PSY102: BIOLOGICAL BASIS OF BEHAVIOUR

MOTIVATION AND THE REGULATION OF

INTERNAL STATES
LEARNING OBJECTIVES

 Discuss motivation and homeostasis

 Understand hunger and its mechanisms

 Discuss obesity

 Discuss eating disorders

MOTIVATION AND HOMEOSTASIS

 Motivation
 Set of factors
 Initiate, sustain, and direct behaviours

 Why we do what we do

 No motivation centre/area in the brain

MOTIVATION AND HOMEOSTASIS

 Motivation theories
 Instinct theory
Instinct
 complex behaviour
 Unlearned

 Occurs in all members of a species

MOTIVATION AND HOMEOSTASIS

 Theories of motivation
 Instinct theory
 Humans are guided by instincts
 Became popular  since fallen out of favour

 Does not explain why

MOTIVATION AND HOMEOSTASIS

 Theories of motivation
 Drive theory
Body maintains a condition of homeostasis
 Any system is in balance or equilibrium
Need is met drive reduces/goes away
Drive
 Aroused condition
 Individual has to engage in action
MOTIVATION AND HOMEOSTASIS

 Theories of motivation
 Drive Theory
Does not explain all motivation
 Some behaviours/motivations are beyond tissue
needs
Better to define drives as brain states
MOTIVATION AND HOMEOSTASIS

 Theories of motivation
 Incentive Theory
 People are also motivated by external stimuli
 Incentives can be a factor in physiological stimulation too
MOTIVATION AND HOMEOSTASIS

 Theories of motivation
 Arousal theory
 Behaviour led by desire to maintain preferred levels of
arousal
 Sensation seeking
MOTIVATION AND HOMEOSTASIS

 Homeostatic Drives
 System has set points – point of equilibrium
 Deviation from set point
 Initiatesa drive  engages in behaviour back to
equilibrium  homeostasis achieved
MOTIVATION AND HOMEOSTASIS - DRIVES

 Temperature regulation
 Have to maintain internal temperature within
certain limits
 Humans are endothermic
Can regulate internal temperature automatically
 Not truly intentional
Exothermic – require external stimuli
MOTIVATION AND HOMEOSTASIS - DRIVES

 Temperature Regulation
 Preoptic area of hypothalamus
Containswarm-sensitive and cold-sensitive cells
Respond to
 Temperature of blood flowing
 Input from temperature receptors in body

Integrate information  initiate regulatory

response
MOTIVATION AND HOMEOSTASIS - DRIVES

 Thirst
 Body is 70% water
 Critical to bodily functions
 Two types of thirst
 Osmotic thirst
 Hypovolemic thirst
MOTIVATION AND HOMEOSTASIS - DRIVES

 Thirst
 Osmotic thirst
Fluid content decreases in cells
Blood is more concentrated than usual  Water
is drawn from cells into the bloodstream
Detected in organum vasculosum lamina
terminalis (OVLT)
 Communicates with median preoptic nucleus of
hypothalamus  initiates drinking
MOTIVATION AND HOMEOSTASIS - DRIVES

 Thirst
 Hypovolemic thirst
Blood volume drops due to loss of extracellular
water
Feel weak

Detected by receptors where large veins enter

the heart
 Signaled by vagus nerve to nucleus of solitary tract in
medulla  median preoptic area of hypothalamus
MOTIVATION AND HOMEOSTASIS - DRIVES

 Thirst
 Hypovolemic thirst
Detected by receptors in kidneys
 Release hormone called Renin  increase presence
of angiotensin II (hormone) stimulates subfornical
organ (SFO) median preoptic nucleus
MOTIVATION AND HOMEOSTASIS - DRIVES

 Thirst
 Time lag between drinking and arrival of water in
tissues
 Must stop drinking before feeling satisfied
 Satiety mechanism
 Satisfaction of appetite
 Receptors in stomach monitor presence of water

 Infusion of water in liver  presence of water receptors?

HUNGER

 Complex drive
 Eating provides energy and fuel for activity, growth
and repair of tissue, and maintaining body
temperature
 Variable set point

 Variety of different kinds of nutrients

HUNGER – ROLE OF TASTE

 Distinguish between nutritious, nonnutritious,

and toxic
 Diet requires variety/combinations of nutrients
 Choose right foods in right amounts
HUNGER – ROLE OF TASTE

 5 primary taste sensations

 Sour

 Sweet

 Bitter

 Salty

 Umami

 Complex taste is a combination of primary

sensations
HUNGER – ROLE OF TASTE

 Preferences
 Sweet – fruits and carbohydrates
 Slightly salty – chloride and sodium ions

 Umami – proteins

 Avoid
 Overly sour – spoiled
 Bitter - toxic
HUNGER – ROLE OF TASTE

 Taste neurons  thalamus  insula (primary

gustatory area in frontal lobes
 Pass through nucleus of solitary tract in medulla
(NST; link to thirst)
 Specialised areas for different taste sensations
HUNGER – ROLE OF TASTE

 sensory-specific satiety
 The more you eat of a specific food, the less
appealing it becomes
 Variety of foods  eat more

 Happens in NST
HUNGER – ROLE OF TASTE

 Learned taste aversion

 Avoidance of foods associated with illness or poor
nutrition
 Usually learned between ages 6 – 12
HUNGER – ROLE OF TASTE

 Learned taste preferences

 Preference for a flavour of food that contains a
nutrient
 Nutrients that aren’t directly tasted

 Requires pairing of taste with a benefit  constant

over several days
 Smell has a significant effect
HUNGER - DIGESTION

 Process
 Occurs primarily in small intestine
 Food is broken down into usable forms
Carbohydrates  simple sugars incl. glucose
Proteins  amino acids

Fats  fatty acids and glycerol

 Under control of autonomic nervous system

HUNGER - DIGESTION

 Absorptive phase
 Few hours
 Body lives off nutrients arriving from digestive
system
 Increased glucose  shifts from sympathetic to
parasympathetic NS
HUNGER - DIGESTION

 Absorptive phase
Insulin
Hormone

Allows body to take up glucose for energy

and to store excess nutrients
Diabetes
Inefficientuse of insulin
Chronically hungry
HUNGER - DIGESTION

 Absorptive phase
 Storage of nutrients for energy later
Glucose  glycogen (short term)
Glucose  fats

Fats  triglycerides
HUNGER - DIGESTION

 Fasting phase
 Blood glucose level drops
 Body uses energy stores
 Secretion of glucagon
convert glycogen back to glucose  nervous
system
Break down of fats  muscles and organs

 Starvation
– muscle proteins broken down 
amino acids  glucose
HUNGER - DIGESTION

 Phases of digestion
 Lateral hypothalamus
Initiateseating
Controls feeding behaviour

Metabolic reactions
HUNGER - DIGESTION

 Phases of digestion
Paraventricular nucleus (PVN)
Initiates
eating (less effectively)
Rehulates metabolic processes
Body temp, fat storage, cellular metabolism
HUNGER – STARTING A MEAL

 3 major signals
 Glucoprivic hunger – low supply of glucose
 Lipoprivic hunger – low supply of fatty acids

 Ghrelin - Stomach’s store of nutrients depleted

HUNGER – STARTING A MEAL

 Glucose and fatty acids

 Monitored by liver
 Deficit vagus nerve  NST  arcuate nucleus of
hypothalamus  release neuropeptide Y and
agouti-related protein PVN and lateral
hypothalamus  increase eating and reduce
metabolism
HUNGER – STARTING A MEAL

 Ghrelin
 Hormone produced in stomach
 Released into bloodstream as stomach empties

 Reaches arcuate nucleus  passes through blood-

brain barrier
 Levels rise before each meal  decline sharply
after eating
HUNGER – ENDING A MEAL

 Satiation adjusted according to nutritional

value of food
 Optimal satiation involves interaction
 Mouth

 Stomach

 Intestine
HUNGER – ENDING A MEAL

 2 signals
 Stomach volume
 Cholecystokinin
HUNGER – ENDING A MEAL

 Stomach volume
 Stretching
stomach  vagus nerve  NST
 Dependent on nutritional value too
 Release peptides brain monitors nutrients
 Vagus nerve or blood stream
HUNGER – ENDING A MEAL

 Cholecystokinin (CKK)
 Peptide released as food passes duodenum
 Detects fats gall bladder inject bile fats broken
down
 Stimulate vagus nerve receptors NST 
hypothalamus
 Affects meal size
HUNGER – LONG-TERM CONTROLS

 Peptide YY
 Appetite suppressing hormone
 Released in intestine  response to food

 Bloodstream  arcuate nucleus  inhibits NPY-

releasing neurons (initiates eating)
 Slow acting – does not affect current meal
HUNGER – LONG-TERM CONTROLS

 Leptin
 Hormone that inhibits eating
 Secreted by fat cells

 Amount in blood is proportional to body fat

 Regulates meal size – response to long term stores

of fat
HUNGER – LONG TERM CONTROLS

 Insulin
 Levels proportional to body fat
 Act on arcuate nucleus
 InhibitsNPY neurons
 Activate POMC cells – inhibit PVN and lateral
hypothalamus
HUNGER – LONG-TERM CONTROLS

 Orexin
 Neuropeptide

 increases appetite and induces eating

 Activated by – leptin/glucose are low; ghrelin is
high
 Neurons located in lateral hypothalamus

 Activate NPY neurons and inhibit POMC cells

OBESITY

 Body Mass Index (BMI)

 Divideweight (kg) by height (m2)
 25-29 = overweight

 30-39 = obese

 40+ = morbidly obese

OBESITY

 Associated with numerous health risks and

reduced quality of life
 Environmental influences
 Diet

 Activity
level
 Sleep deprivation
OBESITY – GENETIC INFLUENCES

 Adoption and twin studies – moderate

relationship
 Several genes linked with obesity
 Rare in population
 More than 40 genetic variants contribute to obesity
and fat distribution
OBESITY – GENETIC INFLUENCES

 Epigenetic characteristics
 Inheritable traits result from modification of gene
expression
 Methylation – attachment of molecules to a gene

 Accounts for more variation in obesity

OBESITY

 Reduced metabolism
 Basal metabolism – energy required to fuel the
brain and other organs
 Lower basal metabolism linked to increased weight
gain
 Shifts with weight gain/loss
OBESITY

 Treatments
 Dietary restriction
 Exercise

 Medication – not promising

 Increaseserotonin activity  reduce carb intake
 Leptin  protects against weight loss in deprivation

 Obesityis an addiction
 Surgery- gastric bypass
EATING DISORDERS – ANOREXIA NERVOSA

 Obsessive disorder
 Restricts food intake
 Maintains weight and dangerously low levels
 Excessive diet and exercise
 Body image distortions

 Do not seek help

EATING DISORDERS - ANOREXIA

 Two subgroups
 Restrictors

 Binge-purgers
EATING DISORDERS - ANOREXIA

 correlates
 Deficitsin brain volume
 Dysfunction in areas involved with reward, emotion,
and processing of bodily information
 Obsessive-compulsve traits, harm avoidance, adn
perfectionism
EATING DISORDERS - ANOREXIA

 Increased levels of NPY and ghrelin

 Decreased levels of leptin
EATING DISORDERS – BULIMIA NERVOSA

 Binge-purge cycles
 Often look normal weight

 Increased ghrelin levels does not decrease

as much after meals
 PYY does not increase as much after meals
EATING DISORDERS – BINGE EATING DISORDER

 Frequently eat large amounts of food during

short periods of time
 Feelings of loss of control

 Typically overweight
EATING DISORDERS - FACTORS

 Environmental
 Culturalnorms
 Family environment – lack of control
EATING DISORDERS - FACTORS

 Genetic
 High heritability (56% - anorexia; 54-83% bulimia;
45% binge eating)
 Polygenic

 Comorbid psychological disorders

EATING DISORDERS - NEUROTRANSMITTERS

 Serotonin
 Involved in eating behaviour and psychological
correlates of eating disorders
 Low levels in anorexia

 Imbalanace in activity at serotonin receptors

 Increasedbinding 5HT1A - inhibits neural activity
 Decreased binding 5HT2A - increases activation
EATING DISORDERS - NEUROTRANSMITTERS

 Dopamine
 Low levels in anorexia
 Eating increases dopamine release
EATING DISORDERS - NEUROTRANSMITTERS

 Cannabinoids
 Play role in food intake and reward
 Anorexia and bulimia – more cannabinoid receptors
in insula