distance from observer to object in mm)

multiplied by one fifth of the height of the smallest letter

should be, with good vision, around 4 um, the width of a photoreceptor

26
Q

define protanope, deuteranope and tritanope

A

protanope lacks red/L cones
deuteranope lacks green/M cones (but still have normal vision spectrum)

these both confuse red and green

tritanopes lack blue cones (s cones) which is rare

swap ope for omaly and it’s defective cones, not completely missing cones

27
Q

what happens when you move a finger toward/away from the nose?

A

eyes move disjunctively - opposite directions to one another
towards nose - eyes converge, move in
away from nose - eyes diverge, move out

28
Q

how does the corneal reflex work?

A

this is the on that results in blinking like if you blow on the eye
sensory part = CN V the trigeminal nerve
motor part = facial nerve CN VII

29
Q

why does the pupil dilate/constrict in response to changes in light level?

A

constrict - brighter light - restricts light entry to prevent photoreceptor saturation and to give greater depth of focus by removing scattered light

dilate - lower light - increases light entry to increase potential of action potentials in retinal ganglion cells, but this sacrifices visual acuity

30
Q

how does the pupil dilate/constrict?

A

dilate - radial muscle constricts (circular relaxes) PNS
constrict is the opposite of that, including the other system, the SNS

31
Q

why do both eyes dilate even if one is covered?

A

because both eyes are innervated in parallel, a lack of consensual reflex can indicate a neurological disorder

32
Q

the accommodation reflex - what three things happen?

A

convergence of the eyes as seen in the focus response (looking at an object closer)

accommodation of lens (relaxed ciliary, taut suspensory if you are flattening the lens and vice versa)

accommodation of the pupil - constriction of the pupil increases depth of focus by reducing peripheral scattered light

33
Q

what does an EOG measure?

A

potential difference between the cornea and retinal pigmented epithelium

34
Q

what is the point in smooth pursuit?

A

it keeps the fovea on the object once located, whether you are moving and need to correct drift away, or the object is moving and you need to follow it

35
Q

what does an EOG of saccadic eye movements show? why doesn’t the feeling of this movement annoy us when e.g. reading?

A

large saccade = changing lines when reading
very small saccade = skipping between prominent words

this cannot be felt by a person due to saccadic masking, optic nerve stops sending signals for it

36
Q

optokinetic nystagmus - what does it look like and what does each bit represent?

A

its for stabilising the gaze if you’re moving you’re head for example

has a fast phase - saccadic movement

slow phase - smooth pursuit movement

37
Q

does smooth pursuit require visual stimuli?

A

yes

38
Q

define vestibular nystagmus and how the vestibular system and brainstem work together

A

the ability of a person to hold their gaze on an object while rotating the head/spinning

brainstem does the quick movement, the vestibular system is responsible for the slow movement opposing the direction of the spin

inertia of endolymph pushes the cupula in the opposite direction to the direction of rotation

39
Q

their are 5 tastes - what are they, what are they indicated by, our preference, and why we need to detect it

A

salty - vital electrolytes - prefer high alt - required for many processes

sour - high acidity - we avoid this - helps us avoid rotting food and GI tract injuries

sweet - sugars - high sugar content is preferred - required for growth and energy

bitter - diverse chemical structures - we avoid this - helps us avoid toxic/poisonous substances

umami - amino acids - we prefer high amino acids - needed for protein synthesis, as NTs etc…

40
Q

describe the physiology of the tongue

A

we have 2000-5000 tastebuds
bumps = lingual papillae, there are different kinds:

central/filiform - detect texture

circumvallate (at back) - where most taste cells are found

foliate (around outside and the front) similar to small circumvallate

fungiform - these lingual papillae have taste buds on top, unlike the others

the taste cells have microvilli to increase SA at the taste pore, different taste cells for watch kind of taste

41
Q

which of the tatses use GPCRs and which use LGICs?

A

GPCRs = bitter, sweet, umami

LGICs = salty (ENaC) and sour (Na+ and H+ ion channel)

42
Q

how does transduction work in taste cells?

A

taste cells are just receptors, transduction occurs when molecules like Na+ or H+ move into the cell, it depolarises, so voltage gated calcium ion channels open, calcium causes exocytosis of neurotransmitter to sensory afferent fibres

43
Q

what experiment showed that different taste cells give different info to the brain (e.g. I want more/less of that)?

A

each taste cell is specific to one taste, so sweet will only have sweet receptors
researchers engineered a bitter molecule and receptor, put bitter receptors in sweet cells, and the mouse wanted more of this bitter substance because the sweet cell communicates to the brain that this is something sugary we want more

the bitter receptor receptor was put into bitter cells and the bitter molecule was not liked that time

44
Q

give an overview of how the olfactory system works

A

Odurants enter, dissolve in a mucus layer over the olfactory epithelium (these are the peripheral nervous system receptors)
Cilia of the epithelium in the mucus detect the odorants
A graded potential occurs in the dendrite/cilia? of the receptors, if big enough an AP occurs at the axon segment

45
Q

does each receptor cell detect each odorant? do the APs converge in the same area of the brain?

A

no, each cell only expresses one kind of receptor protein, the information of different odorants can then be combined to detect specific smells

all go to the olfactory cortex in forebrain, but the neurons from receptor cells of different types converge in a their own glomerulus

46
Q

fun facts about olfactory epithelium?

A
  • they can be regularly replaced
  • a stronger smell = bigger graded potential = more frequent action potential
47
Q

human olfactory epithelium totals to what area?

A

10cm^2 (a dog is 170)

48
Q

there’s a lot of smells - give bodily evidence for this

A

350 odorant receptor proteins, 3-5% of our genome
each cell only expresses one kind of receptor but multiple odorants can bind to the receptor

we can combine these 350 possible bits of info with different combos being registered as different smells

49
Q

explain the transduction pathway used by olfactory epithelium

A

odorant receptor proteins are GPCRs using G-olf alpha subunit

it acitvates adenylate cycclase - ATP to cAMP - binds to non-selective cation channel, causing depolarisation of the cell

Ca2+ gated chloride channels are opened from the inside as Ca2+ enters, Cl- moves out further depolarising the cell (allows for lower odorant levels to cause a response and be detected)

then this propagates all the way up, past the soma, to the axon initial segment and onwards if graded potential is large enough, there’ll be an AP

50
Q

explain the different olfactory connections in the brain

A

from glomeruli in the olfactory bulb:

olfactory bulbs to olfactory cortex to perceive the smell, then to the hippocampus (or can go directly from olfactory bulb) as smell is strongly linked to memory

from olfactory cortex to amygdala for emotional response

olfactory bulbs directly connected to hypothalamus, from here there is a link to the reticular formation which is important in ‘visceral responses - like gagging at a bad smell