Embryology 4 Flashcards
how does ectoderm differentiate between epidermis (skin) and CNS/PNS?
- if ectoderm receives BMP signals is normal ectoderm
- if doesn’t receive BMP signals then becomes neural ectoderm
How deactivate neural BMP?
- node & notochord (head mesoderm) provide anti-BMP inhibitory molecules
- allow overlaying ectoderm to ignore BMP instructions to become epidermis
- allows the ectoderm’s default neural fate to proceed
What is the natural fate of ectoderm?
-all ectoderm is poised to become neural; but prevented from doing so by BMP signals
Where does head ectoderm/ the BMP-inhibiroty signals come from?
- as Hensen’s node regresses, head mesoderm lays don and forms notochord
- notochord & node release the signals at the cranial end of the primitive streak
Steps of neural tube formation?
1) neuroectoderm forms neural plate
2) neural plate invaginated to form groove
3) neural folds appear on each side of neural grooves
4) neural folds fuse to form neural tube (loosing contact w/ some old neighbor cells and making contact with new ones)
What does the neural tube form?
-the brain & spinal cord
How make the neural plate
- opposite& adjacent to primitive streak ectoderm tissue thickens & flattens to become the neural plate
- starts thickening on anterior side…moves posteriorly
- made around the notochord
Notochord involvement with the neural plate?
- is a distinctive rod underneath the forming tube
When does the neural tube close?
- 22 days is theorized, but is always completely closed by 28
Steps of neural tube closure?
1) fusion of tube begins in cervical region, proceed in cranial & caudal directions
2) fusion temporarily delayed at poles, creates cranial and caudal neuropore
Mechanisms of neural tube closure?
- originally believed had 1 bilateral zipper that closed tube from 1 closing point
- now believe have 3-5 closing points, not as uniform; is complex
broad 3 steps in neural tube formation?
1) thickening
2) elevation
3) closure
* doesn’t happen EVERYWHERE; can have secondary neurolation instead*
secondary neurolation
- instead of cells forming a circle, cells accumulate together then cells/tissue are cut out of center to form tube
- see multiple holes/ lumen that then fuse
- often done in the tail region mice
- is evidence of it in human
secondary neurolation in humans?
- at our caudal end
- happens later (after 28 days)
- the ventral aspect of neural tube
Spina Bifida? Main types?
- Abnormal closure of the caudal neural tube during weeks 3 & 4; ranges in severity
- causes splitting of the vertebral arches
1) Spina bifida occulta (most common)
2) Spina bifida cystica
Spina bifida occulta
- have missing bone (lamina) section w/ exposed dura
- have spinal cord w/ nervous sytem in tact
- rarely locomotive defect but are missing spinal cord cover
- -usually in 1 or 2 discs (sometimes 3)
- occurs up to 5% of population,
- often can carry and not notice, may just look like harry mole on lower spine w/ no seocndary effects
Spina bifida cystica 2 types
1) Meningocele: Protrusion of meninges
2) Myelomeningocele: Neural tissue protrusion; typically very truamtic
Spina bifida meningocele
- Protrusion of meninges
- from no symptoms, to very severe
- spine is in normal place, no nerve damage, missing lamnia bone cover
Spina bifida Myelomeningocele:
- protrusion of the neural tissue (much more severe) because the neural tube is outside the spine
- leg-muscle &trunk weakness sometimes paralysis
- leads to leakagge of spinal fluid, get developmental effects
karytoype 2 malformation
-seen with Spina bifida Myelomeningocele, when have leakage of spinal fluid, causes hypothalamus to sink down into spinal column, leads to brain clogging & swelling
Rachischisis (split spine)
- severe/ complete form of spina bifida
- tube not closed, have very long “split” of spine
- very few cases make to term, suaully don’t survive as babies
Exencephaly
- failure of cephalic (anterior, cranial) part of neural tube to close
- Vault of skull doesn’t form; necrosis of malformed brain occurs
- leads to anecephaly (lack of brain)
- brainstem remains but fetus lacks mechanism for swallowing, hydramnios occurs in last 2 months of gestation.
hydramnios
- when excess amniotic fluid accumulates during pregnancy due to baby not being able to take up fluid very well since lungs are damaged
- ends up drowning in the fluid
Exencephaly vs. Spina bifida
Exencephaly in failure to close the anterior/cranial/ cephalic part of the neural tube
Spina bifida is the failure to close the caudal part of the neural tube
Human primoridal germ cells?
- mature into gametes
- PGCs are induced in mammals near the initiation of the Primitive streak, shortly before gastrulation
- they then move out of embryo during gastrulation into the endoderm of the yolk sac wall (near the allantois and connecting stalk)
- migrate from the yolk sac to the developing gonads later in development
Why do PGCs migrate away from the embryo in development then have to come back?
- PGCs are in charge of maintaining genetic info for next generations, if exposed to gastrulation signals; may risk integrity of the genetic info
- move to a natural env that lacks organizer differentiation signals therefore they don’t differentiate until they reach their respected gonads
How PGCs get back into the embryo? How get to gonads?
- movement of allantois and pinching of endodoerm brings germ cells into embryo
- specific attachments of extracellular molecules, & chemoattractants direct to gonads
- chemorepllents keep them from going into other spaces
How do the primordial germ cells move to their desired location?
- basement membrane guides to goand region
- cells grab ECM, acts as road/pathway of laminae so they know are going in right direction
- llamepodia and flamellipodia probe env, trying to ID good things to grab/bad things to avoid
- process enables contact between cells, that group together in gonad regions to form gonad structure
how PGC know to be sperm or egg?
- testes have seminferous cords w/ future sperm in center
- if male PGCs fail to colonize, end up lost in diff location, they adopt female charcateristics
- wont develop into oocyte but will develop characteristcs of oocyte
- being located in the testes is the defining factor of gonads Maturing into sperm rather than egg
male/female reproductive organs indifferent stage?
1) indifferent stage: in both genders; have gonads, mullerian duct, mesonephros
* differences in development due to response to the same sex hormones*
Male development form indifferent stage?
-mesonephros
becomes epidysis
-mullerian duct disappears
Female development form indifferent stage?
-mesonephros
disappears
-mullerian duct becomes Fallopian tubes & uterus
embryo folding locations?
1) anterior: Head fold 2) posterior: tail fold 3) lateral fold on lateral side of embry
Head fold
Foregut formation and Cardiogenic primordium brought caudally to Chest region
Tail fold
Hindgut is formed and Connecting stalk is now ventral to the embryo instead of caudal
Lateral fold
- Part of Umbilical Vesicle becomes Midgut;
- Dorsal mesentery suspends the midgut
- Umbilical cord forms from connecting stalk as it narrows
- Amnion covers over the umbilical cord
placenta
-made by feto-maternal combination
-ensures resources for growth of embryo
-first few days done w/ only resources provided in the egg
-
placenta functions:
Nutrition, Respiration, Excretion, Protection
and Hormone production.
fetal vs maternal parts of the placenta?
Fetal: develops from chorionic sac
1) syncytiotrophoblast,
2) cytotrophoblast
3) extramembryonic mesoderm
Maternal: derived from endometrium of uterine wall
when is implantation completed? what does it consist of?
- chorionic sac formation
- completed 2 weeks after fertilization
chorionic sac formation
1) Extraembryonic somatic mesoderm and trophoblast form chorion
2) chorion forms wall of chorionic sac
3) extraembryonic coelom is beginning of the chorionic cavity.
What is suspended in this Chorionic sac? How is it suspended?
- embryo, amniotic sac, and umbilical vesicle
- suspended by the connecting stalk
How make the primary chorionic villi?
1) syncytiotrophoblast invades endometrium; breaks down glands & vessels.
2) Maternal blood fills lacunae. lacunae get larger & form network
3) network forms intervillous spaces of the placenta
4) cytotrophoblast proliferates, makes extensions into syncytiotrophoblast= primary chorionic villi.
lacunae
- spaces/bubbles within the syncytiotrophoblast
- fill with maternal milk to nourish embryo
- are isolated cavities
primary chorionic villi.
-cytotrophoblast proliferations that makes extensions into syncytiotrophoblast
what induces cytotrophoblast proliferation?
-induced by the underlying extraembryonic mesoderm (hypoblasts)
primary villi
-first stage of chorionic villi (week 2)
- trophoblastic shell cells (cytotropoblast)
form finger-like extensions into maternal decidua (maternal endometrium; lacunae)
Secondary villi
- Week 3
- second stage of chorionic villi development
- extraembryonic mesoderm grows into villi, covers entire surface of chorionic sac
what forms the chorionic plate?
-the basal region
Tertiary villi
- Week 4
- 3rd stage of chorionic villi
- mesenchyme differentiates into blood vessels & cells forms arteriocapillary network, fuse with placental vessels, developing in connecting stalk
- stalk now communicated & providing resources to embryo
Stem villi
“anchoring villi”
- villi that attach to maternal tissues via cytotrophoblastic cells (which now surround all the chorion)
- Branch chorionic villi grow from the sides of it
primitive cardiovascular network?
- the network that existed before the embryo received resources from mom’s blood, before placenta etc were created
- vasculature connected embryo to the yolk
- only using resources in egg, as exhaust resources; developed new vasculature around wall of chroion through chorionic villi
Placental Circulation
1) Fetal blood is pumped to the placenta via umbilical arteries
2) Fetal blood returns via a fetal veins
3) Maternal blood never mixes with fetal blood in placenta cuz it remains in the intervillous spaces
4) Endometrial arteries pump blood into intervillous spaces & veins drain the blood
intervillous spaces
- is the critical barrier made by lacunae network
- are little bubles in synctiumtropopblast, where maternal blood is deposited
- from this region, chorionic villi able to suck in resorues & throw out waste
- contain endometrial (mom) veins & arteries and chorionic stem villi (fetal veins/arteries)
Vasculature of the chorionic sac?
- it is not extensive; instead the stem villi have grown massively near the connecting stalk (what provides embryo the resources from mom)
- branching chorionic villi have branched into the intervillous space, contain thinner stem villi collected materials from maternal blood, then go to thicker stem villi near chorionic stalk, then into the stalk to be transported to baby
Microchimerism
- idea that we have a micture of cells
- some maternal cells stay in fetus & some fetal cells stay in mom (chimeras)
- debate if an accident or have true function, potentially help w/ immune system training & protection
- potentially you carry cells from older siblings to
The Decidua
- Thick layer of modified mucous membrane that lines the uterus during pregnancy and is shed after birth w/ placenta
- wraps around embryo…but not a part of the embryo
- part of the endometrium
what is the decidual reaction?
-the change undergone by the endometrium after implantation
The Decidua 3 parts?
- Decidua basalis
- Decidua capsularis
- Decidua parietalis
Decidua basalis
- forms the maternal part of the placenta
Decidua capsularis
- the superficial part overlying the fetus where villi no longer exist
Decidua parietalis
- includes all remaining parts of the decidua
