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Motivation and
the Regulation of
Internal States
Hunger: A Complex Drive
Hunger: learning factors
• Much of what we eat is culturally driven or learned
– Basic food preferences (5 tastes)
– Some physiological need
– But mostly learning!
• Learned taste aversion:
– the avoidance of foods associated with illness or poor nutrition
– Often occurs in one trial.
• Learned taste preference
– Preference for the flavor of a food
– Probably developed to remember taste of food that contains a needed
nutrient.
– Often we choose a food based on taste, not nutrient contents!
communicating about
food depends on the kind
of animal we are!
• What is a poison or bad food?
• How do humans figure out a food is rotten or poison?
• How do other animals judge “bad food”- what clues do they
use?
• Why might we learn after only 1 experience that a food is
bad- why don’t we keep eating food that made us sick?
Garcia Effect or
Conditioned Taste
Aversion
• Grp I: Tasty Water--> Nausea
– Good Conditioning
• Grp II: Bright Noisy Water-> Shock
– Good conditioning
• Grp III: Tasty Water--> Shock
– No conditioning
• Grp IV: Bright Noisy water--> Nausea
– No conditioning
A “biologicAl boundAry”
• Look at the TYPE of stimuli that are being used:
– Categorize each as an internal or external event
• Grp I: Tasty Water--> Nausea
• Internal
Internal
• Grp II: Bright Noisy Water-> Shock
• External
External
• Grp III: Tasty Water--> Shock
• Internal
External
• Grp IV: Bright Noisy water--> Nausea
• External
Internal
• Can’t learn ACROSS modalities very well!
Important Properties
• Just takes once!
• All animal species show it
•Can remember the poison for a VERY long time!
• Novel stimuli condition more readily than familiar
stimuli
•Different Cues for different species:
• quail: color of food
• monkeys: texture
• rats: taste and smell
•In social animals- can transmit stimulus socially
Uses
• Humans: dietary restrictions and
smoking cessation programs (but
will switch brands and tastes)
• Can develop CTA with
Chemotherapy- must watch pairing
good food with nausea
• Most important use: Wildlife
Management:
– Coyote management
– Wolf management
– Bear management
keep your dog out of
the garbage?
•
Starting and stopping
eating
• What starts and stops eating? Complex factors
• Local theories: Cannon & Washburn
– Hunger = sensation arising from gastrointestinal tract
– Tied to some “sign”:
• Increase in gastric juices
• Full stomach
– Balloon experiment: swallow balloon and fill/empty it
• Subjects with filled balloon ate less, reported feeling more full
• But, still ate!
• Central theories: homeostatic physiological processes
– Starting process
– Stopping process
– Selection process: what to eat and when!
Process of digestion
• Digestion begins in the mouth, where food is ground fine
and mixed with saliva.
• Saliva:
– provides lubrication
– contains an enzyme that starts the breakdown of food.
• Digestion proceeds in the stomach:
– food is mixed with the gastric juices hydrochloric acid and pepsin.
– Broken down more before enters intestines
• Small intestine
– Receives partially processed food from stomach
– Stomach releases food gradually so the small intestine has time to do its job.
digestion
• Duodenum
– Initial 25 cm of small intestine
– Digesting primarily occurs here
– Carbohydrates are metabolized into simple sugars, particularly
glucose.
– Proteins are converted to amino acids.
– Fats are transformed into fatty acids and glycerol.
• Area postrema:
– Area of brain outside the blood-brain barrier
– Most posterior portion of brain
– Exempt from blood-brain barrier functions, so toxins can activate it
to induce vomiting.
Phases of digestion
• Absorptive phase
– The few hours following a meal
– body lives off the nutrients arriving from the digestive system;
• Insulin release:
– hormone that enables body cells to take up glucose for energy and certain cells
to store excess nutrients.
– The pancreas secretes during absorption phase
• Storage: Some of the glucose is converted to glycogen and
stored in a short-term reservoir in the liver and muscles.
• Fat reserves: Any remaining glucose is converted into fats
and stored in fat cells, also known as adipose tissue.
Digestion phases
• Fasting Phase
– Eventually the glucose level in the blood drops
– body must falls back on its energy stores
– This is the fasting phase.
• The pancreas ceases secretion of insulin
– starts secreting the hormone glucagon,
– glucagon causes the liver to transform stored glycogen back into
glucose.
• When levels are low enough, starts signals for eating again.
– but; social and environmental cues can also trigger “hunger”
Initiation of hunger
• Three major physiological changes with hunger:
– Glucopruvic hunger: low glucose signaled to brain
– Lipoprivic hunger: low fatty acids
– Ghrelin: neuropeptide in stomach
• Liver monitors
– glucose level
– fatty acids in blood passing from liver to small intestine
– Monitors fatty acids via hepatic portal vein
• Vagus nerve carries signals from liver to NST in medulla
• NST sends signals to arcuate nucleus of hypothalamus
– vital hypothalamic structure
– monitors the body’s nutrient condition.
– This is like the thermostat in temperature regulation
Initiation of hunger
• The arcuate nucleus sends signals to the PVN
(paraventricular nucleus)
– Also part of hypothalamus- ventral medial part
– initiates eating, though less effectively than the lateral hypothalamus,
– regulates metabolic processes such as body temperature, fat storage,
and cellular metabolism.
– Modulates control via two nerotransmitters:
• Neuropeptide Y (NPY); serotonin
• Lateral hypothalamus: master control of eating
– initiates eating
– controls several aspects of feeding behavior as well as metabolic
responses.
Critical initiation
hormones
• NPY (neuropeptide Y)
–
–
–
–
released from the PVN and lateral hypothalamus
Released in response to signals from the arcuate nucleus
dramatically increases eating
But reduces metabolism.
• Gherkin
– Peptide that is synthesized in the stomach and released
during fasting.
– Also induces eating
– Involved in eating disorders such as Prader Willi syndrome
• 2.5 x higher in individuals with Prader Willi’s
• Gherkin blocker may be an important dietary manipulation
Prader Willi Syndrome
• Genetic disorder: due to malfunction of cell division
– caused by a gene missing on part of chromosome 15.
– most patients missing genetic material on part of the father's
chromosome;
– others have two copies of the mother's chromosome 15.
• the genetic changes occur randomly. Patients usually do not have a
family history of the condition.
• Symptoms
– Newborns with this disorder small for gestational age; males have
underdeveloped genitals
– difficulties with sucking and swallowing; problems with weight gain
– May seem floppy and feel like a "rag doll" when held; weak cry
– Facial changes, such as "almond-shaped" eyes and a small,
downturned mouth; Skin differences
– Very small hands and feet compared to the body
Prader Willi Syndrome
• Affected children have intense craving for food; will do almost
anything to get it.
– results in uncontrollable weight gain and morbid obesity.
– Morbid obesity may lead to lung failure
– also low blood oxygen levels, right-sided heart failure, and
death.
• Signs and tests
–
Abnormal glucose tolerance
–
Above normal level of the hormone insulin in the blood
–
Failure to respond to luteinizing hormone releasing factor
–
High carbon dioxide levels; low oxygen
• Obesity is the greatest threat to health.
Prader Willi Syndrome
Manipulating
onset of eating
• Stopping eating: Blocking NPY or gherkin or damage to LH or PVN greatly
disrupts eating
• Starting/maintaining eating: Injections of NPY into PVN results in
huge increase in eating
– Rats may gain 6x or more body weight
– Can also induce by lesioning PVN
– Really can’t stop eating!
• During extreme deprivation: NPY reduces metabolism and increases
motivation to eat
– By decreasing metabolism, conserve body fat/glucose stores
– At same time, make animal more active, thus more likely to get food
– Also suppresses sexual behavior• Again conserves energy
• Also lessens chances of producing nonviable offspring
Signaling an
end to a meal
•
Mouth factors:
– Full mouth
– Chewing
– Learning
•
Stomach factors
– Full stomach is a cue to stop
– Phillips and Powley (1996):
• Inflated cuff to close off stomach/duodenum
• Infused glucose into stomach
• Infused saline into stomach
• As long as stomach felt “full” – ate less
•
Also respond to caloric intake
– High calorie soup produces greater reduction in eating than low-calorie
soup
– Issue of diet drinks: may eat MORE when drink diet drinks- not get
satiety signal
•
Optimal factor: mouth+stomach+intestines signal to brain
Signaling an
end to a meal
• Stomach and intestines respond to food by releasing various
peptides that brain uses to monitor intake
–
–
–
–
Some peptides respond to carbohydrates
Some to fats
Some to proteins
Some to mixes
• Peptides induce pancreas, liver, gallbladder to secrete
appropriate enzymes indo duodenum
– Allows appropriate digestion of specific nutrients
– Signal to brain which nutrients digested via vagus nerve or
bloodstream
Satiety hormones
• CCK (cholecystokinin)
– The best known of the satiety signals
– a peptide hormone that is released as food passes into the duodenum.
– CCK detects fats and causes the gall bladder to inject bile into the
duodenum, which breaks down the fat so it can be absorbed.
– Relatively short term regulation
• PYY (peptide YY3-36)
– Another appetite-suppressing peptide hormone
– released in the intestines in response to food
– carried by the blood stream to the arcuate nucleus; inhibits the NPYreleasing neurons.
– Note: non-neural route to the brain thus action is too slow to limit the
current meal;
– instead it decreases calorie intake by about a third over the following
12 hours.
– LONG term regulation
Satiety hormones
• leptin.
–
–
–
–
–
Fat cells secrete leptin
inhibits eating
The amount of leptin in the blood proportional to body fat.
Leptin helps regulate meal size,
Regulates in response to long-term stores of fat rather than the
nutrients contained in the meal.
• Can demonstrate effect of these hormones: VMH
lesions (much like Prader Willi’s syndrome)
– Increase parasympathetic activity in vagus nerve
– Enhances insulin release
– Creates persistent absorption phase in which more nutrients are stored rather
than used
– Animal MUST overeat to maintain normal energy level
– BUT: also becomes obese because of huge storage