Development of the NS Flashcards
gastrulation
single-layered blastula reorganised to multilayered gastrula, 4,000+ cels
in frogs blastula with ectoderm(skin), mesoderm and endoderm, cells move to mesoderm now under ectoderm at top (see diagram in notes)
blastula
hollow sphere of cells with ectoderm, mesoderm, endoderm, during early stage of embryonic development
Neuralation
after gastrulation, folding in vertebrates to form neural plate to neural tube
chicken neural tube closure vs human
chicken is zipper from anterior to posterior so slower at back-end
human not zipper but happens in phases (looks like a vag lol)
human neural tube closure (3 weeks old)
1 - spinal cord 2 - brain 3 - front (near face) 4 - back skull 5 - posterior end (near butt)
3 defective neural tube closure in humans
anencephaly
encephalocele
meningomyelocele (spina bifida)
anencephaly
number 2 brain doesn’t close so aborted or don’t live long
encephalocele
number 2 - parts of brain protrude outside skull in sac of skin
usually live, mental disability varies
if number 4 (back of skull) then don’t live
meningomyelocele
spina bifida
spina bifida
folic acid relation
most common
number 5 (near butt)
80-90% survive
varying disability (paralysis, bowel, bladder control, hydrocephalus, learning)
altered folate metabolism from env. or genetics so affect cytoskeleton
hydrocephalus
CSF accumulates
human neural tube structure (embryo)
3 sections of primary brain vesicles - forebrain, midbrain, hindbrain
5 chambers of secondary brain vesicles - cerebrum, thalamus/hypoth/epithalamus., midbrain, pons, cerebellum, medulla oblongata
what is compartmentalisation of neural tube controlled by?
TFs like Hox, Krox20, Otx, Emx2
neural fate of ectoderm
becomes neuroectoderm which is diff from the rest
but needs mesoderm (in vertebrates) for signalling
BMPs
bone morphogenic protein
stops ectoderm becoming neuroectoderm
Lateral inhibition
cells compete to adopt neural fate
all proneural neuroectoderm cells are competent to become neurones but not all do
all cells have Notch receptor and Delta ligand
Notch
Delta
receptor, all vertebrates, glial/skin cells, expressed in neural plate
ligand, all vertebrate neurones, expressed in neural plate
Drosophila evidence of lateral inhibition
regulation of how much delta controlled by Acheate-scute - suppression or enhancement
suppressor-of-hairless switch on enhancer-of-split so switch off achaete-scute
delta gets upper hand so acheate-scute wins
this happens in vertebrates too but diff genes (neurogenin and neuro D)
brainbow
genetic technique shows diff coloured types of neurones (thousands of neurones not just 4 main unipolar/bipolar/pseudouni/multi
asymmetric division of neuroblasts
- components in cell start to move - realignment of metaphase plate so have apical and basal of cell
- Numb protein on basal part - so when divide daughter cell has Numb, stem cell is without Numb
Baz/Pins/Insc apical so only in neuroblasts - 2ndary ganglion is diff to 1st GMC (ganglion mother cell) - diff things inside each time so age and change competency (what it can become)
invariant lineage
diff embryos have same cells so follow division of specific cells (invertebrates)
vertebrates development
almost same as invertebrate development
most similar is retina development (progenitor change TF profile, change competency)
determined by timing of division - neuroblasts divide near surface of neural tube then climb radial glia and migrate to cortex then sideways and change TF depending on where end up
position depends on time
neuronal diversity mediated by…
and explain
chemical gradients
in neural tube, signalling molecules (not TF) like BMP in dorsal and Sonic Hedgehog in ventral tell neurones what to become (diffuse dorsal to ventral)
neuronal diversity dorsal and ventral
dorsal (top) - PNS (neural crest cells) and sensory neurones
roof plate in middle of dorsal tip - conc in BMP
ventral (bottom) - motor neurones, V1 and V2 interneurones
floor plate in middle of ventral - conc in Sonic Hedgehog
gradients define what type of motor/inter (conc decreases as move away)
all happens while neural tube forming
anterior-posterior patterning (front to back)
Hox genes in vertebrates pattern neural tube (brain and spinal cord)
combinatorial code of TFs to specify individual neurones
codes pretty much same, few TFs make difference to identity of neurones
code homologous in all animals
code driven by TF profile from neuroblasts/patterning molecules/Hox from diff env.
spina bifida and folic acid
risk in pregnancy from diet - changes methylation status of proteins and DNA so change gene expression
take up folic acid in diet and forms 5-MeTHF (required to make methionine)
vitamin B12 required for metabolism so makes methionine for methylation
without folate, homocysteine builds up and affects development of fetus
can get rid of it but not if genetics altered, affect cadherins and cytoskeleton
