Exam 1 Flashcards
(212 cards)
1
Q
Embryology
A
study of embryo until time of parturition
2
Q
Parturition
A
Birth
3
Q
Development
A
morphological, biochemical and physiological differentiation of an individual (embryology & gametogensis & after birth)
4
Q
Differentiation
A
generation of cellular diversity (fertilized egg specialized into different cell types)
5
Q
Morphogenesis
A
creation of form and structure
6
Q
Growth
A
increase in size
7
Q
Germinating
A
giving life
8
Q
Ontogeny
A
growth and development of individual from fertilization to birth
9
Q
Zygote
A
the fertilized egg
10
Q
Embryo
A
developing organism form cleavage to birth (2 cells)
11
Q
Fetus
A
developing embryo (in human after 3 mo.)
12
Q
What are the two major accomplishments of the developmental process?
A
- Generates cellular diversity and order with each generation
- Ensures the continuity of life from one generation to the next
13
Q
What are the 7 stages of embryogenesis?
A
- Fertilization (zygote formation)
- Cleavage (embryo, morula)
- Blastulation
- Gastrulation
- Organogenesis
- Germ cell formation
- Larval stage
14
Q
What are the three layers formed in gastrulation?
A
- Ectoderm
- Mesoderm
- Endoderm
15
Q
How do we approach the study of embryos (3)?
A
- Anatomical
- Experimental
- Genetic
16
Q
What are the four parts of the anatomical study of embryos?
A
- Comparitive
- Teratology/Medical Embryology (limited since we can’t experiment on human embryos)
- Evolutionary
- Fate Mapping
17
Q
Historical Perspective: the anatomists. How did they believe the embryo formed?
A
Epigenesis
Parts of the embryo arise in succession
18
Q
What did Aristotle believe in?
A
Oviparity, vivipaarity, oviviparity
Major cleavage patterns
Functions of placenta and umbilical cord
Mensus gave material, semen gave form and animation
19
Q
Historical perspective: who was William Harvey? What did he believe? He was the first to observe what?
A
Ex ovo omnia All animals from eggs 1st to observe chick blastoderm Blood islands form before heart Amniotic fluid functions as shock absorber
20
Q
Epigenesis vs Preformation
A
Epigenesis: organs of embryo develop de novo
(aristotle / harvey)
Performation: tiny babies live inside of us. all generations that will ever be are within you. All orgas are pre-formed, simply required growth
21
Q
What are two supporting contemporary theories of preformation?
A
- Infinite divisibility (things can be infinately small to serve their purpose)
- Limited time (creation to apocalypse)
Predate cell theory (didn’t understand there was a limit to how small things can be)
22
Q
What are the two schools of preformation?
A
- Ovist
2. Spermists
23
Q
What did Spallanzani believe?
A
Preformation
Experimented with frogs; put pants on them and stopped semen from transferring = no offspring
Established that sperm was needed to trigger the generation of offspring
24
Q
Who were the Baltic Boys? What did they do?
A
Rathke, von Baer, Pander
Rathke - proposed how pharyngeal pouches, reproduction/extretory/respiratory system developed
von Baer - mammalian egg and notochored
Pander - primary germ layers induction
25
What were the 4 von Baer's Principles?
1. General features appear earlier in development than specialized features (general features of all vertebrates (arches, notochord)
2. Generalized features give rise to more specialized (general skin gives rise to scales, feathers, hair, etc)
3. Embryos do not possess adult features of lower animals (gill slits of mammals don't look like adult gill fish)
4. Higher animals are never like lower animals, only like their early embryos (I was never a monkey)
26
Medical Embryology has no experimental data, so what do physicians utilize?
Physicians utilize nature's "experiments"
| 2-5% of infants have observable anatomical abnormalities
27
What are the 3 main causes of birth defects?
1. Malformations (genetic events)
2. Disruptions (exogenous causes)
3. Random Chance
28
Malfomraitons often appear as ______
Syndromes
29
What is Piebaldism? What gene contains the defect? What is the result?
Syndrome
Defect in KIT
Specific neural crest cells, RBC, germ, peripheral nerve cells fail to proliferate
Loss of pigment cells (white on forehead and stomach), loss of ear cells, loss of gut neurons
Overall: deafness, digestion issues, anemic, sterile, lack of pigment
30
99% of Dwarfism is a result of what malformation? What does this cause? (Peter Dinklage)
Defect in FGF4, FGFR3
Cartiledge cells lay the formation of bone develope,ent
FGF4 inhibits cartilege cell production > achondroplasia > limited bone growth (weiner dogs too)
31
What are teratogens?
Exogenous agents causing abnormalities
| ex. chemicals, viruses, radiation
32
Tell me the story of Thalidomide. How many infants were affected? How many pills did it take? When was the susceptibility period for the mother? What did the children develop (symptoms)?
It was given as a mild sedative to alleviate morning sickness, effected 7,000 infants
1 pill was sufficient
Susceptibility during day 35-50 of menstaul cycle (20-36 days post conception)
Children developed phocomelia (long bones deficeint/absent)
Heart defects, absence of external ears. malformed intestines
33
What was the big developmental biology lesson form Thalidomide?
The symptoms the child faced (absence of ear, absence of arms, etc) was dependent on the days after last menstruation
So, it told us when different parts of the embryo were developing at day 34, 38, 42 and so on
It also told us that exogenous agents in general will effect different pieces of development depending on when it is introduced
34
What is gestational age?
The gestatial age is how long a woman has been pregnant
Gestatial age = 10 weeks
Embyro age = 8 weeks
35
Who is Thomas Quasthoff?
A thalidomide baby that is now an opera singer
36
Homology vs Analogy
Homology: Evolutionarily linked, same face bones from forengial arches
Analogy: not embryologically linked, developed separately, wing of a bird and butterfly
37
What is Fate Mapping?
Tracing cell lineages through development to figure out what they will ultimately become
38
What are the two types of cell movements?
1. Mesenchyme cells
| 2. Epithelial cells
39
How do mesenchyme cells move?
Move independently as a herd
| ex. Zebra
40
How do epithelial cells move?
Move as a unit
| ex. people linked arms and moved together
41
What are the 6 fundamental professes driving morphogenesis?
1. Direction and number of cell divisions
2. Cell shape changes
3. Cell migration
4. Cell growth
5. Cell death
6. Changes cell membrane or secreted products
42
When was the first fate map created? From what organism?
1906
Conklin
He mapped a chicken egg
43
What are the different ways you can fate map?
Flourecent, dyes, GFP in genetics
44
What are the 4 major techniques of Experimental Embryology?
1. Defect: destroy portion of embryo (how does it develop lacking these cells?)
2. Isolation: remove portion & observe development (how do singular cells develop)
3. Recombination: replace original part with part from another region (diff part of same embryo)
4. Transplantation: one portion replaced by part from another embryo
45
What are the three fundamental forces of experimental embryology?
1. Forces outside the embryo
2. Forces within the embryo/cells
3. Forces ordering cells into tissues
46
What is an example of a force outside of the embryo affecting development?
Temperature
In reptiles
Higher temperatures (above 34) are males
47
How does climate change affect reptiles that rely on temperature to determine sex?
Increasing temperatures and fewer trees > increased number of male reptiles
48
What is another example of a force outside of the embryo affecting development?
Development of both females and males in the same Echiuroid worm
Female: if larvae land in sand, larger
Male: if larvae land on female proboscis, lives symbiotically inside female reproductive organs and acts as a gonad
49
What are sequential hermaphrodites?
Organims that transition from one sex to the other or to a combination of both
50
Protandry
Male to larger female
51
Protogyny
Female to larger male
52
Protogynous hermaphroditism
Female to hermaphrodite
53
Protandrous hermaphroditism
Male to hermaphrodite
54
Dimorphism
Females and males look different
55
Which sex is typically higher energy?
Females - takes more energy to make eggs than sperm
56
What are simultaneous hermaphrodites?
both reproductive parts at the same time
57
Differentiation
development of specialized cell types
58
Commitment
developental fate of cells is restricted
59
Go from differentiation through the stages of commitment to a fully differentiated cell
True
60
What are the two stages of commitment
1. Specification
| 2. Determination
61
Specification
Autonomous differentiation in a neutral environment
| Still reversible
62
Determination
```
Autonomous differentiation regardless
Assumed irreversible (regardless of outside influence)
```
63
What are the only cells in your body that are not fully differentiated?
Stem Cells
| Stem cells can differentiate OR make more of themselves
64
What are the three basic mechanisms of specification? What organisms do we see these mechanisms in?
1. Autonomous specification (most invertebrates, inherited transcription factors, asymmetrical eggs)
2. Conditional specification (all vertebrates & some invertebrates)
3. Syncytial Specification (most insects)
65
What is autonomous specification?
- mosaic development
- determinal specification
- Fate is set from very beginning, predetermined
- Morphogens
66
Morphogens
Generates morphology (ex. TF)
67
Who was L. Chabry? What did he do?
1st to demonstrate autonomous specification
| Pull it apart and it will still develop into specified pieces
68
Summary - Autonomous Specification. It is characteristic of what kind of organism? The specification is achieved by what? where? Cells can't change fate if _____ is lost
1. Characteristic of most invertebrates
2. Specification by the differential acquisition of cytoplasmic molecules present in egg
3. Cells can't change fate if blastomere lost
(You get half a person if you split the cell)
69
What are the 2 characteristics of conditional specification?
1. Each cell has the potential to become any of the many different cell types
2. Interactions with other cells/factors restricts fate
(You get twins if you split the cell)
70
Who was Wilhelm Roux? What was his big achievement?
Frog Mosaic development
At the two-cell stage, he killed one cell > the dead tissue was still able to influence the living cell > still end up with dead half and live half
71
What is something unique about the nine-banded armadillo?
They have 4 identical twins every time they reproduce
72
Who was Hans Dreisch? What was his big achievement?
Urchin development
Echinoderms = only group of invertebrates that are conditional specification
If you split up the 4 cells > get 4 fully formed structures
Also noted, location in the blastomere dictates fate!
73
What is syncytial specification?
Seen in insects
Multinucleate cell structure
Nucli replication > multiple nuclei > signal gradient > different development
74
What are the three typesof cell-cell interactions in development?
1. Cell Adhesion
2. Cell Migration
3. Cell Signaling
75
What is differential cell affinity?
When germ layers are developing you can scramble them up and they will still cluster on the inside and outside the way they should
This is because the endoderm has the strongest cell adhesion (surface tension) and the epiderm has the weakest
76
What is surface tension?
The strength it takes to seperate two cells
77
What generates surface tension between cells? (2)
1. Cadherins (cell-cell)
| 2. Integrins (cell-ECM)
78
What are cadherins?
Calcium dependent adherein molecules
79
What is one way to cause cells to dissociate?
Remove calcium > targets cadherins > lose cell-cell adhesion
80
What are catenins?
Linked to actin in the cytoskeleton to give the cell strength
Connect Cadherins to the cytoskeleton
81
What are two factors that can affect Cadherin strength?
1. Number of cadherins
| 2. Types of cadherins
82
What is a homotypic binding? Example?
When two of the same molecules bind together
| ex. Cadherin-Cadherin binding
83
What are the 4 types of cadherins?
1. E-cadherin
2. N-cadherin
3. P-cadherin
4. VE-cadherin
84
What is the main location of E-cadherins?
epithelia
85
What is the main location of N-cadherins?
neurons, heart, skeletal muscle
86
What is the main location of P-cadherins?
placenta, epidermis, breast
87
What is the main location of VE-cadherins?
endothelial cells
88
What are protocadherins?
No strong connection to the cytoskeleton (in comparison to classical cadherin)
Function is more directional than strength
89
What are integrins?
Connect ECM-Cytoskeleton inside cell
| Has two subunits (alpha and beta)
90
What does the alpha component of integrins bind to? The beta?
Alpha: binds ECM to cell membrane
Beta: binds ECM to Talin to Actin (cytoskeleton)
91
What does integrin-binding require?
Divalent ions (ex Ca2+)
92
What are talin, vinvulin, a-actinin protiens?
Linker proteins connecting integrins to the actin
93
Talk me through epithelial to mesenchyme transition
To move from epithelial to mesenchyme the cell needs to lose cadherin connections from paracrine factors
94
Metastasis is an example of what?
Epithelial to mesenchyme transition
95
What are the four stages of cell migration?
1. Polarization (2 distict sides; leading and lagging)
2. Protrusion of leading-edge (uses actin; globular > filamentous)
3. Adhesion to ECM
4. Release of lagging edge
96
Invagination
infolding of region of cells
97
Involution
in-turning of an expanding outer layer
98
What are the two driving forces for Involution?
1. Intercalation
| 2. convergent extension
99
Ingression
Migration of individual cells to interior
100
Delamination
Splitting one cell layer into two or more
101
Epiboly
Spreading of epithelial surface sheets to enclose deeper layers of embryo
102
Intercalation
Going from 2 layers to 1 longer layer
103
Convergent Extension
Going from lots of layers to fewer longer layers
104
What are the 4 types of cell signaling?
1. Juxtacrine: 2 cells that are touching (homo or heterotypic)
2. Paracrine: general area
3. Endocrine: (via blood)
4. Autocrine
105
Define induction, inducer, and responder
Induction: message
Inducer: sender
Responder: responser
106
Competence
The cells have to have the capacity to do their job
107
Time regulation can place a role in making sure everything is in place in regards to cell signaling and development
True
108
Sequential cell signaling
a > b > B > c > C
109
Reciprocal cell signaling
a > b > B ....... back to a > A
110
Placode
a region that's going to form something else
111
Talk me through the formation of the eye (cell signaling)
lens placode > signals to neural ectoderm to become optic cup > optic cup signals to lens placode to become lens (reciprocal signaling) > developing lens signals to epidermis to become cornea (sequential signaling)
112
What are the two types of cell signals?
1. Instructive interactions "do this"
| 2. Permissive interactions "you can do this"
113
Tell me about the experiment with the heart and cell signaling
1. Removed cells with detergent, so just ECM is left
2. Introduced progenitor cells
3. ECM gives progenitor cells permission to become heart cells
114
What are the two types of specificity of induction?
1. Regional Specificity
| 2. Genetic Specificity
115
What is an example of regional specificity of induction?
If you take the dermis from the wing, thigh, and foot and then layer the wing epidermis over it, the epidermis will become the wing, thigh, and foot despite being wing epidermis because the dermis is telling the epidermis what to become
116
What is an example of genetic specificity of induction?
If you take a section of the frog gastrula and put it in the newt gastrula > the newest will have frog tadpole suckers
Likewise if you take a section of the newt gastrula and put it in the grog gastrula > the frog will have newt balancers
**both have competent cells, so they received the signal to develop, but they can only develop into the cells they have the genetics for**
117
What is a morphogen gradient?
The concentration of the morphogen will determine the type of cell
118
What are the 5 major families of signaling pathways?
1. FGF
2. Hedgehog
3. Wnt
4. TGF-beta
5. RTK pathway
119
Talk me through RTK pathway
Ligang > RTK > GEF > Ras > Raf > MEK > ERK > Transcription Factor > Transcription
120
Talk me through FGF & JAK-STAT pathway
Ligand > receptor > JAK > STAT > STAT dimerization > transcription
121
A mutation in the gene for FgfR3 causes what?
Thanatophoric dysplasia
Mutation in gene for FgfR3 causes the premature constitutive action of the STAT pathway > premature production phosphorylated Stat1 protein > cartilage growth stops before birth > narrow chest, extremely short limbs > thanatophoric dysplasia
122
Talk me through the hedgehog pathway
Hedgehog --| patched inhibits smoothened --| Ci protein made activator > transcription
123
Talk me through the Wnt pathway
Wnt > Frizzled/LRP5/6 > Disheveled --| B-catenin --| transcription
124
Talk me through TGF-beta & smad pathway
TGF-beta superfamily ligand > receptor II > receptor I > smad activation > smad dimerization > new transcription
125
Talk me through Juxatrcine signaling
Delta ligand on singnaling cell > notch receptor > protease cleaves notch > peice of notch acts as TF > activation of CSL
Normally CSL has repressor sitting on it
126
What are the 4 phases of gametogenesis?
1. Formation & Migration of PGCs
2. Mitotic Increase in Germ Cell Numbers
3. Meiotic Reduction in DNA/Chromosome Content
4. Differentitation & Maturation
127
What are PGCs?
Primordial germ cells
| All gametes are derived from PGCs
128
PGCs can differentiate into what?
Either sperm or eggs (dependent on sex of adult)
129
PGCs acts as ____ cells for all future gametes in individuals
Stem cells
130
How do PGCs get to the gonads during development?
They migrate
131
What do Vasa cells(?) do?
bind and activate germ-cell-specific genes
132
What do Nanos & Pumilio do?
Block RNA translation for somatic gene expression > prevent replication of germ cells > prevents apoptosis
133
What do Tudor & Piwi do?
Silence genes
134
The PCGs are isolated to a specific end of the embryo in a highly conserved process
True
135
Chromosome diminuation
Pieces of chromosome break down > unique cells
136
Stem cells are the only cells with all _______ intact
chromosomes
137
Nanos localization
Half of the egg with yolk ad half the egg without yolk due to gravity
Nanos will localize in yolk
138
What does DAZL protein do?
Regulate mRNA translation = makes PGCs competent
| No DAZL = no PGC
139
Why does PGC migration occur?
To seperate the events that lead to somatios and germ cells
| Germ cells inherit supresed to not be somatic
140
Where do PGC migrate to?
Genital ridge along the hindgut
141
What is Retinoic acid? What does it do? What is it produced by?
Influences germ cells and gonads
Dictates initiation of meiosis
Produced by mesonephric kidney
142
The re-initiation of meiosis in PGC happens when?
In males it starts at puberty
| In females it starts before birth
143
What is Stra8?
Stimulates DNA replication round and enter into meiosis (works with retinoic acid)
144
How are retinoic acid (RA), Stra8, and meiosis related?
RA > Stra8 > Meiosis
145
What is Cyp26b1?
Inhibits RA, stops the progression of meiosis in males before day 13.5
146
What sex if Cyp26b1 found in?
Males
147
What is Nanos2? What sex is it found in? When?
Inhibits Stra8
In males
After day 13.5
Determines male fate
148
Talk me through spermatogenesis in terms of mitosis and meiosis
Primodial germ cells > E12.5 = prospermatogonia = mitotic arrest > birth > proliferation > puberty > meiosis > fertilization > zygote
149
Talk me thorugh spermatogenesis in terms of DNA methylation
Low Levels of DNA methylation with primodial germ cells and during prolifertion & migration
High levels of DNA methylation in prospermatogonia (mitotic arrest, proliferation, meiosis)
Low levels after fertilization
150
What does methylation on DNA do?
Supresses gene expression
151
What are imprinted genes?
can be tissue specific
certain genes that just aren't expressed because they're always methylated
Ex. mom's is expressed and not dad's
152
What is Prader-Willi syndrome? What chromosome is affected? Which sex does it affect the most? What are the symptoms/
Chromosome 15: dad's version is defective and mom's version is imprinted (blocked)
Typically in males
Weak muscles, constant appetite
153
What do the PGCs turn into once they reach the genital ridge? (males)
Incorporate into sex cords and remain until maturity and then hallow out into seminferous tubules
154
What is the initiation of spermatogenesis at puberty regulated by? (2)
BMP8b
| RA
155
What do Sertoli cells differentiatie from?
Epithelium
156
What are spermatogenic germ cells are bound to Sertoli cells by what? (2)
1. N-Cadherins
| 2. Galactosyltransferase on PGCs
157
What is the role of Sertoli cells?
Nourish and Protect spermatogenic germ cells
158
What do galactosyltransferases do?
Bind and transfer sugar (how sertoli cells nourish speratogenic germ cells ?)
159
Two sertoli cells can link together to form what? What is this structure important for?
Link together to form a testis blood barrier
| Important because sperm are haploid and the body might think they're foreign
160
What is the order from spermatogonia to sperm?
Spermatogonia > primary spermatocytes > meiosis I > secondary spermatocytes > meiosis II > spermatid > spermatogenesis > mature sperm
161
Type A, intermediate, and type B spermatogonia are all examples of ____ cells
Stem cells
162
What is the first step towards commitment to become sperm?
A4 > either become intermediate, replicate, or die off
163
What is the signal for spermatogonia to become spermatocytes?
GDNF
164
What is GDNF dependent on?
Dependent on conc
Low conc = supports spermatogonia to become spermatocytes
High conc = renewal (spermatogonia to more spermatogonia)
165
What supports the transition to spermatogenesis?
SCF
166
Spermatogonia, spermatocytes, and spermatids linked?
Cytoplasmic bridges
167
Why do developing sperm need to be linked by cytoplasmic bridges (2)?
1. Important for coordination
2. Need proteins for transcription and translation that come from the X chromosome (which only half the secondary spermatocytes and on would have)
168
What is the difference between cellular and nuclear maturation?
Nuclear maturation is the division of the nucleus etc
| Cellular maturation begins with spermatid and is the creation of the polar bodies - it is not a cell division
169
What is the point of residual bodies in spermatogenesis?
1. decrease the size of the sperm = eliminate extra size
| 2. Lose cytoplasmic bridge (so they can move individually)
170
What are the 3 major components of sperm?
1. Head - acrosome & nucleus
2. Middle piece - mitochondria
3. Tail - locomotion
Membrane surrounds the entire thing
171
What is the acrosome? What does it do?
Cellular vesicle that releases enzymes to get to egg surface and bind to egg
172
What is the centriole? What does it do? (3)
mTOC
1. Nucleatic center for microtubles
2. Help assemble tail
3. Contribute to spindle in zygote
173
What is the acrosomal vesicle?
Extratory vessicle
| Golgi derived structure
174
In nuclear condensation of spermiogenesis __ histones are replaced by _____
H1 histones are replaced by protamines
175
When are protamines translated?
Protaamines are translated in early spermatid
176
Histones:solinoid
Protamine: ______
Doughnuts (annulus)
177
What are the 3 main functions of the mitochondria in sperm?
1. Produce ATP (for cell life)
2. Regulate calcium
3. Clear ROS
178
The flagella uses ATP produced primarily by what?
Glycolysis in the cytoplasm
179
What is the structure of the axoneme?
9 & 2
| with the inner and outer dynein arms connected with radial spokes
180
What is nexin?
The space between theinner and outer dyenin arms in the axoneme
181
What are dynein?
Motor protein that walk using ATP in the plus direction
182
What are Kinesin?
Motor protein that walk in the minus direction
183
What are linker proteins?
Connect the inner and outer dynein arms so that when the microtubles move they bend
184
What is the structure of a microtubule dublin?
A ring of 11 dyenins and a ring of 13 dyneins overlapping
185
What is katageners syndrome? What is the cause? What are the symptoms?
Flagella lack dynein arms > dysfunctional flagella > effects all cilia in the body
Can lead to detracardio, respiratory problems, infertility
186
What is citus invertus totalis? What causes it? What are the symptoms?
Nodal cilia are non-functional
| The symmetry of your body is flipped
187
How many days does it take for spermatogenesis? What does that mean in terms of hr/testicle rate?
65 days
| 1x10^8 sperm/hr/testicle
188
How many sperm are in an ejaculationg/ (~2mL)
2x10^8
189
What sperm count is considered sterile?
< 1 million
190
How many sperm will a man make in his lifetime?
1-10 trillion
191
Why are testes outside of the body?
To keep them cool
192
Sperm can have many different morphologies depending on the organism
True
193
What are the 3 main classes of hormones?
1. Peptides (lipophobic)
2. Steroids (lipophilic)
3. Monoamines/amino acids (ex epinephrine and norepi)
194
Peptides have extraceulluar receptors
True
195
Sterioeds require what to navigate the circulatory system?
Carriers
196
What is GnRH? Where is it made? What does it target? What does it do?
Gonadotrophin releasing hormone
Produced by hypothalamus
Targets anterior pituitary
Stimulates Gonadotrophin release
197
What are the 3 gonadotrophins discussed in class? What class of hormone are they?
1. FSH
2. LH
3. ICSH
Peptides
198
What is FSH? Where is it produced? What does it target?
Follicle stimulating hormone
Produced in pituitary
Males: target sertoli cells
Females: target Ovarian follicles
199
What is LH? Where is it produced? What does it target?
Lutenizing hormones
Produced in pituitary
Targets ovaries
200
What is ICSH? Where is it produced? What does it target? What does it do? It is the male equivalent of what?
Interstitial Cell Stimulating Hormone
Produced in pituitary
Targets Interstitial cell of lytig to produce testosternone
"Male LH"
201
What are the 3 sex hormones?
1. Estrogen
2. Progesterone
3. Testosterone
202
What can estrogen be converted into (3)? Where is it produced? What does it target?
Estradiol, estriol (placenta), estrone (postmeopause)
Produced in gonads and adrenal gland
Males: targets germinal cells
Females: everything
203
Where is progesteorn produced? What does it targert?
Females: produced by ovaries and endometrium/placenta
Males: produced by adrenal/testis
Females: targets breast tissue, endometirum, pituitary
Males: turns into tesosterone
204
What is the most potent form of testosterone? Where is it produced? What does it do?
Most potent form is DHT
Produced in gonads and adrenal gland, and in females in ovay
Males: targets everything
Females: controls libido, muslce mass, fat distirbution
205
What are the 4 sex glands?
1. Hypothalamus
2. Anterior Pituitary
3. Gonads
4. Adrenal Glands
206
What does the hypothalamus produce?
GnRH
207
What does the Anterior Pituitary produce?
Gonadotrophins
208
What do the gonads produce?
Androgens and Estrogen/Progesterone
209
What do adrenal glands produce?
Testosterone and estrogens
210
Talk me through the male hormones from GnRH through the results
Hypothalamus > GnRH > anterior pituitary > FSH > blood > sertoli cells > 1. produce ABP (androgen binding protein) 2. produce CYP19 (converts testosterone to estradiol) 3. produce AMH (antimullerian hormone) 4. blood testis barrier 5. produces GDNF
211
Talk me through the male hormones starting with ICSH
ICSH > stimulates lydig cells > produce testorsterone > sertoli cells > ABP + testosterone > seminal fluid > effect developement of sperm
sertoli cells > inhibin > block anterior pituitary
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What does the build up of testosterone do?
Build up of testosterone > block hypothalamus and anterior pituitary
