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homeostasis
process that keeps the body variables in a fixed range/set point
negative feedback
actions that lower inconsistencies in the set point
allostasis
body anticipates needs and avoids mistakes
basal metabolism
energy used to maintain body temperature at rest
brown adipose cells
metabolizes and produces heat by burning fuel like muscles and releasing it like muscle contractions
ectothermic
dependent on external heating sources
endothermic
mechanisms used to keep core at a constant temperature
evaporation
used to cool the body in a hot environment
generating heat
mechanisms that increase body heat in a cold environment
shivering
used to maintain body temperature
reproductive cell environment
cool
hypothalamus physiological effect
causes shivering, sweating, blood flow change
preoptic area/anterior hypothalamus (POA/AH)
sends signals to hindbrain’s rapne nucles (controls physiological reactions); controls body temperature
infections
make immune system release prostaglandins and histamines; POA/AH raises set point for body temp
fever
shivering/sweating when body temp deviates from new level; can kill bacteria and makes immune system work harder
vasopressin
constricts blood vessels (raises blood pressure) to compensate for decrease in blood volume; OVLT + SFO cells tells pituitary gland to release it
antidiuretic hormone (ADH)
lets kidneys reabsorb water from urine (more concentrated)
osmotic thirst
caused by eating salty foods, drive to drink water to restorenormal state
hypovolemic thirst
cause by losing fluids through bleeding/sweating
ostomic pressure
water flows from low to high concentration
sodium accumulation
happens when you eat something salty; high solutes outside membrane
OLVT + SFO
check for ostomic pressure and sodium content in blood; sense water loss and increase ostomic pressure
angiotensin II
constricts blood vessels to help make up drop in blood pressure; detects blood pressure and triggers thirst (LOW BLOOD VOLUME)
angiotensin
is released by neuromodulator and responds to hypovolemic thirst - and restores lost salts and water
sodium-specific hunger
need to consume salty tastes thanks to sodium deficiency
aldosterone
released by body’s sodium reserve is low and helps retain salt (LOW SODIUM)
lactase
intestinal enzyme, needed for metabolizing lactose
stomach distension
main signal to end a meal
sham feeding
animals eat and swallow continually without being satiated
vagus nerve (cranial nerve)
conveys info to the hypothalamus about stretching the stomach walls
duodenum
area where nutrients are absorbed; nerves here inform the brain about distension and type and amount of nutrient
Cholecystokinin
released by distension, produces satiety by constricting sphincter muscle so stomach holds contents and fills up AND enabling the vagus nerve to send signals to hypothalamus to send a neurotransmitter that can cross the blood-brain barrier
insulin
enables glucose to enter the cells and prevents blood glucose levels from rising too sharply; is released by pancreas before/after meals
after a meal
blood glucose drops, insulin drops, and glucose enters slowly so hunger increases
glucagon
stimulates the liver to convert some glycogen into glucose; pancreas enables release
high insulin
increased weight
diabetes
disorder of glucose absorption
type 1 diabetes
autoimmune attack reduces/eliminates pancreas’s ability to produce insulin
type 2 diabetes
pancreas produces insulin, but cells don’t respond to it
untreated diabetes
blood glucose level rises, but not much glucose enters the cells
leptin
signals brain about fat reserves
low fat reserves
low leptin; you eat more and are less active
axons functions
affects taste sensations and salivation response to taste (cortical cells increase this) + hormone, insulin, digestive secretion
sexual selection
genes that increase an individual’s mating probability /offspring also spreads in the population
turner syndrome XO
y chromosome never got copied; missing or part of second X chromosome or two full X chromosome
Klinefelter syndrome XXY/XXYY/XXXY
extra copy of chromosome; masculine features + self-identification but infertile
mullerian ducts
precursors to female internal structures
wolffian ducts
precursors to male internal structures
SRY gene
causes undifferentiated gonads to develop into testes
androgens
testes increase growth of testes and produces more of these
vasdeferens
duct from testis into the penis
Mullerian-inhibiting hormone (MIH)
mullerian ducts degenerate into penis and scrotum, into vagina and uterus; produced by testes
male testes
androgens increase and estrogens decrease
female ovaries
estrogens increase and androgens decrease
estrogen
helps in memory and cognition; produced by adrenal glands
steroid hormones
androgens (testosterone) and estrogens (estradiol)
progesterone
prepared the uterus for implantation of fertilized ovum and pregnancy maintenance
steroids
bind to receptors, enter the cells to activate specific proteins and bind to chromosomes to activate/inactivate specific genes
organizing effects in sex hormones
long-lasting (puberty)
activating effects in sex hormones
temporary, continue while hormone’s present (hormone levels affect sex drive)
high testosterone
develops male pattern
low testosterone
develops female pattern
high dihydrotestosterone
penis and scrotum development
low dihydrotestosterone
clitoris and labia development
estradiol in prostate gland
produces fluid that protects sperm cells when ejaculated (during sex)
female hypothalamus
cycle patterns of hormone release (menstrual cycle)
male hypothalamus
hormones released more steadily
alpha-fetoprotein
prevents estradiol from entering cells; female brain not exposed to estradiol thanks to this
girls with high testosterone
play more with toy trains
oxytocin
stimulates uterus contraction during delivery of babies and stimulates mammary gland to release milk; helps reduce anxiety and calms after orgasm
male sexual arousal
androgens are essential
D1 and D5 receptors
increase sexual arousal
D2 receptors
high dopamine concentration, causes orgasm
after orgasm
serotonin increases and testosterone goes down
serotonin
decreases sexual activity and blocks dopamine
impotence
inability to have an erection, poor blood circulation
menstrual cycle
produced by hypothalamus, pituitary glands, and ovaries; period of change in hormones and fertility in 28 day cycle
follicle stimulating hormone (FSH)
stimulates follicle growth in the ovary; stimulates nurture ovum and creates estradiol and estrogen
@ middle of menstruation cycle
follicle gains more receptors to FSH and produces lots of estradiol- effects on follicle increase
lutenizing hormone (LH)
released from anterior pituitary; leads to release of ovum from follicle
increased FSH and release of LH
increased estradiol
FSH + LH
follicle releases ovum from uterus (most fertile time)
corpus luteum
remainder of follicle; releases hormone progesterone
progesterone
prepares the uterus for fertilized ovum implantation and blocks further release of LH
pregnancy
FSH isn’t needed; estradiol and progesterone increases and serotonin 3 (s)
menstruation starts
lining of uterus is cast off and estradiol and progesterone decreases
pre-ovulatory
rise in attention seeking behavior, peak fertility at midcycle
birth control pills
prevent pregnancy by changing feedback cycle in the ovaries and pituitary
combination pill
prevents FSH and LH from releasing ovum and prevents ovum from implanting in the uterus; thickens cervix mucus (sperm can’t reach ovum)
prolactin
stimulates milk production up after birth
arcuate nucleus (hypothalamus)
set of neurons for hunger signals; get their input from insulin and leptin (and amygdala)
NPY/AGRP
hunger neurons
POM/CART
satiety neurons
ghrelin
triggers stomach contractions when starving and increases appetite in hypothalamus
hunger cells
inhibit the paraventricular nucleus which inhibits the lateral hypothalamus → excites the lateral hypothalamus so there’s INCREASED eating
satiety cells
excite the paraventricular nucleus which releases melanocortin and glutamate
melanocortin
helps limit food intake
orexin
increases activity (food searching) and promotes wakefulness
lateral hypothalamus
controls insulin secretion, changes in taste responsiveness, and facilitates feeding; increased DRIVE TO EAT t if stimulated
damage to lateral hypothalamus
refusal of food and water; kills neurons and interrupts axons containing dopamine