T6 (Fys) The case of the colour-blind man Flashcards

0
Q

What is the reason and result of glaucoma?

A

Decreased drainage of aqueous humour from the anterior chamber causes increased intraocular pressure, limiting the blood flow in the eye which leads to retinal damage.

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1
Q

Which structures are denoted by ‘the uveal tract’?

A

The sclera, ciliary body and the iris.

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2
Q

Explain the following: emmetropia, myopia, hyperopia, presbyopia.

A

Emmetropia: normal accomodation
Myopia: nearsighted (eyeball too long)
Hyperopia: farsighted (eyeball too long)
Presbyopia: age-related farsightedness

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3
Q

What is a cataract?

A

Opacities in the lens caused by for example UV light.

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4
Q

What layers does the retina concist of?

A
  1. Pigment epithelium
  2. Photoreceptor outer segments: cones and rods
  3. Outer nuclear layer: receptor cell somas
  4. Outer plexiform layer: receptor - bipolar cell synapses, horizontal cell projections
  5. Inner nuclear layer (lateral information flow): horizontal cell soma, bipolar cell soma, amacrine cell soma
  6. Inner plexiform layer: amacrine cell - ganglion cell synapses, bipolar cell - ganglion cell synapses
  7. Ganglion cell layer: ganglion cell somas and axons (to optic nerve)
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5
Q

Why are the light-sensitive cells part of the outermost layer of the retina, instead of being in the innermost layer (closest to the light)?

A
  1. The membranous disks which houses the light sensitive photopigment are constantly regenerated and shed (into the pigment layer where they are phagocytosed).
  2. The pigment epithelium regenerates photopigment after light exposure, supplying the retina with fresh pigment.
    (3. Optimum blood flow exists in the pigment layer only, vital for photoreceptor function.)
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6
Q

What is the basic principle for visual signaling of the retina action potentialwise, and what values can the n. opticus membrane potential take?

A

Light reception leads to hyperpolarization. In total darkness the membrane potential is at ca - 40 mV, the hyperpolarization extreme is ca -65 mV.

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7
Q

What ions, receptors, and how, is the receptor membrane potential controlled in darkness vs. light?

A

In darkness: Levels of cGMP in the outer segment are high, opening membrane channels that allow influx of Na and Ca ions which depolarize the cell. Simultanious efflux of K ions acts to counter bakance the charge difference.

In light: cGMP levels decrease, closing the cation channel. The K ion efflux then causes hyperpolarization.

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8
Q

What is the basic structure of the photopigment rhodopsin?

A

Retinal (aldehyde of vitamin A) coupled woth several opsin proteins (there are many different).

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9
Q

How does phototransduction occur in rods?

A
  1. Rhodopsin in the disk membrane encapsulates retinal
  2. A photon turns retinal from 11-cis form into all trans form
  3. Transducin is activated, which activates a phosphodiesterase which hydrolyzes cGMP
  4. The outer membrane hyperpolarizes
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10
Q

How can little light cause even a noticeable change in the membrane potential?

A

Signal amplification:

  • one molecule of activated rhodopsin can activate 800 tranducin molecules (ca 8% of transducin on disk surface)
  • each phosphodiesterase can catalyze breakdown of 6 cGMP molecules
  • ultimately ca 200 ion channels close from the action of one photon (1 mV change)
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11
Q

How is phototransduction ended?

A

Rhodopsin kinase phosphorylates activated rhodopsin, after which arrestin binds to it, hindering further phototransduction.

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12
Q

How does the retinoid cycle work?

A
  1. All-trans retinal dissociates from opsin into cytosol of the outer segment
  2. Conversion into alk-trans retinol
  3. Transportation into pigment epithelium by IRBP (interphotoreceptor binding protein)
  4. Enzymatic conversion into 11-cis retinal
  5. Transportation into outer segment by IRBP (interphotoreceptor binding protein) and combination with opsin in receptor disk
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13
Q

Explain the ‘light adaption’ of phototransduction amplification.

A

Light induced closure of cation channels leads to a decrease in inner Ca ion concentration. This increases the activity of guanylate cyclase (synthesises cGMP), rhodopsin kinase and affinity of cGMP-gated channels for cGMP.

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14
Q

Explain scotopic, photopic and mesopic vision.

A

Scotopic: vision using only rods
Photopic: vision using only cones
Mesopic: vision usin both rods and cones

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15
Q

How do the convergences or rods and cones compare (receptor to bipolar cell ratio)?

A

Rods: 15-30 rods to 1 bipolar cell
Cones: 1 cone to 1 bipolar cell

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16
Q

How do cones and rods differ in adaption to light, e.g. brightest possible exposure?

A

Rods: 600 ms to adaption
Cones: 200 ms to adaption

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17
Q

Outline the connection of rods to rod ganglion cells.

A

Unlike the cone bipolar cells, rod bipolar cells first synapse with an amacrine cell (gap junctions and chemical synapses with terminals of cone bipolars) which then synapse with ganglion cells in the inner plexiform layer.

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18
Q

What specifies the foveola?

A

It is entirely rod free.

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19
Q

How do the cone colours and wavelenghts correspond?

A
blue = Short
green = Medium
red = Long
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20
Q

What two types of dichromatism are there? What other types of colour-blindness exists?

A

Protanopia: lack of red-sensing cones
Deuteranopia: lack of green-sensing cones

Anomalous trichromats: require higher intensity stimulation of a certain colour (protanomalous/deuteranomalous/tritanomalous trichromats)

21
Q

How do light spots and dark spots get perceived/interpreted by the cones in the retina?

A

Based on ganglion receptive fields and increments and decrements of light intensity in the center of the receptirve field (luminance contrast).

Light spot in center: cone is hyperpolarized, on-center bipolar cell depolarized, off-center bipolar cell hyperpolarized, on-center ganglion cell fires, off-center ganglion does not fire

Dark spot in center: cone is depolarized, on-center bipolar cell hyperpolarizes, off-center bipolar cell depolarizes, on-center ganglion does not fire, off-centre ganglion cell fires.

22
Q

How is the sign change achieved in the on-center, off-center circuit?

A

On centre: cone to bipolar synapse is metabotropic and closes Na ion channels, changing the sign

Off-centre: cone to bipolar synapse is ionotropic (as is bipolar-ganglion synapse for both on- and off-centered cells), opening Na ion channels, preserving the sign (sign-conserving)

23
Q

How is light adaptation achieved on ganglion/bipolar level?

A

Sensitivity of the ganglion cells for a spot of light is relative to the surrounding background lighting a.k.a. center-surround mechanism. This is based on surround antagonism mediated by horizontal cells (somas in inner nuclear layer, synapses in outer plexiform layer).

24
Q

Explain the physiological basis of the surround antagonism phenomenon.

A

Horizontal cells synapse with photoreceptor cells in the outer plexiform layer. The mechanism activates when illuminance of off-centre area matches that of on-centre area, where surrounding photoreceptors decrease the release of glutamate, causing hyperpolarization of horizontal cells. This leads to a decrease of GABA release from horizontal cells onto presynaptic membranes of the on-center photoreceptor synapses, increasing the latter’s level of depolarization and thus inhibiting light-evoked transmission by the on-center ganglion cell.

25
Q

How much of the axons of the optic nerves cross sides at the optic chiasm?

A

Ca 60%.

26
Q

What is the difference between the optic nerve and the optic tract?

A

The nerve contains ganglion axons from only one eye whilst the tract contains axons from both.

27
Q

Describe the retinogeniculostriate pathways/primary visual pathway.

A

Optic nerve - optic chiasm - optic tract - thalamus dorsal lateral geniculate nucleus - optic radiation (part of inernal capsule) - primary visual cortex (V1)/striate cortex/Brodmann’s area 17(calcarine fissure of occipital lobe)

The optic tract also targets the hypothalamus (circadian rhythms), pretectum (pupillary and lens control and reflex) and the superior colliculus (orienting movements of head and eyes).

28
Q

Explain how the pretectum plays part in pupillary constriction.

A

Projections from the pretectum synapse with the Edinger-Westphal nucleus which are close to the nucleus of CN III. These contain preganglionic parasympathetic neurons that pass via CN III to terminate on neurons in ciliary ganglion which innervate constrictor muscles of the iris.

29
Q

What is the diagnostic value of the pupillary reflex?

A

Clinical testing of left- and right-side sensory and motor neurons by observing the direct and the consensual responses of the pupils when shining light in either is possible.

30
Q

Where does the suprachiasmatic nucleus lie and which neural pathway is it involved in?

A

Ut lies in the hypothalamus and is involved in the retinohypothalamic pathway (“influences the broad spectrum of visceral functions that are entrained to the day-night cycle”).

31
Q

How can light-triggered circadian rhythm be maintained in animals deficient in rod- and cone-mediated reception?

A

The ganglion cells responsible for mediating circadian rhythm via projections to hypothalamus and pretectum themselves contain light-sensative photopigment (melanopsin).

32
Q

What makes up the binocular field of vision?

A

Left: the nasal visual field of the right eye and the temporal visual field of the left

Right: the nadal visual field of the left eye and the temporal visual field of the right

33
Q

How is peripheral vision perceived?

A

Monocularly, each eye’s most medial part of the nasal retina receiving it.

34
Q

The tractus opticus mediates a contralateral field of view. What does this imply?

A

It implies that the tract contains visual feed from both eyes.

35
Q

Distinguish between anopsia and scotoma.

A

Anopsia: “relatively large visual field deficit(s)”
Scotoma: a smaller visual field deficit

36
Q

What symptoms present int homonymous hemianopsia?

A

Complete loss of binocular vision of one side.

37
Q

What symptoms present in a lesion of the chiasma opticum?

A

Bitemproal hemianopsia/heteronomous hemianopsia (loss of peripheral field of vision on each side).

38
Q

What symptoms present in homonymous quadrantanopsia and why?

A

Loss of upper quarter field of vision due to contralateral lesion of Meyer’s loop.

39
Q

What kind of damage commonly presents with macular sparing.

A

Damage to the cortex.

40
Q

What types of discrimantion do cortical visual neurons make of visual input? Why?

A

Mostly based on orientation of edges (preferred orientation) but also movement direction and spatial and temporal frequency. This has been shown to be an efficient way of encoding natural scenes from nature.

41
Q

How are cells ordered in the neocortex as pertaining to a certain orientation preference?

A

Similar orientation preferring cells are found in one radial column.

42
Q

How eye-specific are the cells in a given column in the striate cortex?

A

Most cells are binocular. Only cells in layer 4 are strictly monocular (contains alternating eye-specific ocular dominance columns, geniculate neurons terminate here). Most neurons (neuron columns) are however either right or left polar.

43
Q

What are the layers of the striate cortex?

A

1, 2/3, 4A, 4B, 4C, 5, 6, white matter

44
Q

What is diplopia?

A

The phenomenon of double vision.

45
Q

How does stereopsis occur?

A

Diplopia makes for focus of an image on two non-corresponding parts of each retina. These are coordinated by neurons in the striate cortex specific to retinal disparities behind or in front of the plain of disparity (far neurons and near neurons). Tuned zero neurons “respond selectively to points that lie on the plane of fixation”.

46
Q

The retinogeniculate pathway is concisted of two lateral pathways. Which are these and where do they project?

A

These are the magnocellular (M ganglion cells) layer and parvocellular (P ganglion cells) layer. These project into layer 4Cα and 4Cβ respectively

47
Q

What differences are there between M and P cells?

A

M cells have larger receptor fields, faster conduction velocities and respond transiently to visual stimuli. P cells on the other hand respond in a sustained manner and can also distinguish colour (on-center cones sensing one wavelength, off-center cones sensing another).

48
Q

What is the role of the koniocellular pathway and where is it found?

A

The K cell pathways exists between the P and M cell layer. It transmits some short wavelength light.

49
Q

What other visual processing areas (extrastriate) of the cortex are there and what are their functions?

A

MT (middle temporal area, target of dorsal stream): responds selectively to the direction of a moving edge without noting colour, failure of results in cerebral akinetopsia

V4 (target of ventral stream): selective response to colour without noting movement, failure of results in cerebral achromatopsia (?)

50
Q

What problems arises from misfunction of the ventral and dorsal stream respectively?

A

Ventral (temporal lobe): recognition of objects and faces (?)
Dorsal (parietal lobe): recognition of objects based on position(?)