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Neuro M101B > Module 1 Lecture 5: Target Selection > Flashcards

Module 1 Lecture 5: Target Selection Flashcards

1
Q

topographic map

A

ordered projection of a sensory surface (eg skin or retina) or an effector system (eg musculature) to regions in the CNS

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2
Q

defining feature of topographic maps

A

neighbor relations in the sensory surface are preserved in target area

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3
Q

where does optic topographic mapping occur

A

back of retina, superior colliculus, tectum, lateral geniculate nucleus, visual cortex

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4
Q

chemoaffinity hypothesis

A

2+ cytochemical gradients in the retina and tectum stamp the RGCs and target with matching chemical codes (identity) to establish the observed mapping

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5
Q

roger sperry’s experiment

A
  1. cut the optic nerve of an amphibian
  2. rotate the eyeball 180 degrees
  3. wait for regeneration
  4. assay for visual behavior
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6
Q

result of roger sperry’s experiment

A

animals behave as if their world is turned around
- never learn

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7
Q

where does the nasal retina map to

A

posterior tectum

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8
Q

where does posterior retina map to

A

anterior tectum

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9
Q

what causes topographic mapping between the retina and the tectum

A

built-in, anatomical features, rather than experience

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10
Q

first step of Bonhoeffer’s experiment

A

prepare cell membrane from anterior and posterior tectum (chick)

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11
Q

second step of Bonhoeffer’s experiment

A

deposit membrane in very thin alternating stripes

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12
Q

third step of Bonhoeffer’s experiment

A

test how retinal axons across the nasal temporal axis grow on stripes

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13
Q

fourth step of Bonhoeffer’s experiment

A

treat posterior membranes with protease or PI-PLC (phsphatidylinositol-specific phospholipase C), which cleaves PI

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14
Q

results of Bonhoeffer’s experiment

A
  1. nasal axons have no preference
  2. temporal axons prefer anterior membrane
  3. preference lost with membrane treatments; consistent with repulsive influence from posterior membranes
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15
Q

conclusion fo Bonhoeffer’s experiment

A

glycosylphosphatidylinositol (GPI)-linked cell surface protein enriched in the posterior tectum triggered repulsion of temporal axons

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16
Q

what does ephrin-5A do

A

causes growth cone collapse

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17
Q

where is ephrin-5A found

A

enriched in the posterior tectum

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18
Q

two types of ephrins

A
  1. ephrin-A: GPI linked
  2. ephrin-B: transmembrane domain
    - 8 ephrins in mammals
    - As bind As, Bs bind Bs
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19
Q

what are ephs

A

receptor tyrosine kinases; important to cell proliferation and survival, as well as migration and axon guidance

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20
Q

what kind of signaling do ephrins do

A
  1. forward signaling (ephrin:Eph)
  2. reverse signaling (Eph:ephrin, the ephrin expressing cell responds)
  3. bidirectional signaling: both cells respond
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21
Q

what is the gradient in the tectum

A

posterior to anterior high-to-low ephrin-A5 and -A2

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22
Q

what is the gradient in the retina

A

temporal to nasal high-to-low EphAs

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23
Q

how does the posterior tectum affect axons from the temporal retina

A

repelled

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24
Q

relationship between temporal retina axons and the posterior tectum with ephrin-A2, A5 double mutants

A

they can target the posterior tectum

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25
Q

if topographic mapping is based on repulsion, then how do nasal axons avoid the anterior tectum?

A

counter gradients and reverse signaling:
- tectum: A-to-P high-to-low EphAs
- retina: N-to-T high-to-low ephrin-A5
- axons from nasal retina are repelled from anterior tectum due to ephrin reverse signaling

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26
Q

what system guides the axon maps from the retina to the superior colliculus and the dorsal lateral geniculate nucleus, from the dorsal lateral geniculate nucleus to visual cortex, and visual cortex back to the previous stuff?

A

EphA and ephrin-A counter gradients

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27
Q

do counter gradients of EphB and ephrinBs exist, and what do they do?

A

yes, exist alongside non-graded expression in the D-V axis of the retina and the medial-lateral axis of the superior colliculus

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28
Q

what do Cajal-Retzius cells express

A

multiple Eph receptors and ephrin ligands

29
Q

wildtype Cajal Retzius cells vs EphB1/B2/B3 triple mutants

A

wildtype cells display contact dependent repulsion; EphB1/B2/B3 triple mutants cluster

30
Q

what is required for wildtype Cajal-Retzius cell distribution

A

contact-dependent repulsion

31
Q

hypotheses for why the CNS is built up in layers

A
  1. protect info –> minimize entropy
  2. minimize energy
32
Q

what happens if Robo2 is mutated

A

RGC axons spread across depth of tectum; some project to multiple layers and have diffuse terminal processes

33
Q

what happens if Slit is knocked down

A

same as if Robo2 is mutated

34
Q

what happens if Slit is overexpressed

A

same as if Robo2 is mutated

35
Q

what happens if Collagen IV is mutated

A

no Slit and RGCs looks same as if Robo2 is mutated

36
Q

where does Slit protein accumulate

A

in the basement membrane, under the skin cells
- stays there by sticking to Collagen IV

37
Q

steps for development of retina

A
  • optic vesicles extend from neural tube
  • turn into cups (now two layers)
  • overlying ectoderm thicken and invaginates; will become the lens
38
Q

where does most computation occur in the retina, and what types

A

inner plexiform layer
- visual features such as light on/off, edges, colors, direction of motion

39
Q

where does the vertebrate retina originate from

A

pseudostratified neuroepithelium
- retinal progenitor cells (RPCs) are connected to both apical and basal laminae and divide preferentially at the apical domain

40
Q

is the retina built inside-out?

A

no

40
Q

recoverin function

A

marks photoreceptors

40
Q

what kinds of gradients of development exist in the retina

A

spatial, in addition to temporal
- central retina develops ahead of peripheral retina

40
Q

how do bipolar cells target to the OPL and IPL

A

by retracting the apical and basal processes of retinal progenitors

40
Q

where do bipolar dendrites form

A

at the BPL

41
Q

where do bipolar axons form

A

at the IPL

42
Q

order of addition to IPL

A
  1. amacrine cells (2nd born)
  2. retinal ganglion cells (1st born)
  3. bipolar cells (last born)
43
Q

where do tyrosine hydroxylase (TH) - expressing dopaminergic amacrine cells predominantly stratify

A

within the S1 sublamina of the IPL in wild-type

44
Q

where are Sema5A and 5B expressed

A

in the developing mouse outer nucleoblast layer (ONBL)

45
Q

what happens in Sema 5B and 5A/5B mutants

A

dopaminergic amacrine neurons, which normally have projections in the S1 layer of the IPL, mis-target into the INL

46
Q

where do melanopsin expressing intrinsically photosensitive RGCs predominantly stratify

A

in the S1 sublamina of the IPL in wild-type

47
Q

what is the working model of targeting to the IPL

A
  • during early retinal development, class 5 semaphorins are expressed by cells in the ONL
  • contact with Sema5-expressing tissues biases the extension of neurites, such as those of tyrosine hydroxylase-expressing dopaminergic amacrine cells (DACs, ‘TH’)
  • following initial redirection, DAC neurites extend into the OFF layers of the IPL
48
Q

characteristics of PlexinA4 and Sema6A proteins

A

expressed in a complementary pattern in the developing inner plexiform laeyr

49
Q

ipRGCs and DACs relationship

A

synaptic partners (make synapses together)

50
Q

what happens in PlexA4 mutants

A

both ipRGCs and DACs extend far deeper into the IPL
- new extensions appear to overlap

51
Q

what happens in Sema6A mutants

A

same as in PlexA4 mutants

52
Q

what cells express PlexA4

A

DACs, not ipRGCs

53
Q

Sema6A functioning in deeper layers of the IPL

A

keeps PlexA4 expressing DAC processes confined to the S1 layer

54
Q

characteristic of ipRGC targeting

A

may be dependent on its direct interactions with DAC processes

55
Q

class 5 semaphorins function

A

direct the neurites of DACS (‘TH’) to the IPL

56
Q

ipRGC (‘M1’) targeting to the S1 layer of the IPL characteristic

A

may be guided by its interactions with DACs

57
Q

examples of homophilic binders

A

Cntn2,3,4, Sdk1, Sdk2, Dscam, DscamL
- do not interact with each other

58
Q

what does RNAi-mediated knockdown of Cntn2 cause

A

disruption of Skd1 expression layer

59
Q

CAM-code model of IPL layer targeting

A

each synaptic lamina has a unique combination of homophilic cell adhesion molecules, encoded by related genes of the immunoglobin superfamily
- misexpression and knockdown experiments show that these cell adhesion molecules can be sufficient and necessary for targeting synaptic terminals to specific sublaminae

60
Q

what does ONL stand for

A

outer nuclear layer

61
Q

what does OPL stand for

A

outer plexiform layer

62
Q

what does INL stand for

A

inner nuclear layer

63
Q

what does IPL stand for

A

inner plexiform layer

64
Q

what does GCL stand for

A

ganglion cell layer

65
Q
A

Neuro M101B (6 decks)

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