eating behaviour

Question 1

behaviour

Answer 1

response of an organism to a stimulus

Question 2

behaviours can be

Answer 2

unconscious -e.g. reflex of stepping on sharp nail, single doesn’t reach brain

conscious- voluntary

Question 3

higher level behaviour require

Answer 3

motivation

Question 4

motivation

Answer 4

driving force behind a behaviour and can be simple (e.g. the need to urinate, eat, drink) or complex (e.g. the ‘need’ to sing and dance when we’re happy)

Question 5

WC model (old fashioned idea)

Answer 5

the water cistern fills up (increasing motivation) until it reaches its limit

flushing releases the behaviour and the motivation is low

gradually the motivation builds up again until there needs to be another release

works at a crude level for some behaviours but not all

Question 6

pheneas gage

Answer 6

inhibitory sense in frontal cortex destroyed

Question 7

eating is controlled by

Answer 7

the hypothalamus

Question 8

hypothalamus

Answer 8

develops from the diencephalon of the forebrain

central part of the homeostatic mechansims involved in eating (and sexual behaviour)

controls things from autonomic system

Question 9

‘energy balance’

Answer 9

between food in and energy used up

it should be equal

Question 10

anabolism

Answer 10

building up macro molecules

Question 11

catabolism

Answer 11

breaking down macromolecules for energy us e

Question 12

the requirements for energy are continuous otherwise

Answer 12

neurones will kills without glucose in a matter of mintues

Question 13

if anabolism> catabolism

Answer 13

obestity

Question 14

if catabolism > anabolism

Answer 14

starvation

Question 15

requirements for energy change depending on

Answer 15

time of day
time of month
time of year
time of life
level of activity 
state of health

Question 16

a lesion of both sides of a rat’s lateral hypothalamus caused

Answer 16

anorexia

Question 17

bilateral lesions of the ventromedial hypothalamus caused

Answer 17

overeating and obesity

Question 18

historically the lateral hypothalamus was called the

Answer 18

hunger cnetre

Question 19

historically the lateral ventromedial hypothalamus was called

Answer 19

the satiety centre

Question 20

Kennedy (1953)

Answer 20

proposed that the brain monitors fat levels and acts to maintain them ‘lipostatic hypothesis’

a signal from fat to the brain was hypothesised to tell the brain the fat levels

Question 21

1960s Coleman

Answer 21

proposed a soluble factor in obese mice (from the ob gene) ‘fooled’ the brain into thinking fat levels were normal, so the mouse continued eating

Question 22

1994 Friedman

Answer 22

isolated the protein responsible - they called it Leptin (produced by fat)

treating ob/ob (homozygous) obese mice reversed the eating disorders

Question 23

leptin

Answer 23

releasd by fat cells to decrease eating behaviour and increase energy expedniture

Question 24

in times of starvation leptin defiency stimulates

Answer 24

eating behavioural and reduced energy expenditure and reduces reproductive competence

Question 25

high levels of leptin act on receptors on neurones in which nucleus

Answer 25

arcuate nucleus of the hypothalamus

Question 26

the neurones in the hypothalamus activated contain neurotransmitters:

Answer 26

alpha-MSH and CART

Question 27

the neurones in the hypothalamus send projections to

Answer 27

• the lower brain stem and spinal cord
• paraventricular nucleus of the spinal cord
• paraventricualr nucleus of the hypothalamus
• lateral hypothalamus

these inputs stimulate a co=ordinated response to high leptin levels

Question 28

stimulation of the paracentrivular nucleus

Answer 28

acts to release TSH and ACTH from the anterior pituitary gland

Question 29

TSH and ACTH act on

Answer 29

the thyroid and adrenal gladness to increase basal metabolic rate (BMR)

Question 30

stimulation of the brainstem and upper spinal cord increases sympathetic activity causing

Answer 30

raised body temperature (and increased basal metabolic rate)

Question 31

feeding behaviour is inhibited by

Answer 31

somatic motor activity through stimulation of cells int he lateral hypothalamus

Question 32

injection of alpha MSH and CART mimic

Answer 32

effect of raised leptin levels and can be called anorexic peptides (appetite suppressors)

Question 33

low levels of leptin switch off

Answer 33

the effects of alpha MSH and CART

Question 34

falling levels of leptin stimulate other neurones in the arcuate nucleus

Answer 34

these contain NPY and AgRP

Question 35

NPY and AgRP

Answer 35

• inhibit TSH and ACTH secretion
• Activate the parasympathetic nervous system
• stimulate feeding behaviour
• are called orexigenic peptides

Question 36

Gherelin

Answer 36

is released into bloody stream from an empty stomach and stimulates NPY and AgRP release to stimulate feeding

Question 37

sateity singals

Answer 37

are short term signals that are generated when we eat and during initial digestions (the prandial period)
they terminate eating and inhibit future feeding

Question 38

when the satiety signals decline

Answer 38

the orexigenic signals dominate and stimulate feeding again

Question 39

the termination of feeding by satiety factors

Answer 39

distention of the stomach

chloecystokinin and insulin

Question 40

hedonistic motivation

Answer 40

we enjoy eating!

Question 41

mood and food

Answer 41

some foods produce changes in mood via serotonin

post absorption of food (especially carbohydrates) elevates serotonin levels

typical to see carb rich foods during stress