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Developmental Neurobiology 🧠 > Final: Chapter 7 > Flashcards

Final: Chapter 7 Flashcards

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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
Why can Actin-D and Cyclo-H prevent cell death?
because cell death needs proteins
26
When NFG removed, sympathetic neurons...
DIE
27
Experiment: anti-NGF beads
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.
28
Experiment: block antibody in somata of sympathetic neurons,
only 60% neurons survive
29
Trk internalization
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
Experimental evidence (x3) for Trk receptor internalization and such
1) NGF/Trk A/ effector colocalized within endosomal...? 2) increase death when dynein motor protein interfered with 3) block TrkA phosphorylation = decrease survival
31
___ initiates cell death with coreceptor ____
p75 NTR Sortilin
32
___ binds with high affinity to sortilin and p75 NTR
proneurotrophins
33
What happens if you block proNGF and sortilin
decrease in cell death
34
The proNGF/sortilin/p75NTR survival pathway
TRAF6 NIK, stuff with K in it Activates anti-apoptotic genes
35
The proNGF/sortilin/p75NTR death pathway
NRIF: grabs TRAF6 Ask1 --> JNKK (J's activated) Jun- phosphorylated Pro-apoptotic genes activated
36
Name the 3 big survival pathways
AKT RSK ERK (MAPK)
37
Name the 1 apoptosis pathway
JNK
38
Experiment: 1) Remove NGF 2) +JNK 3) +ERK 4) + p21
1) death 2) death 3) life 4) Life, p21 is a cyclone dependent kinase inhibitor (inhibits cdk, which is part of death pathway)
39
What keeps everything in mitochondria?
Bcl-2
40
What inhibits JNK?
MAPK
41
C. Elegans Death pathway
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
What inhibits Bcl-2 to cause death in mammals?
Bax
43
What inhibits IAP so it stops inhibiting capase-9?
Smac
44
mammal pathway:
Bax ----| Bcl-2 --| cyto c ---> Apaf 1 --> caspase 9 --> Caspase 3 --> Apoptosis
45
What keeps apaf-1 and bax locked up?
Bcl-X
46
What 3 things does Bcl-2 have in mitochondria
cyto c SMAC AIF
47
What does BAD do once dephosphorylated?
bind to Bcl-x frees Apaf-1 and Bax
48
What does Apaf-1 do once it's free
forms apoptosome with cyto c
49
What does bax do once it's free?
Free everything from Bcl-2
50
Smac:
binds IAP, free procaspases 9
51
What cleaves procasapase 9?
apoptosome (apaf-1 and cyto c)
52
Caspase 9
cleaves procaspase 3 into active caspase 3
53
Caspase 3
targets ICAD to release CAD
54
Cad joins with __ and goes to the nucleus to do what?
AIF cleave DNA
55
How does lack of NGF cause cell death?
cycline D cdk4 pathway
56
In life pathway: what keeps BAD phosphorylated and inactive
NT kinase activity
57
LIFE: NGF/TrkA: activates SOS and RAS, which decreases
c-Jun
58
LIFe: p21
cdk inhibitor
59
life: p75
no sortiln, TRAF6, NFB
60
Life: ERK, RSK, and AKT promote what
Bcl2 keeping stuff in mitochondria
61
KO bcl-x and bax vs. KO only one
a lot of cell death vs. a LOT of cell death
62
Experiment: NMJ treated with Curare
more cells live Less activity in MOTOR = more survival Why? different systems, different rules
63
Experiment: cochlea removal in chickens
Sensory relies on electrical activity, but the death doesn't happen until E2 when you would actually use it.
64
Experiment: Cochlea removal in a gerbil
p7- 50% neuron loss p9- no neuron loss Activity for survival, once activity already happen, not need to die.
65
Experiment: induce depolarization by adding KCl to neurons
BDNF goes up, more neuron survival
66
Experiment: add BDNF antibody
trophic influence of depolarization eliminated
67
Estrogen vs. testosterone
estrogen: pro-apoptotic, kill male genitals Testosterone: survival factor
68
Experiment: Female and testosterone
SNB and MN death decreases
69
Experiment: male castrated and flutamide (androgen antagonist)
SNB and MN cell death increases
70
Depolarization
survival via NT release | activity (for sensory anyway) increases survival

Developmental Neurobiology 🧠 (11 decks)

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