biopsychology exam 3

the purpose of eating

to provide the body with molecular building blocks and energy

digestion

breaking down of food and absorbing its constituents

salivary glands and parotid glands

are salivated and makes it easier for food to slide down your esophagus

parotid glands

produces enzymes to break down food at a molecular level

stomach

has a lesser role in digestion than intestines, 'holding tank'

hydrocholoric acid

breaks down food in the stomach into small particles

pepsin

breaks down proteins in the stomach

pyloric sphincter

Controls passage of food from stomach to duodenum (small intestine)

duodenum

upper part of the small intestine where most absorption takes place

gallbladder and pancreas

provide enzymes to the duodenum to break down protein molecules to amino acids and starch and complex sugar molecules to simple sugars

amino acids and simple sugars pass more easily through the duodenum wall

lymphatic system

fats are emulsified by bile, which is manufactured in the liver and stored in the gall bladder until it is released by the duodenum

emulsified fat cannot pass through the duodenum wall and is carried through ducts to the ___________ ________

jejunum

Middle portion of the small intestine

continues to absorb fatty acids, amino acids, sugars as the food passes through

ileum

third part of the small intestine

large intestine

The last section of the digestive system, where water is absorbed from food and the remaining material is eliminated from the body

fats are absorbed as

fatty acids and lipids

proteins are absorbed by the duodenum as

amino acids

carbohydrates and complex sugars are absorbed as

glucose

storage

is important so that when we are not consuming food (digestive system is empty) we can still get energy to fuel our bodies and brains without a continuous influx of energy (not in periods of long fasting, usually 12-16 hours)

triglycerides

(~85%) a form of fat stored in the subcutaneous fat tissue

fats

store twice as much energy per gram compared to glycogen - by storing excess glucose as triglycerides, we can maximize how much energy we store.

protein

(~14.5%) amino acids are stored in the muscle

glycogen

(~0.5%) in the liver and muscle tissues

retains a lot of water, increasing water weight and bloating making functioning more difficult

blood glucose

We access energy stores when we need _________ _______ to be available to the cells of our body and neurons

Astrocytes

use glucose in the bloodstream to make lactate - also convert excess glucose into glycogen for temporary storage for when blood glucose is low

lactate

the converted form of glucose that is utilized by the neurons

glycogen

when your blood glucose level is low, ______ is accessed first. fast conversion of ______ to glucose

triglycerides

As soon as blood glucose levels drop, _________ are also being processed to provide fatty acids and conversion to glucose for energy - this process starts early but takes more time, which is why glycogen access is first.

proteins

When there is no more glycogen or triglycerides, ________ are the last to be broken down. Muscle tissue begins to break down and is used for energy - this happens at a starvation level.

cephalic phase

'preparatory phase' triggers your body to prepare for food. Seeing food, thinking about food, smelling food, seeing other people eating food can trigger this. Leads to changes that enhance our processing of food should we actually eat

insulin up to prepare for digestion and processing

glucagon low

fatigue

When Cephalic is triggered but you are not about to eat, the release of insulin can cause a feeling of ________ - may make you feel hungry which prompts you to eat

But 15-20 minutes after the phase is initiated, hunger signals decrease and insulin levels begin to decline again to restabilize

absorptive phase

food has entered your body and moves to the duodenum.

insulin continues to rise

excess food - determined by body's energy pre-eating - is stored, storage promoted by insulin

glucagon remains low

typical processes to pull energy out of storage are not used because glucagon is already low

all energy and nutrients are absorbed and passed to the large intestine

fasting phase

we must tap into our energy storage to have energy to maintain immediate activity level (more active - more energy pulled out, less active - less energy)

insulin levels are relatively low

glucagon levels are high - no more nutrients are being absorbed in the digestive tract to trigger the conversion of glycogen to glucose, and later conversion of triglycerides

glucose is not being used - no conversions occurring. when accessing storage, you are not simultaneously putting more into storage to maintain a stable level of blood glucose.

evolution of tastes

across species, typically prefer sweet, fatty, and salty foods. This preference may have evolved because naturally available foods (prior to farming, etc)

Foods that are sweeter and fatter tend to be higher in "nutrient value" and energy, than less sweet/fatty food; when hunting and gathering, these are better to seek

Salty foods are high in sodium, which is needed for electrolyte balance in the body

modeling of food preferences

we tend to prefer foods that we are exposed to and see other people eating. Preference for flavors that can be found in mother's milk and in the breath of others, molecularly.

Allows members within a species to determine what is safe to eat and what is not.

neophobia

fear of new things, especially food

vitamins and minerals

we prefer foods that are good sources of vitamins and minerals, especially when there is a deficiency

pre-meal hunger

because of a regular eating schedule, at a particular time of day your body has adapted to feel hunger ('prepared' for food.) Physical changes (a rise of insulin, as in the cephalic phase) occur sending signals that it is time to eat, interpreted as hunger signals.

conditioning of hunger

doing something very regularly makes certain things cues for hunger. Certain environmental stimuli (like televisions, if you eat while watching television) can be conditioned to trigger the cephalic phase, increasing insulin release and lowering blood glucose.

Independent from whether or not you have just eaten/have food in your digestive system; a cephalic phase can still be triggered

hunger peptides

chemicals that affect our hunger and satiety responses

NPY and ghrelin

Ghrelin

primarily produced and released by the stomach (and duodenum, pancreas) in response to signals from duodenum (when empty).

The longer you go without food (the longer the duodenum is empty), the more ghrelin you produce and release.

results in perception of hunger

Stimulates appetite and eating behavior - when ghrelin is increased synthetically, people have vivid images of food and increased appetite and perceptions of hunger.

Foods that are higher in nutrient value allow the ghrelin levels to remain lower for longer.

neuropeptide Y

released by neurons in the hypothalamus (from the arcuate nucleus), appears to increase appetite and preference for carbohydrates. When the arcuate nucleus is stimulated, greater desire for carbohydrates

Potent stimulator of eating behavior

Glucose-sensitive cells in medulla oblongata activate NPY neurons; when blood-glucose levels drop, these cells fire and activate NPY neurons

high during fasting, low after eating

satiety signals

a motivational state that occurs when we stop eating even when food is available - choice, not out of necessity.

Presence of Food in the Gut

As we start eating, if we already have food in our gut, we are less likely to eat more. Signals show that your body is already actively absorbing nutrients, you do not need more at this time.

glucose in blood

If your blood glucose levels are rising and staying relatively high, you are less likely to continue eating and seek food soon after.

BG drop, hunger signals rise. BG rise, satiety signals rise

Volume of food (Cannon & Washburn 1912)

expanding the stomach stopped muscle movement, creating feelings of satiety - contracting the stomach created hunger signals (discredited, hunger is attributable to peptides, satiety signals, glucose...)

nutritive density of food

if you eat more nutrient-rich foods, you will eat less. If you eat more lower-calorie, low-nutrient foods, you will eat more of them. 'Quality over quantity,' threshold of nutrients, once met, stop eating.

appetizer effect

If you have an appetizer before a meal, you are more likely to eat your meal/more of your meal. Appetizer triggers the cephalic phase, but you know that appetizers are not your meal, you become hungrier.

social factors on satiety

people tend to eat more (60%) when they are with others. Possibly, biological reason - inconsistency of food means that you feel a need to eat in the presence of others to 'get your share.'

sensory specific satiety

when we begin eating, and start tasting a food, immediately feel a decrease in positive incentive value for the food. As you eat more and more of the food, the positive incentive value decreases - starting with the type of food you are immediately eating, later, applies to other types of food as well.

promote short term satiety to create a more varied diet, an adaptive mechanism evolved to prompt us to eat different types of food

Promote long term satiety to prevent deficiencies

satiety peptides

can also reduce how much we eat at a given time, long term eating

Cholecystokinin (CCK), Peptide YY, Leptin,

Cholecystokinin (CCK)

is released by the upper small intestines (duodenum) in response to fats and amino acids in the duodenum.

More CCK-More Satiety

Stimulates the gallbladder contraction to release bile (which breaks down fat).

Prompts the pancreas to release digestive enzymes

Contracts pyloric sphincter to slow stomach emptying

The longer food remains in your intestinal tract (duodenum) the longer nutrients can be absorbed

More nutrients being absorbed means a decrease in hunger, increasing feelings of fullness for longer.

Peptide YY

secreted by cells in ileum (last section of small intestines) and colon in response to fat and protein presence/absorption proportionate to the number of calories in food

Slows gastric motility; contraction of intestines, increases water and electrolyte absorption by colon

Slowed processing allows for more absorption of various nutrients

Decreases eating for a short period until the intestines are empty

Leptin

secreted by subcutaneous adipose cells (fat cells under your skin), receptors found in brain (arcuate nucleus)

More body fat (larger fat cells) = Less leptin

When you have replenished your triglycerides (healthy max), causes breaks in eating

inhibits release of NPY so that they slow down firing and cause less feelings of hunger

Decreases food intake

Increases metabolic rate

Increases body temperature and activity level

Inhibits insulin synthesis and release as leptin levels rise (right after you have eaten) - the extra insulin is unnecessary, you want the blood glucose to stabilize, not be used up.

desensitized

Long term, with higher leptin levels, people may become less sensitive to the effects of leptin. Metabolic changes that the NPY neurons become _________ by continuous stimulation by leptin; may cause weight gain

serotonin and satiety

Appears to increase short-term satiety associated with a meal

Resisted attraction of highly palatable diet (fattier and sweeter)

Resisted urge to eat high-calorie food - against adaptive evolutionary mechanisms.

Reduced amount of food consumed during a meal

inhibitory effect on NPY receptors 'modulator' - decreased reaction, not a direct inhibitor

Fenfluramine and dexfenfluramine

as appetite suppressants

Taken together to quicken weight loss, but proven to be deadly - heart attacks and strokes. Fenfluramine removed from market, combination no longer prescribed

Increase amount of Serotonin

set point theory

most people attribute motivation to eat with the presence of an energy deficit

Belief that we eat to bring our energy resources backup to an optimal level...energy set point. Homeostasis

glucostatic set point theory

we have a set point where glucose levels have to be steady

However, it has been proven that people do not experience extreme drops/peaks in glucose levels - they remain relatively stable over the hours in the day within a range.

lipostatic set point theory

we have a set point at which we want to maintain our body fat level. We eat because we are using up our energy sources (triglycerides, fats) during the day

However, the change in triglycerides in a day is small. It is impossible to lose the amount of fat necessary in a day to justify this theory. Works better to explain longer-term changes, rather than changes in a day

positive incentive theory

Animals and humans are drawn to eating by the anticipated pleasure of the eating experience (positive incentive value of eating)

Degree of hunger felt at any given time is dependent on all the factors that affect the incentive value of eating

settling point model

Weight tends to drift around a natural "settling" point - shifts depending on bodily changes over time

The settling point is a level at which the various factors that affect body weight reach equilibrium

'Leaky barrel' analogy - more body fat you have, more energy you have available to burn. Increase metabolism. Easier for heavier people to lose weight faster

Readjustment of settling point because of changes maintained over years - short-term changes eventually reach a plateau, no more larger drops or gains

Weight that is less likely to come off later because of newly established state of homeostasis

Original (OLD) View

Ventromedial Hypothalamus

'Satiety center' - firing causes us to eat less. Determined in rat studies

Stimulation of VMH resulted in aphagia (rats stopped eating)

Lesions resulted in:

Hyperphagia (excessive eating)

Increased meal frequency

High insulin levels - constantly in absorptive phase

Gained weight and maintained a high weight relative to non-lesioned rats

Cannot stop eating

Original (OLD) View

Lateral Hypothalamus

'Feeding center'

Stimulation resulted in increased eating (hyperphagia) and drinking (hyperdipsia)

When lesioned:

Aphagia (stopped eating) and did not start eating again, many starved to death unless force fed

Under-ate and underweight

Adipsia (drank a lot less water)

Less arousal

Less movement

Opposition to Old View of Brain Mechanisms for eating

pathways regulating hunger and eating were cut in order to make lesions; may not be the VMH or LH that directly caused inactivity and other side-effects

New View

Hypothalamus

but not just VMH and LH alone causing satiety/hunger but also substances within it

When MCH And orexin-A are released by LMH, increase/stimulate hunger and thereby eating behavior, and decrease metabolic rate

Increase and preserve body energy stores

Foods that are higher in fat/more palatable cause an increase in the MCH and orexin-A released - stimulating taste receptors and nutrient value; evolutionary mechanism

Food deprivation results in increase in MCH and orexin

MCH and orexin are impacted by leptin - satiety peptide. When stores are replenished and leptin is released, these neurons are hyperpolarized - reduction in hunger signal

Melanin-concentrating hormone

one of two peptide neurotransmitters found in a system of lateral hypothalamic neurons that stimulate appetite and reduce metabolic rate

orexin-A

a neuropeptide involved in appetite control

Arcuate Nucleus 'signaling hub'

Produce NPY and AgRP

Neuropeptide Y

stimulates releases of orexin and MCH from lateral hypothalamus

The same NPY neuron when binded to certain receptors can cause either more MCH and orexin release or less; no direct cause/effect.

agouti-related peptide (AgRP)

decreases metabolic rate, causing your body to conserve energy.

Release is activated by calorie deficiency.

Inhibits satiety melanocortin 4 receptor (MC4R) neurons in paraventricular nucleus (of hypothalamus) - to allow hunger behavior to continue until energy store is replenished

Turn-on AgRP (more secretion) = voracious eating, even after a meal

Turn-off AgRP = no eating, even when hungry.

ghrelin, leptin, peptide YY (ileum), insulin (pancreas)

have receptors on AgRP and orexin-A neurons

gastrointestinal tract

stomach and intestine

learning

process by which experiences change our nervous system and as a result change our behavior (relatively permanent)

Excludes behavioral changes resulting from sensory adaptations or fatigue

memory

nervous system changes retained over time and how the changes are expressed (recall)

acquisition

being stimulated by your environment, the information is entering the memory system - what you see, hear, feel, smell...

sensory buffers

related to our senses, for a few seconds, you are able to hold on and maintain thousands of bits of information, seems to be limitless but goes away quickly

iconic memory

lasts less than ½ second, visual information

echoic memory

lasts 3-4 seconds, auditory information

encoding

some of the information acquired is put into short-term memory to be stored

Information put into short-term memory is chosen depending on how much of an emotional reaction it causes, how much you focus on it/care about it

working memory

when information is worked with, processed, used. Conscious activity, not just on what you are interested in. Information from our long-term memory (past) comes into the moment to be considered.

7+-2 (5-9) chunks

can be held in short-term memory as it is rehearsed. Once rehearsing is ended, unless consolidated, this memory can be lost

chunking

small bits of information are combined into more meaningful units to allow for more information to be in short-term memory

storage (into long term memory)

Process of getting information into storage is called consolidation, and involves physical changes at a neural level at synapses.

Once these changes happen, this information is stored for the long-term and can be accessed through retrieval

retrieval

information is pulled from long-term memory to working memory, can be added to (and re-consolidated) and used. With every retrieval, and every pass through working memory, information stored may change.

not all information is re-consolidated, it may fade especially if not rehearsed enough in long-term potentiation (synapses not strengthened)

spaced-out rehearsal

strengthens pathways and allows for long-term memory to be sustained over long periods

explicit memory

memory that is able to be declared, talked about, provided information about

episodic, semantic

episodic

memories for episodes, memories for a time, situation, event that you experienced. Multilayered, with many sensory details

semantic

memories about facts, information, details

implicit

memory for tasks, you are able to do something when prompted, but it is hard to explain in words.

associative conditioning, procedural, priming, non-associative

associative conditioning

things experienced again and again become conditioned to be associated with certain memories.

emotional (amygdala)

somatic (cerebellum)

procedural

memory on how to complete tasks (striatum)

priming

ability to be prompted and recall information that you are not aware of because it is not on the conscious level. Because you have seen it and experienced it before, you are more likely to answer a certain way because it is familiar. (remembering someone's name given their face and letters of it)

(striatum)

non-associative

experiences that you have that you may show a larger or lesser response based on past experiences (like the ticking of a clock) Habituation and sensitization (reflex pathways)

Case of Henry Molaison

traumatic brain injury caused the development of epilepsy and severe episodes of seizures which disabled normal functioning.

Bilateral Medial Temporal Lobectomy

Bilateral Medial Temporal Lobectomy

Removal of medial temporal lobes (MTL) bilaterally to alleviate epilepsy (1953)

-Hippocampus

-Amygdala

-Rhinal cortical areas

Usually, only one side of the brain was removed according to where the seizures originated - H.M.'s seizures originated from both sides

Began to struggle with memory, could not remember introducing himself to people he met post-surgery, could not form new memories.

Retrograde amnesia (memory gaps beginning ~2 years prior to surgery)

Profound anterograde amnesia (could not form new memories, the longer he lived, the bigger the gap in his memory became)

H.M. had normal functioning, including priming, BUT...

digit span + 1

test administrator uses number sequences to test performance for short term memory capacity. H.M. was in "normal" range (5-6 Numbers) as long as his attention was on them alone

block-tapping memory-span test

administrators tap blocks in a sequence, you must repeat it back. Performance in "normal" range for short term

H.M had relatively intact short-term memory, if he rehearsed information - forgetting occurred the instant his attention was shifted

mirror drawing test

Implicit memory, new behavioral skills.

His performance improved with training sessions. Normal sensory-motor learning

BUT He had no conscious recollection of ever performing it before.

His implicit memory was fully intact - could not form long term explicit but could form long term implicit

standard consolidation theory (Squire and Alvarez)

Memories temporarily stored in hippocampus - when there is less activity, the hippocampus will reactivate and retrace the activities you were participating in

Later transferred to a more stable system - hippocampus activates other parts of the brain for long-term storage.

For up to a week, information can be retained and pulled out from the activity of the hippocampus. If it is not transferred elsewhere, it fades

Additional stimulation of the pathway can strengthen the memory/pathway

But does not account for the maintenance of implicit memory in H.M.