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149 Cards in this Set
- Front
- Back
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source of releasing hormones?
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hypothalamus
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releasing hormones from the anterior pituitary that have a positive influence on tropic hormones
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CRH, GnRH, and TRH
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From the hypothalamus, directly innervate the posterior pituitary
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SON and PVN
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from the hypothalamus, directly innervates the anterior pituitary
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portal vein/system
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Gonadotropin Inhibitory Hormone (GnIH) functions
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a novel regulatory hormone
inhibits gonadotropin (LH,FSH) release from pituitary Possibly inhibits release/synthesis of GnRH from hypothalamus When infused into the brain-dec plasma LH and alters sexual behavior (solicitations of males by females) |
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nonapeptide hormone synthesis
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synthesized as part of a larger precursor w/ neurophysin. the peptide bond is cleaved in secretory vescicles and both the nonapeptide and neurophysin are released from the axon terminal.
preprohormone-> prohormone-> target cell (ex: oxytocin & vasopressin) |
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ancestral peptide of vasopressin and oxytocin in mammals for fish and amphibians, reptiles, birds.
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fish: isotocin for oxytocin, vasotocin for vasopressin
Amphibians, reptiles, birds: Mesotocin for oxytocin, vasotocin for vasopressin |
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Actions of neurohypophysial nonapeptides
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main effects are on reproduction and osmoregulation
-reproduction: OT stimulates milk letdown, uterine contractions in parturition. -osmoregulation: AVP (formerly called ADH) |
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What is the Fetal Injection Reflex
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a (+) feedback loop. fetal movement stimulates the cervix, which stimulates oxytocin release. OT stimulates contractions on the myometrium-pushes fetus down farther. the further downward movement of the fetus stimulates more OT release, then more contractions, etc....once given birth the + feedback stops.
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what is the drug given to induce uterine contractions when OT is low?
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pitocin
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the difference between vasopressin and vasotocin
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one amino acid difference
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Primary target of AVP?
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kidneys
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Actions of neurohypophysial nonapeptides
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main effects are on reproduction and osmoregulation
-reproduction: OT stimulates milk letdown, uterine contractions in parturition. -osmoregulation: AVP (formerly called ADH) |
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oxytocin's role in labor
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labor- contraction of uterine smooth muscle (myometrium) during parturition (labor)
-during month 9 there is an inc. (up-regulation in the myometrium and endometrium) of OT receptors (associated w/ inc "irritability" of the uterus.) -estradiol has an influence in inc. OT & OTR thru a composite HRE |
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What is the Fetal Injection Reflex
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a (+) feedback loop. fetal movement stimulates the cervix, which stimulates oxytocin release. OT stimulates contractions on the myometrium-pushes fetus down farther. the further downward movement of the fetus stimulates more OT release, then more contractions, etc....once given birth the + feedback stops.
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what is the drug given to induce uterine contractions when OT is low?
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pitocin
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oxytocin's role in milk letdown
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mammy alveoli are surronded by smooth muscle (myoepithelial) cells that are a target cell for OT. OT stimulates contraction on these cells
suckling stimulate the SON, via touch receptors in the nipples that connect with the brain through a spinal reflex arc, to release/synthesize OT |
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Oxytocin's role in behavioral effects
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mediates behaviors associated with affiliation- establishment of maternal and pair-bonding behaviors (estradiol is necessary for a response to OT's effects in pair-bonding)
associated with social memory |
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the difference between vasopressin and vasotocin
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one amino acid difference
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Primary target of AVP?
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kidneys
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Functions of AVP, and what stimulates its release?
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regulates osmotic balance through: V1a receptors (vasoconstriction) & V2 receptors (water retention)
Stimuli: inc. osmolarity (salt concentration, 1% inc) dec. blood volume (at least 8%) |
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what is euvolemia?
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state of normal body fluid volume (homeostasis)
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what is the result of the activation of the SON by changes in blood pressure?
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action potentials in the SON stimulate the release of AVP
-carotid sinus pressure high--> causes shut down of action potentials in the SON-->results in BP to drop. |
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what are the actions of VP in the kidneys?
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-acts on cells lining the collecting ducts and the descending loop of henle to regulate the resorption of water (facilitates resorption by inc the density of aquaporin 2 (AQP2) channels
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what hormone is similar to the effects of OT in mammalian births but in reptiles and birds?
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AVP
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Species differences in social behavior are underlined by changes in what?
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AVP receptor (V1) distribution in the brain
V1a still VP but binding to a different receptor. |
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describe the VP receptor genes structure and differences
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individual males vary in V1a receptor distributions
the length of the repetitive microsatellite in the promoter of the V1a gene is correlated to the distribution of V1a receptors and social behavior. |
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what is the same thing as a repetitive expansion?
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the microsatellite region
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what mediates differences in social behavior?
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-occurance of microsatellite regions
-brain distribution of V1a receptors -but Via receptor expression cannot explain ALL behavioral variations. |
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what effects on human behavior does differences in V1a receptor expression have?
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-men with a specific genetic variant (microsatellite region) had low scores on the "partner bonding scale"
their wives were also less satisfied ("divorce gene") also are associated between VPR1A repeat polymorphisms and autism. |
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what results in changes in brain expression of V1aR?
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changes in length of microsatellite sequence in promoter region of V1a receptor gene
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what is the mechanism of action of ACTH on cortisol-secreting cells in the adrenal cortex?
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ACTH-> operates thru GPCR with ATP and A.cyclase to produce cAMP-> phosphorylates PKA->CEH (cholesteryl ester hydrolase)
LDL-> acted on by CEH-> cleaves lipid protein- cholesterol-> StAR transports cholesterol into mitochondria for steroidogenisis-> acted on by desmolase-> to produce pregnenalone-> to produce cortisol. |
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what carries cortisol to cells?
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CBGC- cortisol binding protein
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mechanism of cortisol action in target cells
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cortisol normally binds to a nuclear receptor which dimerizes with another bound receptor and the 2 together bind the transcription factor GRE (glucocorticoid response element)
when cortisol in inactive, the HSP and BP come off and cortisol binds and forms a homodimer. cortisol can also interact with a variety of other transcription factors (ex: to mediate immune responses- inflammation, could turn off cytokine production) |
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Physiological effects of cortisol
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alter carbohydrate, lipid, and protein metabolism
anti-inflammitory and immunosuppressive actions nervous system effects |
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What are anabolic and catabolic metabolism?
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anabolic- in liver tissue by stimulating gluconeogenesis (adding/producing molecules ex: glucose in liver)
catabolic- in skeletal muscle and adipose tissues by inhibiting glucose uptake (subtracting/ breaking down molecules in all other tissues. breakdown releases energy for anabolic to occur) |
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what is cortisone?
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a naturally produced hormone in the body that is fast acting and short lived. cortisone injections and cream for the treatment of inflammation, does NOT help pain, by causing a decrease in histamine.
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what is the affect of cortisol on the arachidonic acid pathway?
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cortisol inhibits enzymatic activity of phospholipase A2, which stops the cellular cascade at the beginning, acting as a powerful anti-inflammatory
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what are the different parts of the adrenal glands and the hormones they produce?
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cortex(80-90%):
glomerulosa- aldosterone fasciculata- cortisol reticularis- androgens medulla(10-20%): catecholamines |
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stimuli and function of aldosterone
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aldosterone acts with vasopressin. it is secreted by the glomerulosa and acts on the kidney. kidney has baroreceptors that sense osmolarity/pressure and extracellular volume (volume low->renin excreted by the kidney mediates Na taken back in and K and H excreted)
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secretion mechanism of aldosterone
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renin is secreted by the kidney. it is the rate limiting step. renin-> stimulates an enzyme-> that acts on angiotensin I-> which is converted to angiotensin II-> stimulates adrenal secretion of aldosterone from the adrenal gland.
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true or false: you can survive without androgens from the adrenal gland.
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true
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Production of androgens from the adrenal
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production of androgen steroids by the adrenal gland is minimal compared to these hormones by the gonads.
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what is the primary androgen produced by the zona reticularis?
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DHEA (dihydroepiandosterone)
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what is the main secretion of the adrenal gland and the main tissues is acts on?
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corticol
liver, adipose (fat), and muscle |
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what major blood vessels innervate the adrenal gland?
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aorta from the left ventricle and the inferior vena cava going up to the right atrium.
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what hormone does the zona glomerulosa produce
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aldosterone
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what hormone does the zona fasciculata produce?
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cortisol, corticosterone
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what hormone does the zona reticularis produce?
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androgens (DHEA)
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what hormone does the adrenal medulla produce?
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catecholamines (epinipherine, norepinepherine, and dopamine in very small amounts)
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what is the pathway to the production of adrenal hormones stimulated by a stressor?
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stress (emotional, physical, chemical) on the central nervous system-->hypothalamus--> secretes CRF--> act on the anterior pituitary--> secretes ACTH--< acts on the adrenal cortex--> produces androgen, aldosterone, or cortisol.
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how is ACTH synthesized from POMC?
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genome-> mRNA-> POMC synthesized in both (1)corticotropes (pars distalis)->ACTH-> ACTH and (2) melanotropes (pars intermedia) in the anterior pituitary-->ACTH-->a-MSH or CLIP
(enzymatic activity causes dif hormones to be released from tissues using the same hormone-POMC) |
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in what pattern is ACTH released and when is it highest?
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pulsatile. highest 20-30 minutes after waking up
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cortisol is used by_______ and corticosterone is used by_______.
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cortisol- most mammals and fish
coticosterone- mice, rates, tetrapods (anphibians, reptiles, birds). cortisol and corticosterone have the same effect. |
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what is the distribution of hormones in the adrenal gland due to?
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the differential distribution of steriodogenic enzymes.
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what enhances gluconeogenesis?
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anabolic metabolism
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what inhibits glucose uptake (lipogenesis) and protein synthesis?
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catabolic metabolism
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What are some things stress can cause in an individual?
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infectious disease, heart disease, reproductive failure, and psychological distress.
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what is Psychogenic dwarfism?
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children who stop growing and never go through puberty due to extreme abuse-stress.
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true or false: cortisol elevation for a good and bad stressor are the same.
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true
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what is Sapolsky's definition on stress?
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anything that throws your body out of homeostatic balance.
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define stress response
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a suite of physiological and behavioral responses that help to reestablish homeostasis.
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what happens as the body recognizes a stress response?
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in seconds: the sympathetic NS secretes norepinephrine, and the adrenal medulla secretes epinephrine.
in minutes: the adrenal cortex begins to secrete glucocorticoids, and several other hormones including prolactin, glucagon, vasopressin, and TH are secreted from other endocrine organs. |
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true or false: stress response is generally "non-specific"
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true, many different types of stressors elicit a similar stress response.
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What happens in the HPA axis?
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the adrenal cortex produces glucocorticoids (cortisol, corticosterone)
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what is the purpose of a 'stress response'?
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the main purpose is that it is a survival mechanism
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what are adaptive effects of the stress response?
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-inc the immediate availability of energy
-inc oxygen intake -dec. blood flow to areas not necessary for movement. -inhibit digestion, growth, immune function, reproduction, pain perception. -enhance memory and sensory functions. |
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what is stage one of the general adaption syndrome?
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ALARM: when a threat or stressor is realized, the body's stress response is activated.
1. E is released (main response) (fight or flight response) 2. some activation of HPA axis and cortisol release. |
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what are the effects/ responses to acute stress?
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-shift from energy storage to use
-inc cardiovascular tone -inhibited digestion -inhibited growth -inhibited reproduction -compromised immune function and inflammatory response -enhanced cognition. |
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what are the effects/ responses to chronic stress?
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-fatigue, diabetes
-hypertension -peptic ulcers -psychosocial dwarfism -impotence; anovulation; loss of libido -impaired disease resistance; cancer -accelerated neural degradation during aging. |
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what is Cushing's Syndrome?
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mainly caused by prolonged exposure to high levels of cortisol
symptoms are upper body obesity, high blood pressure and high blood sugar, rounded face, severe fatigue, muscle weakness. etc.. |
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what are pituitary adenomes?
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(most common cause of cushings syndrome) benign tumores of the ant. pit. that result in overproduction of ACTH
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what are phamacological causes of cushings syndrome?
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people who take glucocorticoid hormone for asthma, rheumatoid arthritis, lupus or for immunosuppression after organ transplants.
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what is ectopic ACTH syndrome?
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having benign or malignant tumors outside the pituitary (occurs in the lungs in over 50% of cases)
can cause cushings syndrome |
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what are adrenal tumors?
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usually benign tumors in adrenal tissue with result to excess cortisol production.
can be a cause of cushings syndrome. |
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what effect does maternal attention and care have on the offsprings stress response?
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the more maternal care an offspring gets, the more reduced its stress response is. More care results in lower CRH in the hypothalamus
as care inc, CRH and mRNA dec (linear relationship) |
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what are two factors that vary behavior and the stress response between individuals?
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-some of this variation is inherited (genetic)
- some is shaped by the early rearing environment. *genetic variation not as important as actual behavior of rearing parent* (ex: a baby with genetic mother that gives little care, is switched to a non-genetic mother that gives more care- as a result the baby grow up to be a mother that gives more care.) |
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how does ecology shape stress physiology and behavior?
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social scenarios and rank (dominance) can act as stressors.
differences in the availability of a resource (habitat differences) drives changes in behavior. -can cause behavioral differences in aggression and affiliation -changes in stress reactivity |
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compare different mammal behaviors and the stress reactivity
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behavior: rare food competition, little male-male aggression, rare aggression by females
stress reactivity: lower female and male plasma cortisol levels, shorter and reduced adrenal response to stress, dominant males have lower cortisol levels than subordinate males. Behavior: frequent food competition, much male-male aggression, frequent female aggression stress reactivity: high female and male plasma cortisol levels, longer and more sustained adrenal response to stress, dominant males have higher cortisol levels than subordinate males. |
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which enzyme acts on norepinephrine to convert it to epinephrine?
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PNMT by methylation.
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how does cortisol affect PNMT enzyme synthesis?
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cortisol induces expression of this enzyme.
inc in cortisol-> induces inc expression in tyrosine hydroxylase and PNMT-> through GRE's paired w/ other PNMT receptors or transcription factors-> inc production of epinephrine. |
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where are catecholamines stored?
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in granules in chromaffin cells of the adrenal medulla.
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what are chromaffin cells?
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cells in the adrenal medulla that store catecholamines and are innervated by the splanchnic nerve.
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what is the splanchnic nerve?
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a visceral efferent nerve fiber from the sympathetic division of the ANS that innervates chromaffin cells.
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what increases the secretion of catecholamines from the medulla?
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inc by exercise and stressful stimuli by the release of aceytlcholine from preganglionic sympathetic neurons.
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what to carrier proteins do for catecholamines?
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inc their half life
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what transports (carrier protein) catecholamines?
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albumin- they bind with low affinity but high capacity
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why are catecholamines inactivated quickly?
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because they have a relatively low affinity for their receptors compared to other hormones
-90% of catecholamines dont react and are reuptaken by sympathetic nerve endings in the medulla |
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how are catecholamines excreted?
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once metabolized by MAO, conjugation with glucuronide or glucuronic acid in the liver-> this makes it more hydrophilic so it can be excreted from the body.
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explain how the cardiovascular system is affected by threat/ stressor
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direct innervation of the cardiovascular system by the sympathetic nervous system , and from a rise in plasma catecholamines which then act on the cardiovascular system.
catecholamines cause: inc. heart rate, vasodilation of arterioles in muscle, general vasoconstriction, mobilization of liver glycogen and free fatty acids (the combined effect is to inc BP- hypertensive) |
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what are catecholamines effect on carbohydrate metabolism?
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catecholamines glycogenolytic in the liver-they inc blood glucose
they are also glycogenolytic in muscles- this inc. blood lactic acid (as the glycogen is used to produce energy in the muscle cells) |
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how are catecholamines thermogenic?
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both E and NE rapidly inc cellular metabolism (heat production) and oxygen consumption (calorigenic)
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how do catecholamines effect hibernation?
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they act on brown adipose tissues to activate thermogenesis, contributing to an arousal from hibernation.
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what hormone is related to irritability?
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norepinephrine
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what are the two main receptors in the sympathoadrenal system?
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cholinergic receptors (1st in the stress response)
adrenergic receptors (2nd in the stress response) |
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what is the structure on B-adrenergic receptors?
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they have a 7-transmembrane domain, with a N-terminus that binds to a ligand, and a C-terminus that changes conformation.
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what are the functions of the a-andrenergic receptors?
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(a1-stimulatory, a2-inhibitory)
vasoconstriction, iris dilation, intestinal relaxation, intestinal sphincter contraction, pilomotor contraction, bladder sphincter contraction. |
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what are the functions of the B-andrenergic receptors?
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cardioacceleration(B1)
inc. myocardial strength(B1) lipolysis(B1) bladder wall relaxation(B1) vasodilation(B2) intestinal relaxation(B2) uterus relaxation(B2) bronchodilation(B2) calorigenesis(B2) glycogenolysis(B2) |
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what enzyme deactivates cAMP?
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phosphodiesterase (-)
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what is the mechanism of B-andrenergic receptor signaling?
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they act through adenylyl cyclase to inc. intracellular cAMP- which can alter cellular function (enzyme activity, membrane permeability). and/or alter transcription factors (CREB). cAMP can be inactivated by phosphodiesterase or go on the active (phosphorylate) PKA->which can go on to phosphorylate other enzyme or bind to CREB and have its 2 half sites phosphorylates by PKA-> which goes on to inc transcription protein.
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what is CREB?
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(cAMP response element binding protein)
a transcription factor that has two half-sites that are palindromes. |
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what is each signal transduction mechanism of the 4 andrenergic receptor isoforms?
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a1- acts through phospholipase C pathway to inc IP3
a2- acts to dec cAMP production B1- inc cAMP B2- inc cAMP |
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how can andrenergic receptors seem to have dual functions for epinephrine?
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E can has opposing biological effects because a2 dec cAMP while all other inc cAMP (E might bind to a2 instead of a1)
the "opposing effects" depend on which receptor isoform it binds to. normally, E stimulates a and B receptors simultaneously, but the actions of the hormone on a receptors dominate over B. but in the presence on a-receptor blockage, the response of the 'silent' B-receptor is revealed. |
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what are bioactive peptides?
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peptides that may be produced by the adrenal medulla that influence the function of the adrenal cortex and medulla:
-vasopressin( to regulate catecholamine secretion) -VIP( can inc aldosterone production) -POMC -Opiods(endorphins, proenkephalin) |
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how does the adrenal medulla have a function in steroid conversion?
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transforms some steroid hormone precursors into active steroid hormones.
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what is a colloid droplet?
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a structure in the thyroid gland that is formed at the apex (apical membrane) of a follicular cell, that contains Tg- in Tg is where the synthesis of TH occurs.
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how is I- transported from the blood stream into a follicular cell?
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it is actively transported using ATP by a Na+/I- symporter
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what are DIT and MIT synthesized from, how, and what do they form?
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in Tg, they are synthesized from tyrosine by adding the oxidized I+ to form T3 & T4.
T3 consists of MIT + DIT ( little T3 made compared to T4) T4 consists of DIT + DIT |
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how are T3 and T4 release in the blood stream once they have been synthesized in Tg?
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once synthesized, Tg with bound T4/T3 is endocytoced into the follicular cell -stimulated by TSH binding to its GPCR on the basal membrane-> which stimulates the cAMP pathway-> which causes the endocytosis (endocytosed Tg into follicular cell forms colloid droplet)-> then lysed by lysosomes to release T3 and T4 into the blood stream
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how is Tg "labeled" and why?
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as Tg is being translated, carbohydrates- galactose, mannose, and glycoproteins are being added to the structure (post-translational modification) which "labels" the Tg so that lysosomes can recognize it for degradation.
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where is most of the I- stored in the body?
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the colloid space
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what is the cause of hypothyroidism?
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low I- in the body
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what are all the areas in the body where I- can be stored?
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ECF (extra cellular fluid)
tissues (muscle, liver) a hormone pool (T3 + T4) and in the thyroid gi tract |
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what area in the world seems to have the lowest supply of iodine in the environment?
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most of china and areas near it boarder and south eastern australia.
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what is a way we tried to solve iodine deficiency?
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by making iodized salt.
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where in the body is T4 de-iodinated to yield either T3 or rT3?
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in the actual target tissue
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what is pendrin?
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an I- channel in the lumen at the apex.
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what is the coupling scheme for iodothyronine formation?
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thyroid peroxidase (TPO) converts inorganic iodine to active iodine--> iodination of trosine bound to Tg to make DIT or MIT--> then tyrosine is cleaved to form a free randical--> the free radical allows DIT or MIT bind (coupling)--> to form T3 or T4.
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how is 99.96% of TH circulating in the body?
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bound to a transport protein
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what is the only biomolecule in the body that uses iodine?
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thyroid gland
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what are the TH binding proteins?
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albumin, TBG, TBPA
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what is deiodinase?
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enzyme responsible for TH conversion.
enzyme that converts T4-> T3 in the blood stream . (also T3->T2, T2 not really used in the body, mostly excreted) |
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explain type I deiodinase
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in the liver, kidney, thyroid gland.
substrate preference- inner or outer ring reations catalyzed: T4->T3, T4->rT3, rT3->T2, T3->T2. |
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explain type II deiodinase
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in the brain, pituitary, placenta, adipose tissue.
substrate preference is outer ring reaction catalyzed: T4->T3, rT3->T2 in the brain type II converts T4->T3 so T3 can exert negative feedback on the hypothalamus & pituitary. |
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explain type III deiodinase
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in the brain, skin, placenta
substrate preference is inner ring reaction catalyzed: T3->T2, T4->rT3 |
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what are the divisions of the pituitary gland?
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andenohypophysis: anterior lobe- pars distalis, pars tuberalis
intermediate lobe-pars intermedia neurohypophysis: posterior lobe- pars nervosa. infundibulum- a stalk comprised primarily of naural tissue through which the pituitary is anchored to the brain. |
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what is rathkes pouch?
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it left over from the top part of the mouth that forms the pituitary during development.
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what are two examples of secondary releasing hormones?
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(+) VIP
(+) CRH (+) neuropeptide y (NPY) (+) AVP (+) GHRH |
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give an example of how AVT/AVP expression differs between males and females
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AVP/AVT effects males, IT/MT/OT effects females
gender differences are also apparent in the number of peptide-synthesizing cells and the projections of these cells. |
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what is an example of a diseased state that can be caused by excess cortisol? what is the mechanism?
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cushing's syndrome: can be caused my a benign tumor of the anterior pituitary gland that results in overproduction of ACTH
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what are the categories of adenohypophysis hormones?
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1) simple proteins: GH & PRL
2) glycoproteins: gonadotropins ( LH & FSH), TSH 3) small peptides derived from POMC: ACTH, aMSH |
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what hormones come from the pars distalis?
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GH, PRL, LH, FSH, TSH, ACTH
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what hormones come from the pars tuberalis?
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LH, FSH, TSH
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what hormones come from the pars intermedia?
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aMSH
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explain growth hormone (GH) action and target
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acts on tissues to promote growth: stimulates protein synthesis, stimulates bone and cartilage synthesis.
acts through a mediator: ICF/somatomedin (GH- acts on liver-> which releases insulin like growth factor(+ influence on GH)) (GH somatotropin-> stimulates release of somatomedin (- influence on GH)) |
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explain thyroid-stimulating hormone (TSH) action and target.
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acts on the thyroid gland
-stimulates: the synthesis of TH, release of thyroid hormones, thyroid growth |
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explain luteinizing hormone (LH) action and target.
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acts on gonads
regulates female sex hormones, egg development (oogenesis) stimulates sertoli cells in testes to release local mediators that induce spermatogenesis |
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explain follicle-stimulating hormone (FSH) action and target
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acts on the gonads
regulates ovulation, female sex steroid hormones induces secretion of androgens by leydig cells in testes. |
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explain adrenocorticotropin hormone (ACTH) action and target
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derived from POMC
-stimulates the adrenal cortex to produce corticosteroids -response to stress: fight or flight response; nutrient mobilization -osmoregulation- sea water adaption in fish -development- amphibians metamorphosis; smoltification (transition in fish from salt water to fresh water.) |
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explain melanocyte-stimulation hormone (a-MSH) action and target
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derived from POMC
-in non-mammals affects dispersion of melanin in chromatophore cells in skin -when contracted near nucleus, animal is pale; wen dispersed, animal is dark -stimulates melanin synthesis |
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what does POMC produce in corticotropes and melanotropes?
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corticotropes- ACTH
melanotropes- a-MSH and CLIP |
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what is the median eminence?
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part of the hypothalamus from which regulatory hormones are released. it is integral to the hypophyseal portal system, which connects the hypothalamus with the anterior lobe of the pituitary gland.
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what stimulates oviduct muscle contractions during egg laying in reptiles and birds?
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vasopressin (AVP/VP)
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what connects the kidneys to the urinary bladder?
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ureter
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what is activator protein 1 (AP-1)?
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a transcription factor (heterodimer).It regulates gene expression in response to a variety of stimuli (cytokines, growth factors, stress, and bacterial and viral infections). it binds to a DNA sequence.
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what hormone is immunosuppressive?
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cortisol
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what are prostaglandins?
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mediator that acts on smooth muscle, is a fatty acid derivative. formed by the arachnodonic acid pathway.
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what is formed during post translational modification when a carbohydrate is attached to a protein (galactose, mannose)?
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glycoprotein
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what is RXR? (might not need to know)
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a thyroid hormone nuclear receptor. heterodimer.
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