Hypothalamus and Pitutary Flashcards
Pitutary function is regulated by —– produced in the —–
- neurohormones
- hypothalamus (neuronal system)
In hypothalamus there are many clusters of neurons known as (3):
+ such as + what they do
- Hypothalamic nuclei
- Such as Supraoptic, paraventricular, preoptic nuclei
- They are clusters of neurosecretory neurons that produce hormones that control pitutary function
The anterior pitutary, posterior pituitary, intermediate lobe derivation (3):
- AP: Embryologically derived from dorsal outgrowth of the buccal cavity (roof of the mouth) cells come from non-neurological origin from epithelia cell
- PP: Embryologically derived from the brain (outgrowth from the brain)
- IL: Region in between anterior and posterior pituitary associated with adenohypophysis. Not present in some mammals, birds, hagfish and lamprey
Adenohypophysis contains (3):
- Pars tuberalis (tuberal lobe)
- Pars intermedia (intermediate lobe)
- Pars distalis (anterior lobe)
Neurohypophysis (2)
- Infundibulum (neural lobe)
- Pars Nervosa (neural lobe/posterior putuitary)
Neurophypophysis hormone synthesis (2):
- Secretory cells that produce hormones secreted from PP is synthesized in hypothalamus (supraoptic + paraventricular) and travel down axon (hypothalamic-posterior pituitary stalk)and terminate in neural lobe. The hormones remain in terminal nerve until stimulated then it is secreted in blood vessels in PP.
- There are no secretatory cells in the posterior lobe
Adenohypophysis hormone synthesis (4):
+detection
- All hormones are produced and secreted in anterior pitutary
- Neurohormones are produced by hypothalamus and terminates at median eminenance above the AP. It then enter protal system (hypothalamic-hypophyseal portal system)
- Release of hormone in the anterior pitutary and these hormone target tissue that are cells in anterior pituitary to release hormones.
- Neurohormones released by hypothalamus cannot be detected in bood but the anterior pituitary hormones released by target cells in anterior pituitary are released in blood.
Hormones of posterior pituitary (4):
+ details/structure
- Vassopressin (AVP, Arginine vassopressin; Arg at position 8)
- Oxytocin (OX)
- Each contains 9 amino acids ( 9 diff ones but 2 of cys) and is a nano-peptide
- 2 cys forms di-sulfide bonds making them cyclic and also the cyclic structure allows it to stabilize conformation of the hormones to activate receptors
Hormones of posterior pituitary
There are other structurally different neurohypophysial hormones found within mammalian and nonmammalian vertebrates:
Due to evolution. 8-9 variation of peptide in species
Synthesis of Vasopressin (ADH) and oxytocin (3):
what + signal + neurons
- They are synthesized within the cell bodies of the neurons located in the supraoptic and paraventricular nuclei (DNA synthesis occurs, precursor are cleaved to nanopeptide) of the hypothalamus and then transported to terminals in the posterior pituitary.
- When signals come, 2 things happen:
1. Stimulate of instant release of hormones to blood
2. Stimulate neuralsecretatory cells to start protein synthesis - The neurons either produce oxytocin or vasopression, neither are in the same neuron. Control of secretion are different: secretion of oxytocin has no effect on vasopressin.
Arginine vasopressin (AVP) is also known as:
Antidiuretic hormone (ADH)
Effects of AVP
AVP acts through 2 types of membrane receptors (2):
V1: The V1 receptor mediates vascular smooth muscle contraction such as blood vessels (increases blood pressure)
V2: The V2 receptors produces the renal action of AVP (AVP increases water reabsorption and you pee less when AVP increases)
AVP also acts to facilitate:
- Memory consolidation
- AVP treatment improves short- term memory in aged humans
AVP is a neuron endocrine and also acts as a:
neurocrine (neurotransmitter)
AVP secretion are affected by 2 factors:
- Blood pressure
Baroroeceptors controls production of the hormone by detection in blood pressure changes.
Decreased blood pressure -> activation of baroreceptors-> increase AVP secretion -> results in increase water updatke (V2); constriction of arterioles (V1)-> Increase blood pressure
- Water retenstion
The amount of salt (NA+ concentration in circulation) allows osmoreceptors to detect and control AVP.
Increased blood osmolality/ Na+ (eat lots of salt) -> activation of osmoreceptors in CNS-> increased AVP secrection -> increased water retention (V2)/Na+ secrection (V2) ->Increase in urine concentration/urine osmolality and decrease in urine volue
Relationship between plasma AVP, plasma osmolality and plasma AVP:
Increase plasma osmolality means more plasma AVP (more AVP released) and more plasma AVP means more urine osmolality because all the water is being reabsorbed and the urine is highly concentrated.
Change in blood pressure and production of AVP has a —- relationship
- direct
When AVP goes down, there is a —- in blood pressure
decrease
The AVP response to plasma osmolality is very:
sensitive (1% change activates AVP release)
Summary of the regulation of AVP release:
Simulation
Summary of the regulation of AVP release:
Inhibition
- cold weather pee more
What does oxytocin do in terms of milk? (2)
What + how
- It stimulates milk ejection by contacting the myoepithelial cells in the mammary gland (smooth muscles)
- Suckling stimulates sensory nerves in the areolae and nipples of the breast (Sends signal to brain causeing afferent bervous pathway). This causes increase in firing of neurons and stimulates part of the brain that sends signal to secretory cells in hypothalamus (supraoptic + para) which produce oxytocin directly and start secreting
milk secretion not production
Effect of oxytocin is most …
- prominent after parturition because hormones involved in pregnancy and parturition increase in receptor density in nipples
What does oxytocin do in terms of parturition? (2)
+ cycle
- ## Oxytocin stimulates contraction of myometrium (smooth muscle) which facilitates labor. It does not initiate labour bur produces more and more so that it is important for birth
Hypothalamus, pituitary and target cell relationship diagram:
Anterior Lobe contains a variety of cell types which secrete hormones (5):
WHat are the 3 different familes of peptide hormones of Adenohypophysis:
- Family 1: Growth hormones (GH) and prolactin (PRL) Produced in Ant Pit
- Family 2: Glycoprotein Hormones Produced in Ant Pit
- Family 3: Hormones derived from Pro-opiomelanocortin (POMC) Produced in Ant Pit and Int lobe
Peptide hormones of Adenohypophysis
Family I (2)
Includes + structure
- Includes somatotropin or Growth Hormones (GH) and prolactin (PRL)
- Both GH and PRL consist of approximately 200 amino acids (single chain protein/linear) as they have same ancestor gene
Peptide hormones of Adenohypophysis
Family II (2)
The types + produced
Glycoproteins hormones that include:
1. Thyroid stimulating Hormone (TSH)
2. Gonadotropin Hormones
- Follicle-stimulating hormone (FSH) Produced in Ant Pit
- Luteinizing hormone (LH) Produced in Ant Pit
- Chorionic gonadotropin (Produced in placenta, the chrion; LH-like)
Peptide hormones of Adenohypophysis
Family II (4)
Structure
- Each is composed of two subunits; alpha and beta (noncovalently linked) and does not have strong association
- Seperated subunits have no biological activity (needs to be associated)
- The alpha subunit is the same for all glycoprotein hormones (TSH, LH, FSH)
- The B- subunit are different - confer special functional property
Chorionic gonadotropin (2)
produce + measure
- Present only in pregnancy as it is produced in placenta by chrion
- You measure this on pregnancy test
Peptide hormones of Adenohypophysis
Family 3 (5)
Includes + all have + where they are produced
- Hormones derived from Pro-opipmelanocortin (POMC) includes:
1. Adrenocorticotropin Hormone (ACTH) Produced in Anti Pit
2. Melanocyte-stimulating hormone (a-MSH, B- MSH) Target skin pigmentation Produced in Intermediate Lobe
3. B- endorphin endogenous opioid Produced in Intermediate Lobe
4. B-Lipotropic hormone (B-LPH) Important for lipid metabolism Produced in Intermediate Lobe
They all have the same precursor in different cells
Where is a-MSH produced?
Intermediate lobe
Some exceptions in Anterior Pituitary
How are hormones derived from Pro-opiomelanocortin (POMC) precursors?
- POMC gene is expressed in different cell types producing ACTH, MSH, B-endorphin and B-LPH Gene is in all the different cell type and can produce all these hormones
- POMC derived peptides are cleaved specifically by a family of prohormone convertase expressed diferentially in various cell types Cleave precursor in different places
GHRH (44aa) (2)
- Released on median emmince portal system in anterior pituitary. It acts on somatotropes to release/syntheize GH.
- Main stimulation of GH produced in hypothalamas
Somatostatin (~28 aa)
Peptide that prevents production of GH
IGF-I and GH
- GH produced act on a number of target tissue and in the liver which is the main site of IGF production
- IGF-1 that is synthesized in the liver and secreted into the blood is under the control of GH. It causes negative feedback at brain/pituitary to maintain constant GH level.
Physiological actions of GH (2)
GH/Growth rate and age
Too much GH before puberty can cause:
Gigantism
- produces disproportionately long arms and legs
Usually pituitary tumor that cause very tall abnormal arm and leg length
Too much GH produced after puberty can cause (3):
What/why + symptoms + treatment
Acromegaly deformatities
There is no linear growth. The epiphyseal plate is a thin layer of cartilage located at the ends of long bones. It’s responsible for producing new cartilage cells (chondrocytes), which later ossify (turn into bone), leading to linear growth during childhood and adolescence. As a person reaches late adolescence or early adulthood, hormonal changes (particularly the rise in estrogen) lead to the ossification of the epiphyseal cartilage. When the cartilage is fully replaced by bone, the growth plates “fuse,” and no further longitudinal bone growth is possible. During this process, the chondrocytes (cartilage-producing cells) stop dividing and are gradually replaced by bone tissue. This marks the end of linear growth.
- Enlargment of skull, facial bones, jaw, hands, feet, soft tissue and organs, diabetes, hypertension, muscle weakness, arthritis, gonadal dysfunction, cardiovascular disease.
- Treatment: Tumor removal (usually caused by Pit. tumor) or somatostatin analogs
Describe the graph of hypothyroidism and height:
Thyroid hormone production (2)
- Thyroid hormones are produced in thyroid follicules that are lined with secretatory cells. The inside is filled with a fluid called “colloid”
- There are also blood vessels that take away secreted thyroid hormones produced by the cell
Thyroid Stimulating hormone (TSH) (3)
structure + produced/what
- A glycoprotein consisting of two subunits, a and b
- a-subunit contains 89 amino acid, B-subunit contains 112 amino acids
- Produced in the anterior pituitary and controls thyroid hormone production
Factors effecting TSH release (2):
2: What
1: what + produced where +size + cannot be
**TRH (Glu-His-Pro-NH2): **
- Stimulator of TSH
- Produced in hypothalamus nuclei by supraoptic, paraventicular and goes to anterior pituitary to release TSH. TSH then go in blood and act on thyroid secreting cells (follicles) to release thyroid hormones
- Smallest peptide hormone (3 peptide)
- Cannot be measured in the blood, levels are low, function only to control levels of TSH in anterior pituitary.
** T3, T4:** Increased thyroid hormone levels inhibit (negative feedback) TSH
Thyroid hormones synthesis from scratch (11):
- Supraoptic, paraventicular stimulates release of TRH from hypothalamus to thyrotrope cells in anterior pituitary.
- Thyrotrope cells produce TSH which travels in bloodstream and binds to receptor in thyroid follicule cells.
- This activates a G-protein that activates anylcyclase to convert ATP to CAMP
- CAMP activates Protein kinase A which phosphorylates transcription factors allowing the transcription/translation of thyrogobulin
- Thyrogobulin has tyrosine attached as residues
- Iodide is present in bloodstream as I-. Active transport stimulated by TSH. TSH acts on membrane associated receptors: G-protein and increase CAMP and PK which phosphorylates transporter molecules increasing iodide transport I-. Coupled with Na+ to cross into thryoid follicules.
- Iodide oxidation.
Pentosephosphate pathway is mediated by perioxidase which produces hydrogen peroxide. H2O2 is the most potent oxidizing agent and causes oxidation of iodide I- molecule into iodine I2. Release into Lumen. - Inodination of tyrosyl residue:
I- Is a free radical so it can form reaction and attach to tyrosine residue to make monoiodothyronine or diiodothyronine in lumen. - Thyrogobulin colloid gets endocytosed intp follicular cell and lysosome fuses with the vesicles and cuts: two diiodothyronine detach from thyrogobulin and form oxidative coupling. They bind together and become 2 tyrosine residues (T4). A monoiodothyronine and diiodothyronine forms T3. We have isolated T3 and T4 from thyrogobulin colloid via lysosomal enzymes.
- T4 and T3 fuse with secretatory cell membrane and gets released to bloodstream via exocytosis. Lone iodotyrosines get deiodinased into iodide and recycled.
Function of thyroid hormones: Metamorphosis (3)
What + Ex
- Thyroid hormones stimulate metamorphosis in amphibian larvae
- Thyroidectomized tadpoles remain as tadpoles (Chemical that prevents thyroid hormones prevents metamorphosis)
- Treatment with the tyroid hormone reverses this effect (lose gill, develope lungs)
Thyroid hormones and teeth:
Growth and eruption of teeth are influenced and controlled by thyroid hormones. In hypothyroid children, the eruption of permanent teeth is greatly delayed.
Metabolic functions and thyroid hormones (2):
maintain + in birds and mammals
- Thyroid hormones maintain BMR (can be measured by O2 level)
- In birds and mammals (endothermic= maintain constant temp) thyroid increases O2 consumption and heat production (calorgenesis)
Metabolic effect for mammals in prolonged cold:
