Samenvatting
Summary Comparative endocrinology: overview
this document contains all the information of the course, presented in a mind map to give an overview
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Voorbeeld 2 van de 9 pagina's
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Voorbeeld van de inhoud
Prostaglandins: small lipids derived VitD: calcitriol, secosteroid derivedfrom arachidonic acid – pain, fever ~ from cholesterol (ring structure Synaptic: neuron releases a nt at synaps -> picked up Endocrine: release signal molecules in the
aspirin affects the conversion of broken by UV) -> more active dorms by receptors at the other end of the synaps = local bloodstream (global) or body fluids (regional)
arachidonic acid to prostaglandin G2 in liver and kidneys Peripheral catecholamines
Eicosanoids: lipid hormones derived are metabolized by liver Have aromatic group, derived from Signaling
monoamine oxidase tyrosine (derived from phenylalanine) Water soluble: aa, amines, peptides
from arachidonic acid – involved in
and proteins. Act through receptors
inflammation, modulation muscle Transport: non soluble in blood, Synthesis: bc they can’t pass membrane
activity and clotting Different steroid binding globulin use Catecholamines 1. Tryosine hydroxylase: (+) OH => DOPA
specific plasma binding proteins 2. Dopa decarboxylase: (-) COOH => dopamine
Retinoic acid: isoprenoid derived Most can be nt as well 3. Dopamine β-hydroxylase: (+) OH => NA Types of bioregulators
from VitA – important in animal as neurohormones
Lipid bioregulators 4. PNMT: (+) CH 3 => A (more stable)
development and as cofactor for lipid
hormones Lipid soluble: steroids, eicosanoids,
Amines are stored in vesicles, loaded
retinoids, thyroid hormones. Act
Synthesis: in mitochondria and SER. No storage: rate of by vesicular transporter, released by Amines, peptides and proteins through NR bc they can pass
production controls release calcium triggered exocytosis
membrane
1. Acetyl-CoA + Acetoacetyl-CoA = HMG-CoA Similar to synaptic vesicle Amines Serotonin is also released
2. Reductase: HMG-CoA -> mevalonate fusion, but hormonal from EC cells to control our Derived from tryptophan ->
3. Mevalonate -> mevalonate-PP -> isopentenyl-PP -> release into bloodstream Release is controlled by motility and secretion serotonin via hydroxylation and
geranyl-PP -> Farnesyl-PP -> -> cholesterol rather than synaptic cleft control of release vesicles decarboxylation (~ tyr -> dopamine)
Receptor stimulation dissociates α from βγ;
Synthesis:
α echanges GTP for GDP • Gq: stimulates PLC SYNTHESIS AND ACTION OF Indolamines
1. NAT: (+) acetyl-group to amino-N =>
• Gs: stimulates AC
• Gi: inhibits AC
BIOREGULATORS N-acetyl serotonin
7TMS receptors 2. HIOMT: (+) CH3 => melatonin
Trimeric G-protein: associates with PM through Insulin like peptides: disulphide bonds
Turning off the response to GCPR lipid tail of γ subunit are formed -> middle is cleaved off by Synthesis:
activation
MAPK/Ras pw: downstream RTK protease -> end product looks like 2 parts 1. Transcription in the nucleus
• Endocytosis of LR complex ->
fewer receptors 1. RTK activation -> recruitment 2. Translation to prohormone in RER
Synthesized from genes; water
• P of receptor -> inactivation grb2-SOS Peptide hormones 3. Signal peptide attaches to RER
soluble and act through the
• Degradation 2 messengers
nd 2. Activation of Ras (GTP) membrane, prohormone is packaged
same type of receptors
• Extracellular ligand degradation: 3. Activation of Raf -> activation 4. Vesicle translocates to Golgi ->
terminate signal MAPKK -> activation MAPK Sometimes PH are short, formation storage granules
Glycoprotein hormones: dimeric
4. MAPK goes to nucleus -> gene but pro-peptide long = 5. Additional processing prohormone in
proteins -> big, covered in
regulation RER, Golgi or storage granules
glycosylation groups => allow to more copies of the same
Ser/thr kinase receptors: TGF-β be recognized by receptor peptides ~ make more
1. Ligand binds -> activation R-SMAD 1TMS receptors NR can bind ligand in
RTK: Some hormones activate NR by cytoplasm -> to nucleus
protein
1. Ligand binds -> RTK dimerization releasing zinc fingers from inhibitory
2. SMAD protein form complex with
2. Activation RTK via factors -> allow DNA binding Ligand crosses nuclear
SMAD4 (co-smad)
autophosphorylation on tyrosine Receptors membrane and bind NR
3. Translocation of Smad complex to Nuclear receptors
residues
the nucleus
3. Activated intracellular signal NRs are TF -> control
4. Bind DNA with DNA binding Modular structure: different
proteins that bind the P tyr gene expression
partner -> gene regulation domains – different functions
residues
, Can also affect behavior: Prairie voles are
When osmolarity is high, VOLT neurons Broadcasting acute signals from the Control of growth, metabolism
monogamous, form lifelong pair bonds →
activate release of VP from SON → lower NS (giving birth, circadian rhythms, and development: tropic axes
meadow voles do not form stable pair bonds.
osmolarity by Increasing the reabsorption desirable behavior) (HPT, HPA, HPG, HPH)
Difference is due in part to nonapeptide
of water in the collecting duct (kidneys) Endocrine system
by P aquaporins = opening hormone receptors: prairie voles have extra
Neuro-endocrine cells: direct
receptors in reward areas of the brain! Homeostasis: all the cells in the body are release of hormones from
Ocytocin: causes rhythmic contractions of surrounded by extracellular fluids -> need to be hypothalamic neurons
reproductive tract: birth, ejaculation, milk Nonapeptide hormones maintained ~ VP: control of osmotic homeostasis
ejection (mammary gland)
VOLT neurons outside the BBB have sensory
Sequences have a lot of similarities, though the endings that have osmo-sensors. When Derived from Neural lobe = Median emincence =
diencephalon Pars nervosa pars eminens
pre-cursors are different → effect on the abnormal → synapses with SON in Axons: from
chemical properties (basic vs more neutral) hypothalamus: vasopressin-releasing neurons hypothalamus to
neurohypophysis Neurohypophysis (posterior pituitarty): neurohemal
GnRH: Kp promotes GnRH region, not really endocrine cells per se
GH: ARC -> GRH →
release (promoted by
somatotrope (inhibited
TSH: PVN → TRH (Gq coupled) estradiol = (+) feedback Pars distalis =
by SST) → GH Portal vessels: from hypothalamus Mammalian Pituitary
→ Thyrotrope → (-) TSH → (+) anterior lobe
to adenohypophysis
thyroid gland -> TH PRL:
• ARC → DA → (-) lactotrope → PRL Pars tubelaris =
Mammalian Pituitary Derived from Adenohypophysis (anterior piruitary):
• POA → VIP → (+) lactotrope → PRL connection with
neural ridge glandular structure
ACTH: PVN → CRH + AVP hypothalamus
→ corticotrope → ACTH Pars intermedia =
α-MSH: ARC → DA →
melanotrope → (-) α-MSH
HYPOTHALAMUS AND PITUITARY intermediate lobe
LH/FSH: ARC/POA → GnRH Thyrotroph: TSH: controls thyroid
→ gonadotrope → FSH/LH -> day to day metabolism
Growth promoting actions can be Mammotroph: PRL: direct effect
Eminentia mediana: releasing and THs act synergistically with GH
direct or via stimulation of IGF1 on target tissue. Most of these
release-inhibiting hormones → on several aspects of growth
(adults) and -2 (fetus) → stimulate hormones also affect the brain
control the function of
muscle and other somatic tissues (e.g parental care in male fish =
adenohypophysis Somatotroph: GH Cell types and
change in behavior)
Effects of androgens/estrogens hormones
Part of the forebrain, one Hormones on growth are only partly Direct effects of GH on adipose Gonadotroph (glycoprotein hormones:
function is to mediate
dependent on interactions w GH tissue: lipolysis, gluconeogenesis big dimeric proteins that have highly
the nervous system
control and hormone Pars nervosa: Oxytocin + = release E sources glycosylated surfaces, same α but
systems arginine and lysine vasopressin Corticotroph: different β
• ACTH: control release of stress hormone: • FSH: control release of steroids from
PVN: paraventricular
stimulates the adrenal gland to secrete gonads
Mammalian hypothalamus SCN: suprachiasmatic
POA: pre-optic glucocorticoids • LH: stimulate hormone production in
nucleus: information
• LPH: control lipid metabolism; Precursor gonads
about time of day Areas
Local point of tropic endorphins: opiate-like effects on CNS and
(growth) hormone axes PNS: inhibit release of Substance P from Melanotroph: α-MSH: control metabolism.
ARC: arcurate nucleus; has a more Stimulates melanocytes to produce melanin
→ pws that control spinal ganglion neurons → ↓pain
permeable BBB → neurons can be
growth and metabolism perception
regulated by hormones
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