trying to stay at a set point. regulated by a feedback mechanism starting in the hypothalamus.
cold blooded. can't regulate their own body heat; need to use behavioral regulation to keep warm. snakes rely on the environment.
warm blooded. can generate their on body heat so can use behavioral (regulated in lateral hypothalamus) and physiological (regulated in the POA in the hypothalamus) regulation.
thermoregulation in humans: when cold
1) metabolism of brown fat. brown fat has a lot of mitochondria which produces energy. white fat is for storage. 2) shivering of muscles to generate energy which is translated into heat. 3) increased thyroid activity means increased thyroid hormone which increases metabolism so it increases energy and therefore heat. 4) constriction of cutaneous blood vessels to stop heat loss.
thermoregulation in humans: when hot
1) increase perspiration to put moisture on the surface of the skin and help lose heat. 2) accelerate level of respiration, i.e. panting. 3) cutaneous blood vessels dilate to increase heat loss from blood.
trying to even out ratio of salt to water on each side of the membrane. SALT SUCKS.
isotonic, hypotonic, hypertonic
1) isotonic: in equilibrium. 2) hypotonic: concentration of solute<solvent. this means there is less salt than on other side of the membrane so water lever ends up being lower after osmotic pressure moves water out to even out ratio. 3) hypertonic: amount of solute>solvent. this side will have more water than other side of membrane (salt sucks). NOTE: water travels through aquaporines.
1) intracellular: fluid inside the cell. 2) extracellular: fluid outside the cell, i.e. blood plasma, urine, CSF. 3) interstitial: fluid between cells.
thirst (basic facts and two types)
depends on salt and water. the kidney regulates how much fluid is lost. dehydrated cells shrink and blood vessels put fluid back into the cells. the two types are 1) hypovolemic (aka volumetric): loss of extracellular fluid caused by blood loss, urination, excessive sweating, vomiting and is detected by baroreceptors (in heart and kidneys) that detect a decrease in blood pressure. 2) osmotic (aka osmometric): loss of intracellular fluid by normal sweating, respiration, or eating salty food. detected by osmoreceptors.
1. angiotensinogen (hormone) is released into the blood and converted to angiotensin I by renin (released by kidneys. secreted when baroreceptors detect low bp). 2) angiotensin I is converted immediately to angiotensin II. 3) angiotensin II has 4 effects on body: a) constrict blood vessels so bp increases and renin release decreases b) circumventricular organs (subfornical organ which has angio II receptors so related to hypovolemic thirst, OVLT which has osmoreceptors, area postrema, nucleus of solitary tract) trigger drinking c) vasopressin (aka ADH) is released to decrease fluid loss d) aldosterone is released to cause kidney to retain Na2+
if there is an increase in solute concentration interstitially, it causes water to leave cell which affects firing rate
pathways for thirst
hypovolemic -> baroreceptors (if kidney use angiotensin II, if heart use vagus nerve) ->NST or SO -> POA -> hypo -> trigger drinking. osmotic -> OVLT->POA -> hypo -> drink
when do we stop drinking?
when our cells reach an isotonic level
used for immediate energy. can be stored as glycogen in liver or muscles and as triglycerides in fat
parotid and salvary glands to produce saliva. amylase enzyme produced to start breakdown of carbs
mechanical digestion using churning. HCl to breakdown food and pepsin to breakdown proteins
junction between SI and stomach. controls rate of stomach emptying. releases CCK to cause gallbladder to release bile to help breakdown of fat
villi increase surface area to help absorb glucose and amino acids. lacteals increase surface area to help absorb fats
E. Coli which live off of our undigested cellulose and in return make vitamin K. also absorbs water, minerals, electrolytes
in islets of langerhans has 2 cells. alpa cells make glycogen (released when glucose levels are low) and beta cells make insulin (released when glucose levels are high). also has digestive enzymes which are secreted into stomach and SI and bicarbonate to neutralize stomach acid
produces bile to breakdown fat
cephalic phase of digestion
aka preprandial. before eating when you get ready to eat
digestive phase of digestion
aka prandial. when break things down
absorptive phase of digestion
aka postprandial. when absorb things. glucose stored as glycogen and triglycerides. amino acids stored as protein and triglycerides. fats stored as triglycerides
fasting phase of digestion
between meals when need to take things out of storage. 1st source of energy is liver and then muscle -> short term storage. last source is adipose tissue. fatty acids can be used directly or converted as a ketone
insulin (as a gut hormone involved in digestion)
from beta cells. transports glucose into cells. diabetes type I (stop making insulin) and type II (makes normal insulin but no longer sensitive).
made from alpha cells. helps take glucose out of storage (released when glucose levels are low)
glucose is stored as glycogen in liver and muscle
converting triglycerides to fatty acids and glycerol. glycerol can be converted to glucose and fatty acids can be converted to ketones
CCK (as a gut hormone involved in digestion)
released based on fat -> high fat meal = increased CCK. inhibits gastric emptying by preventing duodenum from opening. stimulates gallbladder to release bile. also possibly a satiety signal
convert glycogen to glucose
convert fat and protein to glucose
convert glucose to glycogen
peripheral factors controlling hunger and satiety
1) social factors (time of day, see food, smell food) 2) taste factors (like sweet and salty, don't like sour and bitter) 3) specific satiety (is eat a lot of same food, will be full of that food but not of other food) 4) learning factors (dietary self selection and dietary deficiencies) 5) stomach factors (contractions=grumble=hungry, nutrient receptors, stretch receptors) 6) set points (glucostats- secrete insulin/glucagon to regulate blood glucose, lipostats- body fat regulation, usually long term)
stimulates appetite when stimulated (feel hungry). is lesion, rat stops eating. if keep it alive, it will recover but will have a lower set point weight. so it decreases body weight if lesioned
inhibits appetite when stimulated (feel full). rat ate until it was fat. if it was lesioned, rat will gain weight and will have a new set body weight that's higher than normal
PVN and ARC
stimulates hunger when stimulated (feel hungry). where hormones are detected and then receptors and transmitters are sent out
missing leptin so rat overeats
inhibits eating. adipokine (produced by fat cells). works with a feedback mechanism -> the fatter you are, the more fat cells you have, more leptin is produced, so hunger is inhibited, lose weight
adipokine. simulates eating. facilitates leptin release. decreased in obese.
insulin (as a hunger signal)
CCK (as a hunger signal)
inhibits hunger. produced by intestines. acts on the brainstem
inhibits hunger. produced by intestines. decreases production of NPY and AgRP
inhibits hunger. produced by stomach. decreases production of NPY and AgRP
stimulates hunger. produced by stomach. increases production of NPY
stimulates hunger (aka increases appetite). released onto PVN
stimulates hunger (increases appetite) because is a competitive antagonist for MC4 receptor which normally makes you feel full
cleaved into alpha MSH which inhibits hunger to decrease appetite
stimulates hunger and is released from LH
orexin (as a hunger signal)
stimulates hunger and is released from LH
stimulates hunger. affects LH
if activated by alpha MSH, feel full. if activated by AgRP, feel hungry.
very good metabolizers. leave a lot of calories in digestive tracts for us to absorb. normally have a higher level for this, but obese people have more than lean people
not as good metabolizers, less in gut
genetic causes of obesity
mutations in genes for leptin, leptin receptors, POMC, or MC4 receptors. also can have normal levels but an upregulation of SOCS3 and PTP1B, which inhibit action of leptin
bypass surgery, drug treatment (sibutramine-increases NE and 5HT to decrease appetite, rimonabant-cannabanoid receptor antagonist, orlistat-decreases absorption of fat by intestines). potential treatment (inhibit MCH NYP ghrelin, PYY MC4 agonist, release fat from storage, block fat storage)
biological rhythms are out of sync with environment
shorter than a day (90 min). sleep cycle
24 hour rhythm
circalunar-monthly and circannual-seasonal cycle
in hypo. projects to pineal gland. master clock
released after light hits the retina and causes an action potential to be sent down retino-hypothalamic tract to the pineal gland
keeps track of time by measuring relative amounts of serotonin. during day when there's light, it makes serotonin and then at night when there's no light, it takes the ser produced during the day and converts it to melatonin to make sleepy
free running clock
if we have no zeitgebers, our body knows to keep our circadian rhythm to almost 24 hours (24:11). almost no variability between people
molecular clock in flies and mice
use clock, cycle, per, cry, and tau. see notes for cycle...very important!
states of consciousness
sleep, daydreaming, unconsciousness, drug use, hypnosis, meditation
levels of consciousness
1. conscious 2. preconscious (something not thinking about but can access any time) 3. subconsciousness (buried deep down but can access unless in an altered state) 4. non-conscious (brain pays attention to but we will never access, like blood pressure)
alpha activity (awake but relaxed) and beta activity (activity during normal day)
stage 1 sleep
very light sleep. theta activity. don't think you're asleep
stage 2 sleep
bigger waves. find sleep spindles (small bursts of action) and K complexes (big spike)
stage 3 sleep
blood pressure and temp down, shallow breathing -> brain processes slow down. delta activity=bigger waves. some spindles and K complexes
stage 4 sleep
really deep sleep. all delta activity and some K complexes. some older people don't even get into this level
Rapid Eye Movements. body in deep sleep (paralyzed) but brain says awake (theta and beta activity). very easy to arouse. when most of dreaming occurs. eyes move because they're scanning dreams. least restful stage
1 2 3 4 3 2 REM. takes 90 min. get many in one night's sleep.
why do we sleep?
1. conserve energy 2. avoid predators 3. restoration and repair (done by deep sleep) 4. develop and expand neural connections/memory consolidation/erase unnecessary memories
fatal familial insomnia
can't sleep. part of brain that degenerates is part that controls sleep
brain areas involved in arousal
basal forebrain (using ACh and some use GABA), tuberomammillary nuclei (use histamine), raphe nuclei (use 5HT) and locus coeruleus (use NE)
brain areas involved in sleep
ventrolateral POA (vlPOA) uses GABA so it inhibits the areas involved in arousal
activates the SWS flip flop switch. it is inhibitory so it inhibits the arousal areas. levels rise during the day and at night, when levels are high, the switch flips and you go to sleep
orexin (as a sleep signal)
aka hypocretin. keeps you awake and alert. so if you activate the orexinergic neurons, it keeps you awake by stimulating the arousal areas. hunger activates orexin so when you feel full, orexin is reduced so the arousal areas are less stimulated
REM off area. LC, raphe nucleus, LH all activate vlPAG to allow you to be awake and alert. the vlPOA inhibits REM off
REM on area. activated by the amygdala
activation synthesis hypothesis
cortical arousal is happening in random areas in the brain. the brain tries to create a story that would make sense with the random areas activated
random onset of REM sleep. when they sleep, go into stage 1 sleep and then right to REM during normal nights sleep. also have 2x more REM sleep than a normal person. its caused by emotional stimuli (amygdala triggers REM on) and the orexin neurons degenerate
loss of muscle tone. feel paralyzed
drug to quit smoking
get vivid dreams and are very tired