Proliferation Flashcards
How may Siamese twins occur? Fission theory:
= theiry that during neurulation, embryonic disc ripps open and duplicate on one end
- the exact duplication may vary
- most likely
How may Siamese twins occur? Fusion theory
= theory that there exist 2 emryonic discs developing simultaneously, which at one point fuse together
- phenotype depends on area of fusion
How may Siamese twins occur? Two is a crowd theory
= idea that there are 2 discs developing along side each other -> their signaling molecules start to interact -> crowding, a mess
What can happen if the neural tube doesn’t close?
- Location dependent
1. Rostral side -> Anencephaly = no brain (sometimes brainstem develops)
2. Caudal side -> Spina bifida- spinal cord neurons start to protrude/grow outside the back
- still possible to survive, but paralyzed down
- moreover there are surgical solutions (repair in the womb)
What are placodes? What do they form?
= patches of neurogenic ectoderm which migrate to a specific site and are further differentiated from the rest of ectoderm
- Examples: otic placode (audition), olfactory epithelium, organ of Corti (inner ear), lens and cornea, cranial nerves e.g. trigeminal, vagus)
How does the integrated network of local signals work? On what kind of things does it have an effect (what is moving)?
Done due to specific signaling pathways coordinated based on location and time
- Moves sensory organs (dorsal ventral axis, placodes = precursors of sensory organs), ganglion cells, facial nerves
- Mechanism:
- Placode cell starts to send attractor signals -> moves neural crest cell towards it -> neural crest cell and placode attach -> change inthe attachment of placode (now it can move) -> placode pushed away -> cycle repeats
How does placode know which direction to move? How does it stop?
All based on from where are the neural crest cells pushing
- If they are pushing from one direction -> that’s gonna be the vector of movement
- if they are all around the placode, thus pushing from all directions -> will remain still
Note: this determines e.g. how far away our eye are (for some it stops earlier than others), although there are some evolutionary limits (e.g. no
How could this account for individual differences in facial features?
The previous process determines e.g. how far away our eye are (for some it stops earlier than others), although there are some evolutionary limits (e.g. no human has eyes on their forehead - that would require complete restructuring)
Explain Cyclopia - what is it, cause, symptoms
Due to issue with signaling pathways -> prosencephalon doesn’t at all or just not completely seperate into two distinct hemispheres => this messes up the routes of placodes (and other e.g. organ formation)
-> eye placodes will get too close and fuse together => Cyclopia
Symptoms:
- one eye (sometimes with 2 pupils)
- small mouth, cleft lip
- Holoprosenephalic proboscis = abnormaly formed nose (+ often on forehead)
Proliferation - how many n. do we have (rate of their development)? When exactly do they develop? And are there some exceptions?
- We have approxiametaly 100 bilion n.
- Develop during the 2nd trimestr of pregnancy
- Except cerebellum - done over the first 2 years (needs experience)
- neurogenesis is still happening in hippocampus and olfactory bulb
How does the process of proliferation work?
Within the neural tube:
- Precursor cells inside the walls of neural tube divide and grow
- Symmetrical division = produce 2 precursor cells
- Asymmetrical division = produce 2 kinds of cells
- Progenitor cell = mitosis continues
- Neuroblast = post -mitosis cell, differentiates into n. or glia
=> N. migrate to the pial surface -> synthesis, DNA replication
=> migrate back down to the neural tube (getting ready for more mitosis
How does the regulation of proliferation work?
Neighboring cells have or do not have Delta ligands -> if yes, they can attach themselves to Notch surface receptor of a signal-receaving cell -> Notch gets cleaved to just Notch intracellular domain (NICD) -> stops Recombining binding protein J (RBP-J) blackadge -> turns Hes genes on (allow for differentiation into neuroblasts)
So what exactly determines whether cell becomes a neuroblast or stays progenitor cell?
All depends on the signals of neighboring cells -> if differentiation occurs -> at some places Delta ligand goes up -> thus, basis helix-loop helix goes up -> differentiation occurs
- If Delta and bHLH are down -> remains a stem cell
Where does mitosis occur -> do the final cells stay there?
Mitosis occurs at the ventricular zone (close to lumen of the neural tube)
-> neuroblasts will migrate up the cortical plate via radial glial cells
-> determines cells specific identity of either neuron or glia and their specific function
In what fashion are the cortical layers constructed?
When cortex is being build with migrating neuroblasts -> layer 1 is first formed -> the next layer (6) passes through the first layer (which can help pushing) and stops superficial to it -> other layers follow this inside out fashion
- later 1 is pushed all the way up?
What types of cells are hidden under GE? Two types and what molecules do they express? Which direction do they travel? What brain areas they also form?
Ganglionic eminences = specific cells used before inhibitory neurons
- migrate in a tangential direction
1. Lateral GE - vasoactive intertinal peptide (VIP) expressing interneurons
2. Medial GE - parvabumin (Par) and Somatostatin (Som) expressing interneurons
- Give rise to Basal Ganglia and parts of Amygdala
