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Developmental Neurobiology 🧠 > Final: Chapter 7 > Flashcards

Final: Chapter 7 Flashcards

1
Q

____ is a family of molecules that promote neuron survival

A

neurotrophins

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2
Q

Survival of neurons helped by

A

interaction with target tissue

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3
Q

3 ways for cells to die

A

1) Apoptosis
2) Autophagy
3) Necrosis

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4
Q

Apoptosis

A

PYKNOSIS: chromatin in crescent shape at nuclear membrane
proteins cross linked, apoptotic bodies pinch off, and are eaten by macrophages

*Surrounding cells protected

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5
Q

Experiment: TUNEL (UTP nick end labeling)

A

enzyme attaches labeled nucleotides to exposed DNA ends `

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6
Q

Autophagy

A

cytoplasm fills with autophages/lysosomes before pyknosis

Later stages of programed cell death

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7
Q

Necrosis

A

mitochondria stop making energy
swelling and explosion of soma

*Effects neighboring cells

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8
Q

Experiment: TUNEL and BrdU

ISEL labeling

A

BrdU: label synthesis of mitosis
TUNEL: counts pyknotic cells

Most apoptotic cells in ventricular zone where birth is happening

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9
Q

Neural crest cluster on NON-ADHESIVE surface =

A

increase in TUNEL labeling

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10
Q

Survival of neurons depends on amount of

A

target tissue

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11
Q

Experiment: Chicken DRG

A

Less cell death if limb

Remove limb: Few DRG/MN (increased death)
add limb: More DRG/MN (decreased death)

Significance? Target provides survival factor

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12
Q

Experiment: Reduce neurons that go to target rather than target itself. Does death happen?

A

No, not pre-oriented to die, need to reach target

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13
Q

Experiment: Hamburger’s mouse tumor

Part 2: Is it soluble?

A

Sarcoma

put inside a chicken.
Increase survival of DRG sensory neurons and sympathetic ganglion cells (SGC).

Part 2: Tumor of choriallontoic membrane

Tumor not in contact with sym/sensory ganglia, BUT share the same blood supply, strong growth effect

Therefore, it’s soluble!

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14
Q

Experiment: The snake venom

A

Snake venom breaks down nucleic acids, use to see fi proton or NA have growth factor

1) DRG and sarcoma + Snake venom
2) DRG + snake venom

Results?: growth in both! But loving the snake venom. Snake venom is a growth factor.

Where? NGF in salivary glands.

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15
Q

Why is pro-NGF cleavage a big deal?

A

cleaved= bioactive version.

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16
Q 
BDNF = \_\_\_ ganglia
NFG= \_\_\_ ganglia
A

BDNF Vestibular

NGF cochlear

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17
Q

Remove TrkA

A

no response to NGF

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18
Q

Transactivation

A

TRK receptors activated in absence of neurotrophins

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19
Q

NGF in PCl2 cells

A

protein phosphorylation

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20
Q

onocogene 3T3

A

genetic rearrangement, fuses with tyrosine kinases (TRKA), induces kinase activity and phosphorylates stuff

RTK: receptor dimer, neurotrophins bind with specificity

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21
Q

PCL2 cells with TrkA -/- KO

A

no TrkA? cell death, fewer axonal projections, unresponsive to NGF

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22
Q

Actinomycin-D

A

blocks TRANSCRIPTION by binding to DNA preventing the movement of RNA polymerase

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23
Q

Cycloheximide

A

prevents TRANSLATION by blocking peptidyl transferase reaction on ribosomes

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24
Q

______ and ____ rescue neurons after NFG deprivation

A

Actinomycin-D and Cycloheximide

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25
Q

Why can Actin-D and Cyclo-H prevent cell death?

A

because cell death needs proteins

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26
Q

When NFG removed, sympathetic neurons…

A

DIE

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27
Q

Experiment: anti-NGF beads

A

1) Anti-NGF = 22% survive
2) Anti-NGF, but put in some NGF = 95% survive
3) Use the beads= 85% survive
Why the beads? make stationary to see if retrograde transmit needed.

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28
Q

Experiment: block antibody in somata of sympathetic neurons,

A

only 60% neurons survive

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29
Q

Trk internalization

A

1) NGF binds to TrkA, dimerization and autophosphorylation of receptor
2) Ligand-R has clathrin dependent endocytosis. Effector proteins recruited and endo-vesicles activated.
3) Endosome is transported retrogradely along microtubules by dynein motor.
4) endosome at cell body, signal to control transcription

30
Q

Experimental evidence (x3) for Trk receptor internalization and such

A

1) NGF/Trk A/ effector colocalized within endosomal…?
2) increase death when dynein motor protein interfered with
3) block TrkA phosphorylation = decrease survival

31
Q

___ initiates cell death with coreceptor ____

A

p75 NTR

Sortilin

32
Q

___ binds with high affinity to sortilin and p75 NTR

A

proneurotrophins

33
Q

What happens if you block proNGF and sortilin

A

decrease in cell death

34
Q

The proNGF/sortilin/p75NTR survival pathway

A

TRAF6

NIK, stuff with K in it

Activates anti-apoptotic genes

35
Q

The proNGF/sortilin/p75NTR death pathway

A

NRIF: grabs TRAF6

Ask1 –> JNKK (J’s activated)
Jun- phosphorylated

Pro-apoptotic genes activated

36
Q

Name the 3 big survival pathways

A

AKT
RSK
ERK (MAPK)

37
Q

Name the 1 apoptosis pathway

A

JNK

38
Q

Experiment:

1) Remove NGF
2) +JNK
3) +ERK
4) + p21

A

1) death
2) death
3) life
4) Life, p21 is a cyclone dependent kinase inhibitor (inhibits cdk, which is part of death pathway)

39
Q

What keeps everything in mitochondria?

A

Bcl-2

40
Q

What inhibits JNK?

A

MAPK

41
Q

C. Elegans Death pathway

A

Proapoptotic EGL-1 inhibits Ced-9
Ced-9 is life: inhibits Ced 4
Ced 4: activates Ced 3
Ced 3: protease, cuts after asparatate residue to activate apoptosis

42
Q

What inhibits Bcl-2 to cause death in mammals?

A

Bax

43
Q

What inhibits IAP so it stops inhibiting capase-9?

A

Smac

44
Q

mammal pathway:

A

Bax —-| Bcl-2 –| cyto c —> Apaf 1 –> caspase 9 –> Caspase 3 –> Apoptosis

45
Q

What keeps apaf-1 and bax locked up?

A

Bcl-X

46
Q

What 3 things does Bcl-2 have in mitochondria

A

cyto c
SMAC
AIF

47
Q

What does BAD do once dephosphorylated?

A

bind to Bcl-x

frees Apaf-1 and Bax

48
Q

What does Apaf-1 do once it’s free

A

forms apoptosome with cyto c

49
Q

What does bax do once it’s free?

A

Free everything from Bcl-2

50
Q

Smac:

A

binds IAP, free procaspases 9

51
Q

What cleaves procasapase 9?

A

apoptosome (apaf-1 and cyto c)

52
Q

Caspase 9

A

cleaves procaspase 3 into active caspase 3

53
Q

Caspase 3

A

targets ICAD to release CAD

54
Q

Cad joins with __ and goes to the nucleus to do what?

A

AIF

cleave DNA

55
Q

How does lack of NGF cause cell death?

A

cycline D cdk4 pathway

56
Q

In life pathway: what keeps BAD phosphorylated and inactive

A

NT kinase activity

57
Q

LIFE: NGF/TrkA: activates SOS and RAS, which decreases

A

c-Jun

58
Q

LIFe: p21

A

cdk inhibitor

59
Q

life: p75

A

no sortiln, TRAF6, NFB

60
Q

Life: ERK, RSK, and AKT promote what

A

Bcl2 keeping stuff in mitochondria

61
Q

KO bcl-x and bax vs. KO only one

A

a lot of cell death vs. a LOT of cell death

62
Q

Experiment: NMJ treated with Curare

A

more cells live
Less activity in MOTOR = more survival

Why? different systems, different rules

63
Q

Experiment: cochlea removal in chickens

A

Sensory relies on electrical activity, but the death doesn’t happen until E2 when you would actually use it.

64
Q

Experiment: Cochlea removal in a gerbil

A

p7- 50% neuron loss
p9- no neuron loss

Activity for survival, once activity already happen, not need to die.

65
Q

Experiment: induce depolarization by adding KCl to neurons

A

BDNF goes up, more neuron survival

66
Q

Experiment: add BDNF antibody

A

trophic influence of depolarization eliminated

67
Q

Estrogen vs. testosterone

A

estrogen: pro-apoptotic, kill male genitals

Testosterone: survival factor

68
Q

Experiment: Female and testosterone

A

SNB and MN death decreases

69
Q

Experiment: male castrated and flutamide (androgen antagonist)

A

SNB and MN cell death increases

70
Q

Depolarization

A

survival via NT release

activity (for sensory anyway) increases survival

Developmental Neurobiology 🧠 (11 decks)

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