Week 4 Flashcards
Induction of Neurulation
-The notochord induces thickening of the overlying ectoderm to form neuroectoderm which gives rise to the neural plate
- The lateral edges of the neural plate elevate to form neural folds
Fusion of the Neural folds produce the neural tube
- Fusion of the neural folds begins in the cervical (neck) region of the embryo and continues cranially and caudally (like a zip)
- As the neural folds fuse, the tube separates from the surface ectoderm
Fusion of the Anterior and Posterior Neuropores
- Anterior neuropore= cranial end
- Anterior neuropore fuses on day 25
- The posterior neuropore fuses on day 28
- The cranial end of the neural tube will form the brain
- The caudal end will form the spinal cord
Failure of the anterior Neuropore- anencephaly
- Forebrain does not form (cognition, memory, speech, vision and hearing)
- A brainstem is present (normally exposed, heart and lungs and some reflexes)
- Rarely a baby with anencephaly may survive for a few years however most are stillbirths or the newborn dies a few hours post birth
Failure of the Posterior Neuropore
- Spinal cord does not form properly leading to paralysis
- spina bifida where there is failure of the sclerotome to crease an arch of vertebrae that protects the spinal cord
- In addition, open neural tube prevents formation of vertebrae
- Flat plate of neural tissue is exposed at birth- high risk of infection
What is Rachischisis?
failure of posterior neuropore to fuse, so we have flat plate of neural tissue (paralysis & risk of infection= high)
Neural Tube Defects (NTDs)
- Anecephaly and rachischisis are known as neural tube defects (NTDs)
- Spina bifida is also classed as a neural tube defect but this is due to abnormal induction of the sclerotome by the notochord
What is the frequency of NTDs & what helps to reduce them?
- Approx 1 in 1000 births in the UK are affected by NTDs
- Folic acid reduces NTDs by 50-70%
Neural Crest cells
- As neural folds elevate and fuse, cells at lateral edge seperate from the neural tube- neural crest cells
- Migrate laterally and ventrally, dispersing widely and differentiating into a variety of structures throughout the body
- Sometimes referred to as the 4th germ layer (only 3 though)
Neural crest cell derivatives
Many different structures that neural crest cells go on to form
Defects in NCC development
-Neurofibromatosis- genetic condition caused by a mutation in neurofibromin 1 (NF1) gene
- NF1 is a tumour suppressor gene that is “switched off” in neurofibromatosis leading to increased cell division
- Benign tumours of the nervous system, skin and cranial bones
Folding of the embryo
- 4th week embryo undegos folding in 2 directions
- Craniocaudal folding (head and tail closer in proximity)
- Lateral folding (left and right side closer in proximity)
- Due to differential growth of the amniotic sac and yolk sac
Lateral folding
Weight of the growing amniotic sac pushes down on the lateral edges of the disc
Craniocaudal folding
- Amniotic cavity expands and fills with fluid head end & tail end are curved around, bringing them closer together
- The yolk sac is pinched at the midgut and forms the vitelline duct
- Cranial caudal folding is drawing in the connecting stalk from extraembryonic mesoderm to form the umbilical cord on the ventral aspect
Ventral wall defects
Ectopia cordis
Gastroschisis
What is Ectopia cordis?
lateral folds fail to fuse in thoracic region leaving heart outside the body
Extremely rare- approx 1 in 5 mill live births
What is Gastroschisis?
lateral folds fail to fuse in abdominal region
Intestines outside the body wall
Occurs in 3.5/10,000 live births
From trilaminar Disc to 3D embryo
So from a trilaminar disc the 2 directional folds (lateral and craniocaudal folding has produced a 3D embryo) caused by weight of the growing amniotic cavity
What are the 8 key features of an embryo on 28 days?
- Lens placode
- Otic placode
- Pharyngeal arches
- Limb ridge
- Vitelline duct
- Umbilical cord
- Allantois
- Heart bulge
