Neural Mechanisms in Eating Behaviour Flashcards
Homeostasis
Involves mechanisms which both detect the state of internal environment + also correct the situation to restore that environment to its optimal state
Eating = increase glucose levels = VMH = Satiety = Stop eating = Decrease glucose levels = LH activated = HUNGER
Lateral Hypothalamus
Damage to rats LH = Aphagia + stimulation elicits feeding behaviour = on switch for eating
Neurotransmitter = Neuropeptide Y = causes rats to begin feeding even when satiated
Repeated injections of NPY = obesity in rats in just few days
Ventromedial hypothalamus
Damage = hyperphagia = rats overeat Stimulation = inhibited feeding = VMH stops feeding as result of many glucose receptors
Damage to nerve fibres in VMH = also damage Paraventricular nucleus
Damage of PVN causes hyperphagia
PVN detects specific foods out body needs = CRAVINGS
Cognitive aspect of food
Images of food we have in memory
Food related sights + smells
Neural control of factors in hunger originate in 2 main brain areas
Amygdala
Inferior prefrontal cortex
Amygdala
Selection of foods on basis of previous experience
Rolls + Rolls:
Rats with Amygdala removed = cause animals to consume both familiar + novel foods indiscriminately
Those with Amygdala would initially avoid novel foods + consume only the more familiar foods
Inferior frontal cortex
Receives messages from olfactory bulb
Odours influence taste of foods,
Damage to inferior frontal cortex is thought to decrease eating because of diminished sensory responses to food odour + taste
Limitations of a homeostatic explanantion
To be adaptive it must both anticipate + prevent energy deficits not just react to them
= Theory that hunger + eating are triggered only when energy resources fall below desired level is incompatible with the harsh reality in which systems evolved
To be adaptive, it must promote levels of consumption that maintain bodily resources above optimal level to help when there is future lack of food
An Evolutionary Approach
Suggest that primary stimulus for hunger + eating is food’s +ve incentive value i.e people eat because they normally develop a relish for particular tastes that are in nature associated with foods that promote our survival
Stress + Hunger
Lutter et al
Body produces extra quantities of hormone ghrelin in response to stress = reduces depressive + anxious behaviours BUT also boosts appetite = comfort eating
Blocking body’s response to ghrelin = may help people with a tendency to comfort eat
Problems with LH
Damage to LH caused deficits in other aspects of behaviour (Thirst + sex)
Research: Eating behaviour is controlled by neural circuits that run through brain not just hypothalamus
Although LH plays important role in controlling eating behaviour, it is not the brain’s eating centre
NPY limitations
Doubt whether normal function is to influence feeding behaviour
Mice manipulated not to have NYP = no subsequent decrease in feeding behaviour
The hunger stimulated by injections of NPY may be experimental artefact
Gold
Lesions restricted to VMH alone did not result in hyperphagia + only produced overeating when they included other areas e.g. PVN
However subsequent research has failed to replicate this studies findings
Syndrome
Kluver-bucy Syndrome
Damage to amygdala + inferior prefrontal cortex = explain this syndrome
P’s show increase appetite, indiscriminate eating + attempts to eat non-food items
Research = food cues no longer accurately represent real reward level of indi
Psychological evidence to support Amygdala
Supports claim that Amygdala participates in emotional processing of olfactory stimuli
Exposure to unpleasant odours produced significant blood flow increases to amygdala where as non-aversive odours didn’t increase blood flow
Increased blood flow to amygdala was associated with with subjective ratings of the perceived of perceived unpleasantness of stimuli
