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Bx Neuroscience > NS Development (Exam 1) > Flashcards

NS Development (Exam 1) Flashcards

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1
Q

what are critical periods in development?

A

periods where parts of NS are more prone to differentiation

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2
Q

what things help make the structures mature?

A

genetic instructions
cell-to-cell signals
interaction b/w child & external environment (think of kitty experiment)

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3
Q

what stage of differentiation are embryonic stem cells at?

A

pluripotent

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4
Q

what stage of differentiation are somatic stem cells at (adult)?

A

multipotent
- tissue specific
eg: neural stem cells (NSC) -> committed to neural fate by either becoming radial glial cells or transit amplifying cells (TAC)

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5
Q

what is a progenitor cell?

A

cell that is restricted to a specific type of neural cell
- limited self renewal

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6
Q

when does neurulation occur in the developmental cycle?

A

gastrulation (3-layered embryo)

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7
Q

what does the endoderm, mesoderm, and ectoderm form?

A

endo = organs
meso = muscle, bone
ecto = NS, skin

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8
Q

what makes up the neuroectoderm? (describe the process of development here)

A

neural plate -> neural groove -> neural tube

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9
Q

in the neural tube, what makes the CNS and PNS?

A

walls of tube = CNS
neural crest cells = PNS

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10
Q

what does the roofplate of the neural tube do?

A

releases induction molecules

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11
Q

what does the floorplate of the neural tube do? what about the lateral floorplate?

A

makes motor neurons for hindbrain & spine
- lateral floorplate (sides) makes sensory relay neuron (2nd neuron)

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12
Q

what are the three primary vesicles? what secondary vesicles do each of them make?

A

prosencephalon -> telencephalon, diencephalon
mesencephalon -> mesencephalon
rhombencephalon -> metencephalon, myelencephalon

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13
Q

what does the telencephalon & diencephalon make?

A

tele = cerebral cortex
dien = thalamus, hypothalamus, optic vesicle

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14
Q

what does the mesencephalon make?

A

middle brain structures

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15
Q

what does the metencephalon and myelencephalon make?

A

met = pons, cerebellum
mye = medulla

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16
Q

what are the two ways of neural induction? (modifying gene expression)

A

steroid hormones
peptide hormones

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17
Q

what is the difference between steroid hormones and peptide hormones? give examples of each (make sure to include where they are located, roof / floor)

A

s = lipophilic, diffusible, RA (roof & floor)
p = lipophobic, needs a carrier
- Shh (floor), FGF, TGF (roof), BMP (roof)

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18
Q

what structures in the brain does FGF’s go to?

A

forebrain, midbrain

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19
Q

what structures in the brain do BMPs go to?

A

spinal cord, cerebral cortex, cerebellum

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20
Q

what releases BMPs?

A

somites

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21
Q

describe the induction pathway of Shh (receptor, what type of neuron it induces)

A

Shh needs a carrier
- binds to patched / smoothened
- activates intracellular molecules (Gli1)
- goes in and binds to DNA
- induces motor neurons

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22
Q

what is holoproencephaly?

A

no bilateral development of the brain (no hemisphere divison) due to Shh mutation
- cyclopean eye
- 1/16k births

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23
Q

what is medulloblastoma?

A

childhood tumor due to Shh mutation
- 60% survival but left impaired
- 1/50k-100k births

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24
Q

what is basal cell carcinoma of the skin?

A

cancer of the skin due to Shh mutation
- 750k cases per year

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25
describe the induction pathway of RA (where it binds and how)
RA diffuses into the cell and binds directly to DNA - localized signal - has a critical period for release
26
what does too much vitamin A lead to? what does not enough vitamin A lead to?
too little = microcephaly too much = ectopic development (abnormal)
27
what are the two factors that help with cell-to-cell signaling?
tropic factors trophic factors
28
what are tropic factors? (three examples)
factors that guide the direction of growth or movement - CAMs, Netrins, Semaphorins
29
what are trophic factors? (three examples)
factors that promote cell growth & survival (nourishment, maintenance) - NFG, BDNF, Neurotrophins
30
describe the four phases of neurogenesis
G1 (cell growth) = attached to both pial and lumen S (DNA synthesis) = nuc moves towards pial G2 (cell growth) = nuc moves towards lumen M phase = loses pial connection
31
describe symmetrical M phase divison
results in 2 identical NSC (mulipotent) - low delta activity - slow, unlimited divison
32
describe asymmetrical M phase division
results in 1 identical NSC & 1 cell that differentiates further - high delta/notch activity
33
describe the process of the delta/notch ligand receptor
notch intracellular domain inhibits transcellular repressor which allows for transcription to occur
34
what direction do PNS cells migrate? what allows for these cells to be mobile?
moves dorsal -> ventral - epithelial cells turn into mesenchymal cells which allows them to be mobile (due to Snail 1 & 2 decreasing the amount of the epithelial adhesion molecules)
35
what three molecules do the PNS cells use to migrate?
CAMs peptide hormones musculoskeletal tissue
36
what are the four paths of migration for PNS cells?
sensory ganglia autonomic ganglia adrenal neurosecretory cells non-neural cells
37
how to CNS cells migrate? what allows for these CNS cells to attach to a leading process?
move along radial glia by using CAMs to attach (think of G1, S, G2, M)
38
describe the range of migration for CNS cells
long-distance - radial glia -> past dividing cells -> cortex, cerebellum, hippocampus - radial glia are ALSO an intermediate for NSC
39
what transcription regulation mechanism helps NSC decide whether to become neurons or glial cells?
active bHLH (basic helix-loop-helix) = neurons inhibited bHLH = glia
40
what are induced pluripotent stem cells (IPSC)?
induced skin cells & fibroblasts by TFs and reverse engineering - gives the cell embryonic stem cell properties (multi -> pluri)
41
what is some of the research out there on IPSC?
- used IPSCs to induce myelination in rats - used RA treated spinal motor neurons in chick embryos to see what cells had axon projections into the ventral root (suggests we might be able to repair damaged neurons)
42
what are some issues with IPSC?
controlling divison (cancer) finding the right induction factors no current human neural treatment
43
what are cerebral organoids?
taking skin cells and turning them into pluripotent neural cells (using IPSC) - mimics brain organization (cortex, choroid plexus, retinal tissue)
44
what is the research out there on cerebral organoids? what happened in the pts?
compared organoids from skin vs cells in microcephaly - microcephaly pts had early developed neurons & progenitor cells that divided strangely & fewer
45
what happens in the brain in microcephaly pts?
decrease in neurogenesis (less progenitor cells) altered mitosis & migration - SMALL BRAIN (less than 2 SD)
46
what does the construction of circuits mean?
growth of axon to target after neuronal migration - uses cell-to-cell signaling (tropic, trophic factors (diffusible & non-diffusible))
47
describe the first step in the construction of circuits (neural circuit formation)
polarity distinction b/w dendrites & axons - neurite growth outward from cell - growth cones branch out in different directions - cytoskeleton redistributes and increase PAR protein and other signaling molecules to induce change in neurite to make an exon
48
describe the second step in the construction of circuits (axon growth cone)
- axon navigates through solid / semisolid protoplasm to reach targets (long distance) - uses tropic factors - has axon expansions to sense their environment
49
what are lamelipodium?
expansion from growth cone, distinct from axon
50
what are filopodia?
extend from lammellipodium - form rapid & disappear
51
describe dendrite polarization and spacing (give an example)
relies on chemoattractive & chemorepellant signaling molecules - Semaphorin3A (sema3A) repels axon and attracts dendrites when put together with sGC
52
what are the two ways dendrites define their synaptic space?
self-avoidance tiling
53
describe self-avoidance (dual repulsion)
repels dendrites from SAME neuron
54
describe tiling (dual repulsion)
repel dendrites from nearby neurons
55
what stops the growth of the dendrites to prevent tangling and give proper spacing?
DSCAM
56
what are non-diffusible axon guidance cues? what are the three main ones?
ligand / receptor - extracellular matrix molecules - CAMs, Cadherins, Ephrin
57
describe how CAMs work as non-diffusible guidance cues
homophilic and embedded in MB to be a ligand & receptor - Ca2+ independent - does fasciculation (bundling of axons into nerve tracts)
58
describe how Cadherins work as non-diffusible guidance cues
homophilic, Ca2+ dependent - influence gene expression & role in final target selection
59
describe how Ephrin works as a non-diffusible guidance cue
- binds to Eph/Tyrosine Kinase receptors = growth promoting - cleavage of ephrin ligand or endocytosis of receptor = growth limiting - cell-to-cell recognition, role in synaptogenesis
60
what are diffusible axon guidance cues? give two main examples
target derived signals - molecules can be both a repellant or attractant - mechanisms are highly conserved - Netrins, Semaphorins
61
describe how Netrin can be an attractant
uses DCC receptors - Netrin 1 midline decussation role (cross over midline in gang) - commissural, sensory, and motor neurons
62
describe how Netrin can be repulsive
Netrin 1 at a distance pushes hindbrain axons away from midline - addition of Unc5 & low PKA activity makes it repulsive
63
describe how semaphorins work
- primarily chemorepellant (sema3A + sGC in dendrites) - membrane-bound, short-range - uses plexins & neuropilins as receptors - increase in Ca2+ causes the filopodia to collapse (repulse) and the cytoskeleton rearranges
64
what is synpatogenesis?
axons reaching targets (cell-to-cell signaling)
65
what will axons not synapse with?
glial cells (CNS) or connective tissue (PNS) - no interaction w/ some targets even when manipulated
66
what happens during synapse initiation? what factors are involved here
growth cone turns into an immature presynaptic terminal - ephrins, CAMs, cadherins on postsynaptics cell (adhesion factors)
67
what does neuregulin (Nrg1) do?
released from presynaptic terminal and binds to the postsynaptic receptor ErbB (diffuses to receptors)
68
what does neurexin do?
on the presynaptic MB that binds to neuroligin - localizes vesicles to be fused - voltage-gated Ca2+ channels
69
what does neuroligin do?
on the postsynpatic MB and promotes clustering of receptors and channels as the synapse matures (released vai proteolytic cleavage) - specific neuroligins for different neurons
70
what happens during synapse maturation?
- neurotrophins secreted in small quantities form target cells - pruning of excess neurons - synaptic rearrangement
71
how does pruning of excess neurons work?
neurotrophins initiate apoptosis of these neurons - need to have appropriate number of neurons to target matches - transplant studies (removing limb bud led to the removal of neurons in SC, adding a limb bud prior to pruning led to the saving of normally removed neurons)
72
what is synaptic rearrangment? what are the two ways synapses rearrange?
ensuring the right number of axons innervate each target cell and there is the right number of targets for each axon - competition, synapse elimination
73
what is synaptic competition?
not W or L, multiple inputs segregate - dependent on pre- & post- synaptic electrical activity - mediated by neurotrophic signaling
74
what is synapse elimination?
initially there are many axons innervating targets (polyneuronal INN), but as it matures, the number of axons to targets decreases - but there is an increase in the number of synapses per target
75
what are the three major functions of trophic interactions?
needed for survival of some neurons in large populations increase axon/dendrite branching connections form & maintain appropriate number of connections
76
what are the four main neurotrophins?
nerve growth factor (NGF) brain-derived neurotrophic factor (BDNF) neurotrophin-3 (NT-3) neurotrophin-4/5 (NT-4/5)
77
what does NGF affect?
- primary sensory dorsal root ganglia - sympathetic neurons
78
what does BDNF affect?
- cranial nerve ganglia - no effect of sympathetic ganglia
79
what does NT-3 affect?
- primary sensory dorsal root ganglia - sympathetic neurons - cranial nerve ganglia
80
does neurotrophin act long distance or locally?
acts locally to regulate growth (only DIRECT exposure, not general)
81
what two receptors do neurotrophin's use? describe the difference
tyrosine kianse (Trk) = specific neurotrophins p75 = all neurotrophins
82
what three things give diversity to the neuronal circuits?
- complex interactions of neurotrophins - their receptors - signal transduction mechanisms

Bx Neuroscience (4 decks)

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