eating behaviour Flashcards
behaviour
response of an organism to a stimulus
behaviours can be
unconscious -e.g. reflex of stepping on sharp nail, single doesn’t reach brain
conscious- voluntary
higher level behaviour require
motivation
motivation
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)
WC model (old fashioned idea)
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
pheneas gage
inhibitory sense in frontal cortex destroyed
eating is controlled by
the hypothalamus
hypothalamus
develops from the diencephalon of the forebrain
central part of the homeostatic mechansims involved in eating (and sexual behaviour)
controls things from autonomic system
‘energy balance’
between food in and energy used up
it should be equal
anabolism
building up macro molecules
catabolism
breaking down macromolecules for energy us e
the requirements for energy are continuous otherwise
neurones will kills without glucose in a matter of mintues
if anabolism> catabolism
obestity
if catabolism > anabolism
starvation
requirements for energy change depending on
time of day time of month time of year time of life level of activity state of health
a lesion of both sides of a rat’s lateral hypothalamus caused
anorexia
bilateral lesions of the ventromedial hypothalamus caused
overeating and obesity
historically the lateral hypothalamus was called the
hunger cnetre
historically the lateral ventromedial hypothalamus was called
the satiety centre
Kennedy (1953)
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
1960s Coleman
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
1994 Friedman
isolated the protein responsible - they called it Leptin (produced by fat)
treating ob/ob (homozygous) obese mice reversed the eating disorders
leptin
releasd by fat cells to decrease eating behaviour and increase energy expedniture
in times of starvation leptin defiency stimulates
eating behavioural and reduced energy expenditure and reduces reproductive competence
high levels of leptin act on receptors on neurones in which nucleus
arcuate nucleus of the hypothalamus
the neurones in the hypothalamus activated contain neurotransmitters:
alpha-MSH and CART
the neurones in the hypothalamus send projections to
- 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
stimulation of the paracentrivular nucleus
acts to release TSH and ACTH from the anterior pituitary gland
TSH and ACTH act on
the thyroid and adrenal gladness to increase basal metabolic rate (BMR)
stimulation of the brainstem and upper spinal cord increases sympathetic activity causing
raised body temperature (and increased basal metabolic rate)
feeding behaviour is inhibited by
somatic motor activity through stimulation of cells int he lateral hypothalamus
injection of alpha MSH and CART mimic
effect of raised leptin levels and can be called anorexic peptides (appetite suppressors)
low levels of leptin switch off
the effects of alpha MSH and CART
falling levels of leptin stimulate other neurones in the arcuate nucleus
these contain NPY and AgRP
NPY and AgRP
- inhibit TSH and ACTH secretion
- Activate the parasympathetic nervous system
- stimulate feeding behaviour
- are called orexigenic peptides
Gherelin
is released into bloody stream from an empty stomach and stimulates NPY and AgRP release to stimulate feeding
sateity singals
are short term signals that are generated when we eat and during initial digestions (the prandial period)
they terminate eating and inhibit future feeding
when the satiety signals decline
the orexigenic signals dominate and stimulate feeding again
the termination of feeding by satiety factors
distention of the stomach
chloecystokinin and insulin
hedonistic motivation
we enjoy eating!
mood and food
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
