Endocrinology Exam 1 (mine)

Negative Feedback loop

biological response where a cell responds to a signal and stops

Endocrine

hormones enteres the blood

Paracrine

one cell makes a hormones that affects other cell

autocrine

hormone that affects same cell

pherocrine

hormone enters atmosphere and affects there

lactocrine

hromone enter the milk and affects the infant

classic endocrine gland

hypothalamus, pituitary, pineal, thyroid, parathyroid, pancreas, adrenal, testis, ovary aka big daddies

non-classic endocrine gland

heart, intestine, gut, kidney, placenta, liver, adipose tissue, more

2 characteristics of hormone

act in low concentrations and have specific receptors (with high affinity and low concentration, and specific mechanism)

cell surface vs nuclear receptor

cell surface- hormone doesn’t actually go through the cell wall, moves the receptor and that changes the chemical reactions inside the cell

nuclear receptor = hormones that can pass through the cell surface bc they’re lipids and go directly bind to DNA

second messenger

hormone doesn’t actually go through the cell wall, moves the receptor and that changes the chemical reactions inside the cell

Hippocrates

father of medicine, 4 humors (phlem, blood, bile, water), and believed that humours could be used to restore imbalances. thought different testis selected gender

galen

big daddy of physiology, initiated concept of a vital spirit that was carried through blood, pituitary is a storage place for mucus

da vinci

was curious about anatomy in the renaissance

michaelangelo

artist interest in anatomy, thought goiter came from bad water

andreas vesalius

first person to describe follicles - sinuses filled with water fluid, identified sperm under microscope

William Harvey

discovered circulation of blood and valves in veins, sets up for a lot of endocrine ideas

Antonie Van Leeuwenhoek

Id sperm under microscope, big daddy of microbiology

Theophile de Bordeu

given credit for writting down the idea/ concept of endocrinology

Arnold Berthold

showed that castration caused the atrophy of the comb in roosters could be prevented by grafting testicular tissue into the birds abdomen (first true endo experiement)

Thomas Addison

linked anemia with a diseased adrenal, discovered addison’s disease (diseased adrenals)

Pierre Marie

looked into people with gigantism (they had tumors in the pituitary gland which caused giant production of GH)

Brown-Sequard

determined that the adrenals were essential for life, developed the brown-sequard method

Oliver and Schafer

extracting hormones from the adrenals, first to show pressor- effects of an adrenal extra

Bayliss and Starling

discovered secretin, distinguied the endo from a simple neural reflex, used the word “hormone”

Von Mering and Minkowski

1889 removed the pancrea from a dog and produced severe and fatal diabetes

Banting and Best

discovered insulin in 1922 (didn’t know what about the pancreas was special at first)

Roslyn Yalow

developped radioimmunoassay technique

Guillemin and Schally

discovered peptide hormone production of the brain

Hypothalamus

full of neurons, located at the base of the brain that regulates body’s homeostasis

Pituitary

2 parts: posterior and anterior lobe

Median Eminence

at the base of the hypothalamus that acts a barrier between the brain and endocrine system

Anterior lobe

AP

Posterior lobe

PP

3rd ventricle

fluid filled space inside hypothalamus

Hypothalamic nuclei

different regions of function in the hypothalamus (similar nuclei have similar functions)

Paraventricular nuclei

hypothalamic nuclei near median eminence

Supra-optic nucleus

hypothamic - above optic chiasma

arcuate nucleus

cluster of neurons in lower parts of hypothalamus, controls hunger, metabolism, hormone release

optic chiasma, mammillary body, anterior commissure

examples of different regions

embryonic origin of the pituitary

PP: brain grew down in embryo

AP: mouth grew up in AP

Rathke’s pouch

embryonic pocket of tissue that forms during the fourth week of development and gives rise to the anterior and intermediate lobes of the pituitary gland

adenohypophysis

part of AP that hormones → into blood

neurohypophysis

part if PP that stores and release hypo hormones

hypophysectomy

sella turcica

dent in bone that hold and protects pituitary

anatomy of a neuron

cell body, long-access + synthesis; all release happens at terminals

portal vessels of the pituitary

2 capillarry vessels that join together from different areas of body but not connected through heart

magnicellular neuron

responsible for oxytocin and vassopresin

parvicellular hypophysiotropic neuron

terminate in capillary bed in median eminence

hypothalamic projection neuron

influencer neuron

kisspeptin neuron

main control of human production, trigger puberty, control fertilty

in situ hybridization

measurement of mRNA (either a florescently labeled probe or radioactive probe)

immunohistochemistry

measurement of protein

hypothalamic releasing factors

peptide that causes hormones to release from AP

TRH

thyroid releasing hormone, stim release from TS hormone → control thyroid (which controls metabolism)

Acidophil vs. Basophil

two main types of hormone-secreting cells in the anterior pituitary gland, distinguished by their staining properties under a microscope

Oxytocin

Vassopresin

Growth hormone, Somatotroph

targets liver + adipose tissue → stim growth and meta of fats + fats

PRL, Lactotroph

targets mammillary gland → prod milk

TSH, Thyrotroph

thyroid gland→ secretin of thyroid hormones

GhRH, Gonadotroph

controls reproduction, development, and fertilty

ACTH, corticotroph

peptide from AP that stim cortisol

Oxytocin target organs and functions

mammillary (milk ket down), uterus (contraction), brain (behavior)

Mechanism that cause oxytocin release during milk letdown

neuroendocrine reflex arc = stim of teets / cleaning of teets

structure of the aveoli and mechanism through which oxytocin acts on the aveoli

spherical structure lined w/ mammillary epithelial structure, surrounded by myoepithelial cells

myoepithelial cells (muscle) contract when oxytocin gets there and squeezes alveoli

Myometrium

muscle laters of the uterus that contracts in response to oxytocin

Uterine contraction/ pitocin

makes contractions longer and stronger

where do oxytocin neurons terminate

posterior pituitary gland

where are oxytocin receptors found

specific parts of the brain (the dark areas)

species differences in oxytocin receptor locations

different species have different oxytocin receptor location (help to prevent interspecies mating)

intranasal oxytocin adminstration

small peptides can be delivered through the nose somewhat effectively

potential effects of oxytocin on “us vs. them” - sapolsky

oxytocin does all the wonderful thing but only if you think of them as an “us” but makes you crappier to “them”

preprooxytocin

precursor protein to breakdown oxytocin

pre

sing peptide

pro

prohormone sequence

neurophysin

carrier that transports oxytocin and vassopressin from hypo → pituitary

gene duplication

2 genes for the same hormone, DNA replicated

pseudogenes

when gene duplication results in non-functional protein

7-transmembrane g-protein couple receptor

come together to make an endocrine

orphan receptors

known receptors but unknown activating molecule/ligand

7-transmembrane g-protein coupled receptor

7 alpha helixes that insert themselves into the membrane of the inside of the cell

orphan receptors

when you know there’s a receptor there but have no idea what the ligand is

g-protein cycle (and component parts)

g-protein, g-alpha, … live in the cell and respond to movement in the membrane

GDP

binds to Gx, when hormones comes in, is exchanges for GTP causes separation of Gx and Gbx, allows for alpha subunit to interact with another unit (ex: PLC and enzyme). This enzyme can then metabolism other things (such as PIP2),

Phospholipase C

(PLC enzyme), job is to metabolize a phospholipid

PIP2

lipid in the membrane, metabolized by PLC = IP3 +DAG

IP3

area below lines that get to be free and float around the cell after PLC metabolize PIP2, travels around the cell, acts a second messenger

DAG

diacoglycerol = top half

IP3 sensative Ca+ channel

opens up ca channels allowing for calcium to flow into the sitosol (when normally there is a very low concentration of Ca+ inside the cytosol)

Smooth endoplasmic reticulum (SERCA pump)

very quickly pump calcium out of the cytosol (back into endoplasmic reticulum), why the “burst of the ca+” /up and down happens

calcium transient

calcium being released inside the cell in response to hormonal signal

Calmodulin - calcium binding protein

binds to burst in Ca+ and is responsible for activating myosin light chain kinsase

Myosin light chain kinase

leads to activation of muscle contraction

tocolytic drugs

molecules given to pregnant women having premature, Work by stopping different areas of oxytocin → muscle contraction

gene knock out mice

gene taken out used to see effect of (ex: taking out oxytocin)

Result of OT KO studies

knock out group successfully created mice with out oxytocin

1.        they gave birth normally (don’t need oxytocin to give birth), this because there is a bunch of hormone/ back up that lead to uterine contraction)

2.        don’t let down their milk (baby dies thus oxytocin is required for milk production)

3.        appear socially normal

evidence for a role of oxytocin in social recognition

if you put mice together, day after day the mice look less and less at each, but KO mice don’t really look at each other

brattleboro rat

naturally occurring mutation in the vassopresin gene (that occurs in the neurophysin area of the gene), caused the rat to pee a lot