Ch 12: Motivation & Regulation of Internal States

Motivation

= factors that initiate, sustain & direct behaviours

• behaviour thats NOT explained solely by outside stimuli, bc our internal states are driving it

→ NO theory fits it perfectly

Instinct

= behaviour thats automatic, unlearned & unmodifiable, occurring in everyone in a species (innate)

ex. animal migration & parental behaviour

• NOT used to discuss humans → use drive theory instead

Incentive & Arousal Theories

Incentive Theory = ppl are motivated by external stimuli, not just internal needs

ex. full → eat more dessert

ex. hungry → still dieting

ex. starting drugs to look “cool”

Arousal Theory = ppl act in ways to maintain a PREFERRED level of stimulation

• thus, they seek out stimulation, not just bc of external stimuli or needs

  • they like being outside of homeostasis

ex. adrenalin junky

Drive Theory (use for humans)

= body drives return to homeostasis (balance)

• Drive = aroused condition

ex. hungry → body drives u to eat

→ CANT explain why we leave homeostasis (ex. eating too much)

Drive Theory: 1. Temperature

→ use drive theory to maintain ideal (set point) body temp

Set point = point of homeostasis the body returns to (can change)

• women have a higher set point, thus need more warmth & perceive bigger differences in temp

Temperature Regulation:

• ECTOthermic animals = need external heat to regulate internal heat

• ENDOthermic animals = have internal heat regulation

via: Preoptic area = contains warmth-sensitive & cold-sensitive cells in hypothalamus of mammals

→ activates something to return to homeostasis (ex. shiver when too cold, or sweat when too hot)

Drive Theory: 2. Thirst

thirst = dry mouth & throat drive when to drink, NOT how much to drink

• detected in: brain, heart & kidneys

Types:

1. Hypovolemic thirst = when blood volume drops from loss of extracellular water ] blood needs water

2. Osmotic thirst = when cells need water

→ can experience both types of thirst at the SAME time (ex. sweat a lot), or have ONLY osmotic thirst (ex. after salty meals)

Drive Theory: 2. Thirst - Brain Structure Involved

via brain/heart signals:

Subfornical organ (SFO) + Organum Vasculosum lamina terminalis (OVLT) = sense & regulate internal water balance TOGETHER

• contain receptors that detect the amount of water in the 3rd ventricles cerebral fluid → tell MnPO

• Circumventricular organs = outside blood-brain barrier w direct access to blood circulation → THUS, talk to blood & ventricle using astrocytes

• Osmoreceptors = fire more as ventricle’s volume decreases (like it plump)

Median preoptic nucleus (MnPO) = integrates signals from SFO & OVLT

• also receives signals from baroreceptors in heart arteries: increased pressure in arteries from liquid → signal MnPO

or

via kidney signals:

Angiotensin II = hormone released by kidneys → stimulates SFO & OVLT receptors in brain via cerebral fluid to notify a drop in blood volume

• takes 10-20 min for brain to realize the deficit is gone & to stop sending stimulatory signals → may over drink

note: act of drinking tells brain we’re satisfying the need FASTER than an injection

Drive Theory: 3. Hunger - role of taste

• food selection varies depending on digestive tracts (ex. humans are omnivores)

• taste primaries: sour, sweet, bitter, salty, umami

→ taste is used to detect what type of nutrients are in the good

• balanced meals activate all 5 taste receptors (on sides of papilla)

  • diff taste cells have diff receptors

  • diff neurons in brain are specialized for diff tastes + they’re in multiple areas

Drive Theory: 3. Hunger - sensory-specific satiety

Sensory-specific satiety = the more u eat a food item, the less appealing it becomes

• innate

• BUT, if well balanced, this is less likely to occur

Learned taste aversion = avoid foods associated with illness or poor nutrition

• not innate (based on experience & familiarity)

Learned taste preference = preference for flavour of food, instead of the nutrients in it

• not innate (based on experience & familiarity)

Drive Theory: 3. Hunger - digestive process (basics)

Area postrema = region in brain (outside the blood-brain barrier to detect directly) that induces vomiting if activated by toxins

ex. throw up bad shrimp

Duodenum = small intestine where most digestion & absorption occurs

Drive Theory: 3. Hunger - digestive process

glucose: from carb digestion → for energy

AA: from protein digestion

fatty acids: from fat digestion in intestine

glycerol: from fat digestion in liver

→ digestive process is controlled by autonomic NS (2 metabolic phases)

1. Absorptive Phase = few hrs after meal + living off nutrients arriving from digestion

2. Fasting Phase = drop in blood glucose → body lives off energy stores

Drive Theory: 3. Hunger - Absorptive Phase

absorptive phase = few hrs after meal + live off of nutrients from digestion

• focus on glucose

→ insulin allows body cells to take up glucose from blood + store glucose in muscle/fat cells

• during parasympathetic activation (to digest)

affected by: Diabetes

• Type 1 = pancreas cant produce enough insulin (WBCs killed the beta islet cells)

• Type 2 = tissues are relatively unresponsive to insulin (not enough insulin receptors) → dont take in glucose

→ thus, glucose remains in blood & cells dont get enough sugar

Drive Theory: 3. Hunger - Fasting Phase

fasting phase = glucose levels drop in blood → body uses energy stores

why we don’t need to be constantly eating

→ pancreas secretes glucagon → causes muscle/fat cells to turn glycogen into glucose

• during sympathetic activation (need energy)

Drive Theory: 3. Hunger - Regulating Hunger

Ghrelin = orexigenic peptide hormone that increases eating by signalling orexin to activate ARC (via AgRP neurons)

• synthesized & released from stomach when it has room, NOT just when hungry

  • released fast

Orexin = neuropeptide that increases eating & wakefulness when starving

→ excites ARC

Arcuate Nucleus (ARC) = hypothalamic center for food intake control

• NPY/AgRP neurons : increase hunger by activating ARC

• POMC neurons : decrease hunger by deactivating ARC

→ sends signals to lateral hypothalamus

Paraventricular nucleus (PVN) = regulates amount of eating & metabolic processes (body temp…)

• signalled by ARC neurons

Lateral Hypothalamus = initiates eating + controls feeding behaviour & metabolic responses (controls chewing, swallowing, insulin production, amount of gastric juices)

Ventromedial hypothalamus (VMH) = produces satiety & increases metabolism

• POMC neurons (decrease hunger) deactivate ARC → increases VMH activity → stop eating

Cholecystokinin (CCK) = hormone that signals satiety when food passes thru duodenum

• limits meal size + aids digestion ] provides satiation after a snack

  • higher CCK DOESNT help w weight loss, bc they just eat more small meals

note: smaller meals allow us to absorb more nutrients

Drive Theory: 3. Hunger - Long-term Regulation of Hunger

PYY = hormone released by intestines → suppresses appetite for LONG period (inhibits NPY release)

• long-term satiation, BUT DOESNT decrease the total amount of food u eat

Leptin = hormone secreted by fat cells already full of fat → INHIBITS NPY release → STOPS eating

• reduces meal size & total daily intake !!

• opposite of ghrelin

→ sent to deactivate ARC via POMC neurons

Drive Theory: 3. Hunger - Summary

role of insulin

• allows uptake of glucose into cells from bloodstream

• activates POMC neurons → deactivate ARC → INHIBITS NPY release → decreases eating

Obesity

malnourished DOESNT equal underfed, it means NOT enough nutrients

use: BMI = weight in kg / height in meters

• a qualifier of obesity or leanness

info:

• a global epidemic bc obese ppl exceed the # not overweight

• increased health risks (correlated)

ex. increased risk of Alzheimers

• CANT be characterized by lack of impulse control, inability to delay gratification, or maladaptive eating style

• no obesity or diabetes gene in humans

  • found in mice tho (db - chromosome 4) & (ob - chromosome 6)

• has multiple genetic factors

• epigenetic factors like methylation have been LINKED to obesity

cause: smoking, pollution, stress

ex. Holland kids were methylated by environmental stressor → became fat

Obesity & dieting

Basal metabolism = energy required (set point) for body survival

• metab will increase/decrease to defend a set point weight

• increase quicker after gaining weight

• accounts for 75% of body energy usage - remainder is split b/w digestion & physical activity

→ dieting eats less than basal metabolism

• 10% weight reduction is more practical + less risk of chronic disease

• standard treatment: dietary restriction

• serotonin could play a role in weight control:

  • eating carbs raises serotonin, but for those that crave carbs, serotonin inhibits ur desire for carbs → THUS, SSRIs lower carb eating

• psych therapeutic approaches: treat out-of-control eating as addictive behaviour

• surgery: gastric bypass (limits meal size by removing stomach cells that release ghrelin) → cant eat as much + feel less hungry

Anorexia Nervosa

= restrict food intake to maintain unhealthy weight

• equal prevalence b/w sexes

• most recover (1/3 in 9yrs, 1/3 in 22yrs )

• body dysmorphia

types:

1. restrictor : reduce food intake

2. binge purgor : restrict food intake & PURGE

results:

• changes in brain structure

  • dysfunction in areas for reward system & body image

  • decreased grey matter - only partially recovers

• loss of ovulation, decrease muscle mass

• HIGHEST mortality rate of ALL psych disorders

Bulimia Nervosa

= binging & purging to control weight

• can have no weight loss or increase in weight

• have higher ghrelin levels b/w meals (tells them they’re hungry)

• lower PYY levels → less long-term satiation

• higher relapses than anorexia

• body dysmophria

Binge-eating disorder

= recently eat large amounts of food in short period

• feels uncontrollable

• feel disgust/shame after → try to hide it

Anorexia, Bulimia, Binge Eating

• bulimia is more heritable than anorexia

• anorexia & bulimia may have social environmental causes + genetic links

  • decreased reward system

• eating disorders are usually comorbid w other psych disorders (depression, anxiety, OCD)

• serotonin may play a role