Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
103 Cards in this Set
- Front
- Back
|
Aldosterone |
Mineralocorticoid from ad. cortex Sodium retention in kidney by acting on the t tubules |
|
|
Cortisol |
Glucocorticoid from ad. cortex Increases carb met, antistress hormone |
|
|
Corticosterone |
Glucocorticoid from ad. cortex Increases carb met, antistress hormone |
|
|
Estradiol |
Hormone from follicles of ovaries Uterine and other female tissue development |
|
|
Progesterone |
Hormone from corpora lutea and placenta Uterine dev., mamm gland dev, maintenance of pregnancy |
|
|
Dihydrotestosterone |
Horm from seminiferous tubules and prostate Male secondary sex characters |
|
|
Testosterone |
Horm from leydig cells Spermatogenesis; male secondary sex characters |
|
|
Glucagon |
Ptn horm from alpha cells of pancreas Glycogenolysis in liver |
|
|
Insulin |
Ptn horm from beta cells of pancreas Glucose uptake from blood; glycogen storage in liver |
|
|
Somatostatin |
Ptn horm from pancreas Inhibits insulin and glucagon secretion |
|
|
Adrenocorticotropic hormone |
Ptn horm from ant. pit Stimulates synthesis and release of glucocorticoids |
|
|
Vasopressin/Antidiuretic horm |
Ptn horm from post pit Increases water reabsorption in kidney |
|
|
Follicle stimulating hormone |
Ptn horm from ant pit Stim dev of ovarian follicles and secretion of estrogens; stimulates spermatogenesis |
|
|
Growth hormone |
Ptn horm from ant pit mediates somatic cell growth |
|
|
Luteinizing hormone |
Ptn horm from ant pit Stim leydig cell dev and testosterone prod in males; stim corpora lutea dev and prod of progesterone in females |
|
|
Melanocyte stimulating hormone |
Ptn horm from ant pit Affects memory; skin color in frogs |
|
|
Oxytocin |
Ptn horm from post pit Stim milk letdown and uterine contractions during birth and orgasms |
|
|
Prolactin |
Ptn horm from ant pit Actions relating to reproduction and water balance Milk prod in mammary glands |
|
|
Thyroid stimulating hormone |
Ptn horm from ant pit Stim thyroid horm secretion |
|
|
Chorionic gonadotropin |
Ptn horm from placenta LH like functions; maintains progesterone prod during pregnancy |
|
|
Mullerian inhibitory horm |
Ptn horm from fetal sertoli cells of testes Mediates regression of Mullerian duct system |
|
|
Inhibin |
Ptm horm form seminiferous tubules and ovaries Inhibits FSH secretion |
|
|
Activin |
Ptn horm from sertoli cells Stimulates FSH secretion |
|
|
Calcitonin |
Ptn horm from C cells of thyroid Lowers serum calcium levels |
|
|
Parathyroid hormone |
Ptn horm from parathyroid gland Stim bone resorption; increases serum calcium |
|
|
Thyroxine/T4 |
Ptn horm from follicles of thyroid Increases oxidation rates in tissues |
|
|
Triiodothyronine/T3 |
Ptn horm form follicles of thyroid Increases oxidation rates in tissues |
|
|
Epinephrine |
Monoamine horm from ad. med Glycogenolysis in liver; increases bp |
|
|
Norepinephrine |
Monoamine horm from ad. med Increases bp |
|
|
Dopamine |
Monoamine horm from hypothalamus Inhibits prolactin release Motor control, motivation, arousal, reinforcement, reward, lactation, sexual gratification |
|
|
Serotonin |
Monoamine horm from CNS and pineal gland Stim release of GH, TSH, ACTH and inhibits LH release |
|
|
Melatonin |
Monoamine horm from pineal gland Affects rep functions |
|
|
Adrenal gland |
Adjacent to kidney. Endocrine cells in outer cortex respond to ACTH by secreting steroid hor to maintain homeo during stress. Neurosecretory cells in central medulla secrete catecholamines in response to short term stress. |
|
|
Androgen |
steroid horm that stimulates dev and maintenance of male rep system and secondary sex char |
|
|
Angiotensin II |
Peptide hor stimulates constriction of precapillary arterioles and increases reabsorption of NaCl and water by proximal tubules of kidney, which increases bp and blood volume |
|
|
anterior pituitary |
Adenohypophysis; portion of pit that dev from nonneural tissue and consists of endocrine cells that synthesize and secrete tropic and nontropic hor |
|
|
Hormone |
Chemical messengers typically produced in endocrine glands that signal a response in certain cells or organs. |
|
|
Endocrinology |
Study of endocrine glands and hormones |
|
|
Berthold's experiment |
Removed the testes of male chicks during development and they didn't develop the red comb or behave as adult males. Some chicks had a teste reimplanted in the abdominal cavity after removal and developed normally. He concluded that the testes release a chemical signal that has widespread effects. |
|
|
Niko Tinbergen's 4 questions |
1. Causation/Mechanism 2. Development/Ontogeny 3. Adaptive Function 4. Evolution/Phylogeny |
|
|
How are hormone/behavior relationships bidirectional? |
Hormones can cause changes in behavior, like T causing a rooster to crow, but behavior can also cause changes in hormone levels. |
|
|
What is the problem with pharmaceutical doses of hormones? |
If pharmaceutical doses of hormones are not physiological doses, then the hormones could bind to receptors that they would not normally bind to. Ex. High doses of T given, subjects were aggressive, concluded that it was due to T, but the T that wasn't bound to T receptors bound to progesterone receptors (similar shape). Progesterone caused the aggression. |
|
|
Ablation and replacement |
Remove the suspected source of the hormone, observe the effects, replace the hormone and see if the effects are reversed |
|
|
Bioassay |
Test the effects of a hormone |
|
|
What are some problems with measuring GCs as indicators of population health? |
- context of stressor can alter GC release (env conditions, food availability, etc) -2 GC receptors with diff functions -must be sure negative feedback is working properly- if not, might get lower max but more overall GC release- measure over longer time -Can't control for or know neonatal experiences, which can affect GC response |
|
|
What happens to GC receptors in response to chronic stress? |
Receptor production decreases in an attempt to compensate for long-term elevation of GCs, therefore, the GCs have a diminished effect |
|
|
Type 1 GC receptors |
High affinity for GCs but are usually saturated at peak circadian concentrations bc GCs vary with circadian cycle. Thought to act primarily in the brain to regulate circadian variation of GCs |
|
|
Type II GC receptors |
Only bound when GCs are high, i.e. after a stressor, and are believed to regulate the classic functions of GCs. These are found throughout the brain and body |
|
|
Functions of GCs |
- direct stimulatory role in coping with a stressor -permissive effects of GCs during SR on systems that are not part of acute SR themselves -GCs turn off aspects of SR when stressor is dealt with -promote recovery from stressor -prime the animal to successfully respond to stressors in the future |
|
|
Integrated response |
total amount of GC released, not just the maximum amount. This takes into account the max amount and duration of stressor. Effects of GCs result from hor-rec interactions over the entire course of SR |
|
|
Negative feedback of GCs |
High concentrations interact with receptors in the brain to turn off the initial steps of the HPA axis (stop hypo from releasing CRH) Levels rise and initially fall even if stressor continues |
|
|
How can early exposure to stressors induce life-long changes in HPA axis? |
When moderate stressors are applied to neonates, the adults have lower GC responses to moderate stressors but same basal GC levels. Occurs bc of an increase in efficacy of negative feedback loop Stronger stressors applied to neonates results in life-long hypersecretion of GCs |
|
|
Stress hyporesponsive (refractory) period |
Period in first few weeks of many mammals where they shut down their ability to respond to moderate stressors. |
|
|
GC acclimation |
Animal no longer responds in same manner to repeated or chronic stressors; results in lower GC responses |
|
|
GC facilitation |
When the acclimation process alters HPA axis physiology such that GC responses to novel stressors are enhanced. |
|
|
What are possible explanations for elevated GCs in population A compared to population B? |
-there are differences in pop health -could reflect natural variation -both are chronically stressed but B has acclimated and A has not -A has acclimated but shows facilitation but B hasn't -B is chronically stressed and can't mount an appropriate response, but A can -A had acute stressor, but B hasn't -B were mod stressed neonates, A not -There are genetic diff in SR |
|
|
Why might different species have different baseline GC levels? |
-Diff # of receptors in target tissue -Diff affinities of those receptors for GCs -Diff capacities and/or affinities of GC binding proteins |
|
|
GC binding protein (CBG) |
Large blood-borne protein that binds GCs and bring them to GC receptors Can act as a buffer to protect target tissues from high GC levels bc only unbound GCs are thought to be active |
|
|
Radioimmunoassay (RIA) |
Competitive binding of antibody and antigen Antibody specific for the hormone placed into reaction tube with labeled hormone. Unlabeled hormone added (sample) and competes for binding with antibody. Measure % of bound labeled hor as proxy for % bound unlabeled hormone |
|
|
Antigen |
Hormone in an assay |
|
|
Enzymoimmunoassay (EIA) and Enzyme-linked Immunosorbent Assay (ELISA) |
Similar to RIA in that there is competitive binding of labeled and nonlabeled (sample) hormone for antibody. Don't use radioactive label, usually chromogenic compounds- color change |
|
|
Chemical Communication |
1. Intracrine 2. Autocrine 3. Paracrine 4. Endocrine 5. Exocrine |
|
|
Intracrine |
Hormones act on receptors inside cell -Cytokines and steroid hormones |
|
|
Autocrine |
Hormone and receptor are on the same cell -Steroids with membrane bound receptors |
|
|
Paracrine |
Hormone produces response in adjacent cell. Hormone not contained- move through space btwn cells Neurotransmitters moving through a synaptic cleft |
|
|
Endocrine |
Hormone travels to target tissue through blood vessels -many hormones |
|
|
Exocrine |
Hormone is released into the environment -Pheremones |
|
|
Describe the typical endocrine system and how it works |
-Stim binds to receptor on horm prod cell -Causes prod of 2nd messenger -Hormone secreted by exocytosis -Diffuses into then out of blood vessel -Binds to receptor on target tissue -2nd messenger prod, cellular effects and biological response |
|
|
Workings of paracrine system |
-Hormone secreted by exocytosis from a nerve ending -Binds to receptor on target cell membrane |
|
|
Exocrine system mechanics |
-Exocrine cells produce exocrine substance -Substance released and collects in ducts -Ducts release substance out of organism and into the environment |
|
|
4 Classifications of hormones |
1. Protein/peptide hormones 2. Steroid hormones 3. Monoamines 4. Lipid-based hormones |
|
|
Protein/peptide hormone |
Composed of chains of AAs Gut, pancreas, liver, hypo, and pit Hypo releasing hormones and and anterior pit horm Most are water soluble so are stored in vesicles and released via exocytosis |
|
|
Steroid hormones |
Derived from cholesterol From adrenal glands and gonads Water insoluble so are not stored in vesicles and require a carrier protein to travel through blood |
|
|
Monoamines |
Derived from single AA From adrenal gland, CNS, pineal gland catecholamines and indol amines |
|
|
Lipid-based hormones |
Prostaglandins From lung, kidney, and various cells |
|
|
How are peptide hormones synthesized? |
-DNA is transcribed into mRNA -mRNA is translated into a pre-pro-hormone -pre is cleaved off via proteolysis to form a pro-hormone -Second cleavage/modification forms the hormone |
|
|
Pre section of hormone |
Facilitates insertion into membrane of ER Hormone then enters ER for further modification |
|
|
Pre-pro section of hormone |
Modified in ER to make the hormone functional It then enters the golgi and vesicle |
|
|
Steroid synthesis |
All start as cholesterol Then form into pregnenolone Then into progesterone Then into a few other transitionary steps before becoming aldosterone or cortisol |
|
|
StAR protein |
Steroid acute regulatory (StAR) ptn Moves hydrophobic cholesterol across outer mito membrane and inner membrane space |
|
|
P-450scc |
Located on the inner mitochondrial membrane Takes cholesterol from inner mito space into inner mito membrane Metabolizes cholesterol into pregnenolone Pregnenolone transferred into the mito matrix |
|
|
What happens to pregnenolone after it gets to the mito matrix? |
It is transferred into the endoplasmic reticulum where it is processed into deoxycortisol Deoxycortisol goes back into the mito matrix and is converted to cortisol, which then leaves through the cell membrane |
|
|
Adenohypophysis |
Anterior pituitary Originates from oral/buccal ectoderm and Rathke's pouch Includes pars distalis, pars intermedia, and pars tuberalis |
|
|
Neurohypophysis |
Posterior pituitary Originates from neuroectoderm Includes pars nervosa, infundibulum, and median eminance |
|
|
CRH |
Stimulate ACTH release from ant pit |
|
|
GnRH |
stimulate FSH and LH release from ant pit |
|
|
Somatostatin |
Inhibit GH release from ant pit Inhibit TSH release from ant pit |
|
|
GHRH |
Stimulate GH release from ant pit |
|
|
PIH |
Inhibit PRL release from ant pit |
|
|
PRH |
Stimulates PRL release from ant pit |
|
|
TRH |
Stimulates TSH release from ant pit |
|
|
Where are receptors located for different hormones? |
Steroid hormones- cytosol/ nucleus Other hormones- cell membrane |
|
|
What are the two options for membrane bound receptors? |
They are internalized and transduction occurs- receptor doesn't span membrane Signal transduction occurs while complex remains in membrane- receptor spans membrane |
|
Explain this |
1. Hormone binds to receptor 2. Gprotein binds to receptor 3. GTP binds to alpha subunit of Gptn and GDP is released 4. Alpha subunit separates and binds to adenylate cyclase with GTP 5. Adenylate cyclase converts ATP-cAMP+Pi |
|
|
cAMP |
Second messenger that activates protein kinases which activate other enzymes using ATP. Eventually inactivated by phosphodiesterases |
|
|
How are protein kinases activated? |
Unactivated, the active catalytic subunits are bound to inactive regulatory subunits. cAMP stimulates the subunits to dissociate and it bind to the regulatory subunit to prevent it from inactivating the catalytic subunits. The catalytic subunits are free to bind and have effects. |
|
|
How do steroid hormones work? |
Receptors are inside the nucleus or cytosol of cell Steroid is lipid soluble and is carried through plasma by carrier ptn then diffuses into cell Steroid binds to receptor to form a transcription factor, which binds to a hormone response element on DNA Transcription of mRNA occurs |
|
|
Steroid hormone with receptor in cytosol |
Receptor bound to HSP so it is inactivated Hormone binds to receptor, HSP dissociates, so it is active Diffuses into nucleus where it acts as a transcription factor to produce ptns |
|
|
Zinc fingers |
Projection on receptor proteins that bind to DNA and begin transcription |
|
|
Hormone response element (HRE) |
Section of DNA that a steroid receptor transcription factor complex recognizes and binds there with zinc fingers Transcription ensues |
|
|
Two categories for hormone cascade feedback |
1. Ultimate hormone feeds back on CNS and hypo Ex. testosterone 2. Function achieved by hormone feeds back on endocrine gland Ex. Blood glucose feeds back on pancreas |
|
|
ADH |
Promotes absorption of water in tubules of kidney resulting in little, concentrated urine |
|
|
Why does alcohol increase urine production? |
Alcohol prevents pituitary secretion of ADH, which reabsorbs water in kidney. Therefore, water is not reabsorbed and leaves the body as urine |
