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Neuro > Eye Mechanics > Flashcards

Eye Mechanics Flashcards

1
Q

What are the five main optic tract destinations?

A
  • dorsal lateral geniculate nucleus
  • superior colliculus
  • accessory optic nuclei
  • pretectal area
  • retinohypothalamic tract
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2
Q

What is the function of the LGN projection destined for the occipital cortex?

A

It serves visual perception

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3
Q

What is the cause of loss of the LGN projection to the occipital cortex?

A

Essentially complete blindness - destroys visual perception

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4
Q

What is the main path of visual perception in the optic tract?

A

From the dorsal lateral geniculate nucleus projecting to the occipital cortex

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5
Q

What is the function of optic fibers that project from the superior colliculus to the dorsal midbrain?

A

Saccadic eye movements that shift visual attention and head movements

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6
Q

What is the effect of loss of the superior colliculus?

A

Sluggish or impaired saccadic visual reflexes

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7
Q

What is the function of the optic tract from the accessory optic nuclei to the brainstem nuclei (dorsal and medial terminal nuclei)?

A

Important for optokinetic nystagmus (smooth eye movements)

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8
Q

What is the function of the pretectal area of the optic tract?

A

Pupillary reflexes (direct and consensual)

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9
Q

What is the function of the retinohypothalamic projection?

A

Regulation of circadian rhythyms

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10
Q

What is the pattern of decussation of nasal retinal fibers?

A

They decussate to the contralateral lateral geniculate nucleus

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11
Q

What is the pattern of decussation of the temporal retinal fibers?

A

They project to the ipsilateral LGN

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12
Q

Where does the upper retina project on the LGN?

A

Medially

upper retina = lower visual field

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13
Q

Where does the lower retina project on the LGN?

A

Laterally

lower retina = upper visual field

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14
Q

Where does the center of vision project in the LGN?

A

It projects to the caudal/posterior LGN

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15
Q

What is the structure of the LGN? What is the function of the layers?

A

It is subdivided into 6 laminae - 1, 4, and 6 get input from the contralateral eye; 2, 3, and 5 get input from the ipsilateral eye

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16
Q

Where does the lower visual field project onto the visual cortex?

A

Upper calcarine banks in the calcarine cortex (medial surface of the occipital cortex)

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17
Q

Where does the upper visual field project?

A

Lower calcarine banks (medial surface of the occipital cortex)

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18
Q

Where do optic nerves from the fovea project in the cortex?

A

Posteriorly with the visual horizon in the fundus of the calcarine fissure

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19
Q

What is the pattern of crossing of the radiations to the visual cortex?

A

Ipsilateral projection from the LGN (so contralateral overall from the eye)

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20
Q

What is the difference in the path of the LGN fibers for the lower and upper visual field?

A

lower field = direct parietal path to the upper bank

upper field = looping path (Meyer’s loop) antero-ventrally to the temporal lobe and then back to the lower bank

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21
Q

Where do geniculate axons of the visual pathway project?

A

To stellate neurons in cortical layer 4 (predominantly) and to a lesser extent layers 6 and 1

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22
Q

What are scotomas?

A

Blind spots labeled as “field cuts”

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23
Q

What is the relationship between visual field and retinal field?

A

They are inverted

upper visual field = lower retinal field

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24
Q

What is calcarine cortex magnification?

A

calcarine neural representation in the region of the macula is greater than proportional

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25
Q

What is the effect of calcarine lesions?

A

Blindness

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26
Q

What is the effect of extrastriate lesions? Temporal, parietal, and ventral occipitotemporal.

A

“psychic blindness” - inability to recognize objects

Temporal = deficits in memory, learning, and recognition

Parietal = visual inattention or visual neglect (right side)

Ventral occipitotemporal lesions = prosopagnosia (inability to recognize faces)

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27
Q

What is the difference between homonymous and heteronymous scotomas?

A

Homonymous = more posterior lesions (signals between both eyes are mixed)

Heteronymous = damage to early portions of the visual pathways (signals between eyes are segregated)

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28
Q

What visual field can temporal damage interrupt?

A

upper visual field deficits (interrupts Meyer’s loop)

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29
Q

What visual field can parietal or occipito-parietal damage disrupt?

A

lower visual field defects

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30
Q

What is a visual receptive field?

A

The region of the retina on which light must fall in order for the activity of the neuron to be affected

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31
Q

What is the effect of a spot of light in the center of an on center neuron? What about light around the center? Diffuse light throughout the cell?

A

On the center: high rate of discharge

Around the center: complete inhibition

Diffuse: minimal activity

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32
Q

What is the stimulation pattern for off center receptive fields?

A

They are excited by a dark spot in the center and inhibited by light spots in the center

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33
Q

What is the difference between the M path and P path from the geniculo-cortical system?

A

M-type = phasic, parietal, for spatial vision

P-type = tonic, temporal, for serving form vision

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34
Q

What is the difference betweens simple cells, complex cells, and hypercomplex cells?

A

simple = cells with orientation selectivity for stimuli

complex = cells that are orientation selective, but without the precise position selectivity of simple cells (on vs. off is a spectrum)

hypercomplex = cells with detectors that extract form information (ex. a “hand” cell)

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35
Q

What is the path of tonic (P-type) cells through to cortex?

A

calcarine cortex –> temporal visual cortex

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36
Q

What is the path of the transient (m-type) cells in the cortex?

A

They fire fast responses in response to visual stimuli

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37
Q

What is the “ventral stream”?

A

The pathways to the temporal cortex, also called the “what” or “perception” pathway

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38
Q

What is the “dorsal stream”?

A

pathways to the parietal cortex, “where” or “action” pathways

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39
Q

Where do neurons of the cortico-cortical paths? What do they do?

A

Neurons in cortex layers 2 and 3, they are important outputs for the visual system

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40
Q

Where do neurons of the corticotectal fibers originate from in the cortex? What do they do?

A

Pyramidal cells in layer 5 of the cortex, connects occipital cortex to the superior colliculus

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41
Q

What does the corticogeniculate pathway?

A

It originates in layer 6 of the cortex and sends axons back to the LGN

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42
Q

What is stereopsis?

A

Depth vision based on slightly different views of the visual scene obtained by the two eyes

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43
Q

What is the difference between convergent/crossed disparity sensitivity and divergent/uncrossed disparity sensitivity?

A

convergent = cells that respond best when images are shifted temporally (responds to near stimuli)

divergent = cells that respond best when images are shifted nasally (responds to far stimuli)

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44
Q

When the optic chiasm is sectioned in a sagittal plan from front to back, as can happen due to a pituitary tumor or a severe blow to the head, the resulting deficit is called “bitemporal hemianopsia.” Why?

a) because the section was complete and occurred due to a single event or at a single point in time, in contrast to the subjects studied by Mitchell and Blakemore
b) because the temporal lobes are damaged when this happens
c) because of the loss of visual information carried in Meyer’s loop
d) because the temporal visual fields (and therefore nasal retinas) of both eyes are blinded
e) because this deficit was first described as a result of a very different lesion, bilateral temporal lobe damage to the optic radiations underlying the cortex

A

d) because the temporal visual fields (and therefore nasal retinas) of both eyes are blinded

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45
Q

The vertical midline, or vertical meridian, of vision:

a) is represented along an anterior-posterior band of the lateral geniculate nucleus
b) is the dividing line between nasal crossing and temporal uncrossed optic fibers
c) is represented at the optic disc
d) is represented at the fundus of the calcarine fissure
e) separates the left eye’s view from the right eye’s view

A

b) is the dividing line between nasal crossing and temporal uncrossed optic fibers

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46
Q

Partial damage to the left lateral geniculate nucleus (to much of its extent but not all layers everywhere) might produce which visual perimetry results?

a) scotoma in left eye, normal right eye vision
b) scotoma in right eye, normal left eye vision
c) nearly homonymous but not identical scotomata of right visual fields of both eyes
d) nearly homonymous but not identical scotomata of left visual fields of both eyes
e) none of the above is possible

A

c) nearly homonymous but not identical scotomata of right visual fields of both eyes

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47
Q

After a head injury, a patient is found through visual field perimetry to be blind in the upper left visual field, with homonymous scotomas, the same when testing either eye. Which is the most likely region of damage?

a) left optic nerve
b) right optic tract
c) Meyer’s loop of the right optic radiations
d) the lower banks of the left and right calcarine fissures in area 17
e) the upper banks of the left and right calcarine fissures in area 17

A

c) Meyer’s loop of the right optic radiations

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48
Q

Based on your knowledge of visual pathways and cortical function, which kind of brain damage would be most likely to cause a loss of some visually-based memory and language skills along with blindness in one upper visual hemifield?

a) left temporo-occipital vascular accident
b) lateral thalamic vascular accident occurring bilaterally
c) pituitary tumor with pressure on the center of the optic chiasm
d) medial thalamic vascular accident
e) bullet wound to the dorsal occipito-parietal cortex, with damage to the upper calcarinecortex

A

a) left temporo-occipital vascular accident

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49
Q

Feature detectors are:

a) concentric center-surround, simple, complex, and hypercomplex neurons
b) lower-order hypercomplex neurons
c) detectors of visual patterns still more complex than those that excite hypercomplex neurons
d) hypothetical, their activity never having been actually recorded in the brain
e) all of the above

A

c) detectors of visual patterns still more complex than those that excite hypercomplex neurons

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50
Q

Disparity refers to:

a) double vision, as would stimulate binocular rivalry; often caused by astigmatism
b) bitemporal hemianopsia
c) inhibitory projections by complex neurons to create hypercomplex receptive fields
d) the sensitive period of development during which visual deprivation has a lasting effect on visual cortex neuronal responses
e) slightly different views seen by left and right eye (bases of steropsis)

A

e) slightly different views seen by left and right eye (bases of steropsis)

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51
Q

What is the main function of the ventral stream pathways?

a) visual perception
b) visual localization
c) visual attention
d) development of plasticity of visuomotor coordination
e) transfer of transient information about visual stimuli

A

a) visual perception

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52
Q

Mononuclear deprivation is:

a) monocular steropsis
b) the source of lamination in the lateral geniculate nucleus
c) ineffective, while binocular deprivation produces selective visual loss
d) a cause of reduction in ocular dominance column size in calcarine cortex
e) loss of cortical neurons representing an orientation notviewed during the critical or sensitive period of development

A

d) a cause of reduction in ocular dominance column size in calcarine cortex

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53
Q

What vision pattern would be produced by lesion 1?

A

Right eye blindness

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54
Q

What vision pattern would be produced by lesion 2?

A

Lateral (temporal) blindness (hemianopsia) in both eyes

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55
Q

What vision pattern would be produced by lesion 3?

A

Left sided hemianopsia

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56
Q

What vision pattern would be produced by lesion 4?

A

Left superior quadrantanopsia

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57
Q

An MRI of a patient shows a lesion in the medial portion of the right lateral geniculate nucleus, the lesion passing through all six layers but sparing the lateral parts of the LGN. Where is the visual field loss?

a) upper left quadrant
b) lower left quadrant
c) upper right quadrant
d) lower right quadrant
e) no loss

A

b) lower left quadrant

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58
Q

A patient complains of “missing things” visually, so you map visual fields and discover the patient cannot see at all in lower left quadrant. The patient appears to have vision in upper quadrant but only after repeated prompting, and it is possible that informal testing without control of eye movements is insufficient. Where is the lesion?

a) right temporal cortex and underlying optic radiations
b) right parietal cortex and underlying optic radiations
c) right fusiform cortex
d) right inferotemporal cortex
e) somewhere on the left, more tests needed

A

b) right parietal cortex and underlying optic radiations

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59
Q

What is the function of the parietal cortex in the visual system?

A

Site where sensory signals from visual system are transformed into motor commands

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60
Q

Where is the frontal eye field?

A

Area located adjacent to the premotor areas of the frontal lobes

61
Q

What is the function of the frontal eye field?

A

Premotor oculomotor command area for eye movements made in a contralateral direction

62
Q

What are the visual effectsof parietal cortex damage?

A
  • limb apraxia (inability to make accurate visually guided limb movements to objects)
  • oculomotor apraxia (difficulty making eye movements to objects)
63
Q

What are the visual effects of damage to the frontal eye field?

A
  • impairs moving eyes to look at the expected location of re-emergence of an object that has been obscured
64
Q

What areas of the cortex are responsible for making smooth ocular following movements to track an object?

A

Parietal and temporal cortical areas along the “dorsal stream” of visual pathways

65
Q

What types of receptors respond to light stimulus for pupilary constriction?

A

Melanopsin containing retinal ganglion cells

66
Q

How do melanopsin containing retinal ganglion cells get activated?

A

They are directly tonically depolarized by light

67
Q

What is the pathway of pupillary constriction starting at the retinal ganglion cell?

A

Retinal ganglion cell –> pretectal neuron in pretectal olivary nucleus –> Edinger-Westphal nucleus preganglionic parasympathetic neuron –> cillary ganglion postganglionic parasympathetic neuron –> pupilloconstrictor muscle in the iris

68
Q

What is the pathway for pupillary dilation beginning at the hypothalamus?

A

Hypothalamus –> intermediolateral cell column preganglionic sympathetic neuron –> superior cervical ganglion postganglionic sympathetic neuron –> pupillodilator muscle in iris

69
Q

What is the brain’s main center for saccadic eye movements?

A

Superior colliculus/optic tectum

70
Q

Describe the visual map along the superior colliculus?

A

Contralateral visual field maps across the superior colliculus with the fovea at the rostral pole

71
Q

Describe the motor error map on the superior colliculus?

A

Neurons deeper in the superior colliculus that cause a saccade - the neurons project axons to regions of the brainstem reticular formation that generate components of the final eye movement command

72
Q

What neurons generate horizontal saccade commands?

A

Neurons of the paramedian pontine reticular formation

73
Q

What is the effect of damage to the paramedian pontine reticular formation?

A

Complete loss of ability to make saccades that direct gazes to the ipsilateral side (smooth tracking and eye rotation intact)

74
Q

What neurons generate commands for vertical saccule movement?

A

neurons of the rostral interstitial nucleus of the medial longitudinal fasciculus

75
Q

What are the pause, burst, and tonic responses of saccades?

A

Pause - omnipause neurons inhibit burst neurons at all times except for the instance of a saccadic movement

Burst - neurons that command a jump in eye position when released from inhibition

Tonic - neurons with steady activity that integrate with burst neurons to create the saccade

all in the paramedian pontine reticular formation

76
Q

What are causes of gaze evoked nystagmus?

A

paramedian pontine reticular formation damage or cerebellar damage

77
Q

What is the main output of neurons from the paramedian pontine reticular formation? What does it do?

A

Ipsilateral abducens nucleus, causes the ipsilateral eye to abduct

78
Q

How do the eyes coordinate lateral movement?

A

Abduction (lateral gaze) occurs via signaling from the PPRF to the abducens nucleus

The other eye is signaled to adduct (medial gaze) by internuclear interneurons in the abducens nucleus that project axons across the midline up via the medial longitudinal fasciculus to the medial rectus portion of the oculomotor nucleus

79
Q

What is the effect of unilateral damage to the medial longitudinal fasciculus?

A

Inability to adduct the eye ipsilateral to the lesion

also called internuclear ophthalmoplegia

80
Q

What is one and a half syndrome?

A

Occurs when the medial longitudinal fasciculus (MLF) is damaged in addition to the paramedian pontine reticular formation on one side –> one eye can’t saccade at all (PPRF damaged and MLF damaged) and the other eye can abduct but not adduct (PPRF functional, MLF damaged)

81
Q

The frontal eye field contrasts with the superior colliculus because its saccade commands are:

a) under executive control
b) quicker to respondto a stimulus
c) more closely related to attention or orientation
d) unable to generate a saccade when the superior colliculus is damaged
e) relayed through parietal cortex

A

a) under executive control

82
Q

Preganglionic neurons that control pupillary constriction are located in the:

a) Edinger-Westphal nucleus
b) pretectal olivary nucleus
c) intermediolateral cell column of the thoracic spinal cord
d) superior cervical ganglion
e) pineal gland

A

a) Edinger-Westphal nucleus

83
Q

Preganglionic neurons that control pupillary dilation are located in the:

a) Edinger-Westphal nucleus
b) pretectal olivary nucleus
c) intermediolateral cell column of the thoracic spinal cord
d) superior cervical ganglion
e) pineal gland

A

c) intermediolateral cell column of the thoracic spinal cord

84
Q

The superficial tissue of the superior colliculus is characterized by:

a) saccade command neurons
b) a motor error map
c) responses closely related to attention
d) a contralateral visual field map
e) input from the PPRF

A

d) a contralateral visual field map

85
Q

The function of the rostral interstitial nucleus of the medial longitudinal fasciculus is to:

a) direct eye movements according to attention
b) direct eye movements according to executive priorities
c) generate vertical saccade burst and tonic command components
d) relay saccade commands to the contralateral medial rectus motor neurons
e) generate one-and-a-half capability

A

c) generate vertical saccade burst and tonic command components

86
Q

The function of omnipause neurons in the reticular formation is to:

a) excite burst neurons
b) inhibit burst neurons
c) excite pause neurons
d) inhibit pause neurons
e) inhibit the substantia nigra pars reticulata

A

b) inhibit burst neurons

87
Q

What eye movement cannot be made after left side MLF damage produces unilateral internuclear ophthalmoplegia?

a) right eye abduction
b) left eye abduction
c) right eye adduction
d) left eye adduction
e) abduction by either eye

A

d) left eye adduction

88
Q

What horizontal eye movement can still be made after left side brainstem damage produces one-and-a-half syndrome?

a) right eye abduction
b) left eye abduction
c) right eye adduction
d) left eye adduction
e) abduction by either eye

A

a) right eye abduction

89
Q

What eye structures are part of the anterior segment?

A

Cornea, iris, lens, and ciliary body

90
Q

What are the three layers of the cornea?

A

epithelium, stroma, and endothelium

91
Q

Why doesn’t the cornea have blood vessels?

A

It has an excess of secreted receptors for VEGF that ties up VEGF and prevents angiogenesis

92
Q

What is the conjunctiva?

A

A loose membrane attached to the limbus and eyelids that prevent foreign materials from getting into the orbit

93
Q

Where is the anterior chamber?

A

area between the cornea and the iris/lens

94
Q

What happens when the eye is too long relative to the optical power?

A

Rays focus on front of retina instead of retina - leads to nearsightedness or myopia

95
Q

What happens if the eye is to short relative to the optical power of the eye?

A

Rays would focus behind the retina leading to far sightedness/hyperopia

96
Q

What is astigmatism?

A

Occurs when the cornea is not uniformly shaped, so major and minor lens axes can have differing powers

97
Q

What is the structure of the lens?

A

Layered laminae (like an onion) of long, narrow flat cells called lens fiber cells

98
Q

How does the lens change shape?

A

When ciliary muscle is relaxed, it lies close to the wall of the eye and the suspensory ligaments are tense and pull the lens flat

  • ciliary relaxed = lens pulled flat*
  • ciliary contracted = lens round*
99
Q

What is cataracts?

A

opaacification of the lens during aging, sometimes associated with diseases (ex. diabetes)

100
Q

Describe the cells that produce plasma?

A

They are part of an epithelium two cells thick that transports several ions actively, which leads to flow of water across

101
Q

Where is aqueous humor produced?

A

Ciliary body

102
Q

What is the main path of flow of aqueous humor?

A

Produced in ciliary body –> forward between the front of the lens and back of the iris (posterior chamber) –> exits eye through trabecular meshwork and canal of Schlemm into episcleral veins

103
Q

What is the path of uveoscleral outflow?

A

Aqueous humor flow goes through the root of the iris rather than the trabecular meshwork

104
Q

What variables control intraocular pressure?

A

total outflow and the conductance of the outflow tract (basically resistance)

105
Q

What is the lamina cribrosa?

A

A collagenous structure that has structural fibers that attempt to maintain the integrity of the globe and allows bundles of optic nerve fibers to pass through it

106
Q

What are the cellular components of the inner nuclear layer of the retina?

A

cell bodies of bipolar, amacrine, and horizontal cells

107
Q

What are the cellular components of the outer plexiform layer of the retina?

A

Photoreceptors connect to rod or cone bipolars and horizontal cells

108
Q

What are the cell components of the inner plexiform layer of the retina?

A

layer where bipolar and amacrine cells connect to ganglion cell dendrites

109
Q

What are the contents of the fovea?

A

Only cone photoreceptors

110
Q

What artery is the entry point of retinal circulation?

A

central retinal artery (branch of ophthalmic artery)

111
Q

What is the artery distribution over the retina and macula?

A

The retina has two layers of capillaries, the macula has more because it is thicker

112
Q

What is the path of venous drainage of the retina?

A

Venules trace the path of arterioles and leave via the central retinal vein

113
Q

What arteries supply the choroid?

A

It is a dense vascular network from long and short posterior cilliary arteries

114
Q

What is the choriocapillaris?

A

capillaries of the inner part of the choroid

115
Q

What is Bruch’s membrane?

A

The basement membrane adjacent to the inner part of the choroid

116
Q

What is the difference between control of retinal vs choroidal flow?

A

Retinal is controlled by metabolic factors and systemic factors, but not autonomics

Choroid is controlled by autonomic factors primarily

117
Q

What cells make up the blood-retinal barrier?

A

Retinal pigment epithelium

118
Q

What causes “floaters” in vision?

A

COndensed areas of vitreous in the vitreous cavity that detatch and float around

119
Q

What are the five classes of neurons of the retina?

A

photoreceptors, horizontal cells, bipolar cells, amacrine cells, and ganglion cells

120
Q

Where is the Muller cell in the retina? What does it do?

A

Spans the thickness of the retina from the inner limiting membrane to the external limiting membrane

Functions as a glia cell - nutrition of neurons, control of circulation

121
Q

What is the function of the retinal pigmented epithelium?

A

It functions to regenerate photopigment in rods and phagocytize the outer segments of rods and cones

122
Q

What is A?

A

Rod

123
Q

What is B?

A

Retinal cone

124
Q

What is C?

A

Horizontal cell

125
Q

What is D?

A

Bipolar cell

126
Q

What is E?

A

Amacrine cell

127
Q

What is F?

A

Ganglion cell

128
Q

What is G?

A

Muller’s cell (glia)

129
Q

What is H?

A

Pigment epithelium

130
Q

What is I?

A

Chromatophore

131
Q

Where is the retina the thickest?

A

In the area just outside the fovea (because second and third order neurons bunch up around the fovea)

132
Q

What part of the retina is used to read and do other detailed tasks?

A

The fovea

133
Q

Why is vision so precise in the fovea?

A

There is a 1:1 connection from cones to ganglion cells, whereas outside the fovea each ganglion cell communicates with thousands of photoreceptors that it cannot differentiate

134
Q

How many types of rods and cones do (most) humans have?

A

One rod - for night vision

Three cones - photopigments for color vision

135
Q

What are the steps of the GPCR signaling pathway of phototransduction?

A

rhodopsin is activated by retinal, which activates transducin (a G protein) –> activates a photophodiesterase to hydrolyze cGMP –> depolarizes the cell and amplifies the light signal

136
Q

How is cGMP restored in the eye?

A

By guanylate cyclase - active in the dark

137
Q

How is trans-retinal converted back to cis-retinal after rhodopsin + GPCR signaling?

A

Occurs in the RPE (rods can’t do it on their own)

138
Q

Does the fovea contain rods, cones, or both?

A

Cones only

139
Q

What are on and off cells in the retinal pathway?

A

bipolar cells

On bipolar cells are depolarized when cones are hyperpolarized (by light)

Off bipolar cells are hyperpolarized in light

140
Q

What types of glutamate receptors do On and Off bipolar cells use?

A

On - mGluR6

Off - kainate-type ionotropic glutamate receptors

141
Q

How does cone signaling work?

A

Cone depolarized by a flash of light –> Off bipolar hyperpolarizes and turns off “off ganglion”, On bipolar depolarizes and turns on “on ganglion”

142
Q

How does signaling work in the “midget pathway”?

A

A pathway in the primate retina - one cone contacts one bipolar cell which contacts one ganglia (one on and one off)

143
Q

What is the pathway of rod signaling?

A

It piggybacks off of cone signaling

Rod depolarizes –> signals to rod bipolar cell (RDB) –> signals to A2 amacrine cell –> signals to the On and Off cone bipolar cells to produce a response

144
Q

Blue cones are found at a relatively low density in the retina as a whole and are specifically excluded from the center of the fovea. How can this pattern be rationalized based on the properties of colored light?

A

Chromatic aberration causes different wavelengths to be focused at different planes - red and green light are better focused at the fovea than blue light, so they are used for high acuity vision

145
Q

What is the utility of splitting cone signaling into On and Off pathways?

A

The world contains both positive and negative contrasts. With this split, increases in spiking from a quiet baseline (which is more metabolically efficient than maintaining a high spike rate all the time) occur for both positive and negative contrasts

146
Q

What two features of primate vision does the midget system support?

A

High acuity and red/green color opponency

147
Q

When a disease such as glaucoma kills a ganglion cell, will it diminish rod vision, cone vision, or both? Why?

A

Both - the rods and cones signalling converges at the level of the retinal ganglion cells

148
Q
A

Neuro (12 decks)

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