Neural Mechanisms and Eating Behaviour

• Hypothamlamus is responsible for homeostasis.
  • body temperature
  • urine levels
  • intake of food and drink

• Decline in glucose levels - hunger
• causes the individual to search and consume food.

• Damage to the LH in rats caused them to stop eating
• Stimulation through NPY brings about feeding behaviour (Wickens)

• Food = glucose levels increase
• VMH causes feelings of satiation and signals stop eating.
• Research founf that damage resulted in hyperphagia (overeating)
• stimulation - inhibit and stop feeding
• Damage also causes damage to the PVN - believed to now cause hyperphagia

• Located at the front of the brain
• influences food choice through previous experience
• Rolls and Rolls - surgically removed the amygdala in rats which then consumed novel foods.

• Hunger mechanism should be adaptive to anticipate and prevent deficits in energy
• claims that hunger/eating behaviour is triggered when energy resources fall below optimal is inconsistent with the harsh environment this mechanism would have developed.

• Alternative explanations
• Primary influence for hunger/eating is food's pos. incentive value

i.e people eat because they develop a taste for foods that promote survivial

• Marie et al - genetically manipulated mice
  • did not make NPY
  • no decrease in feeding behaviour
• suggests NPY injections may only be an experimental side effect and cause behaviour that may not translate into real life scenarios

• Gold - lesions to the VMH alone did not produce overeating
  • only did when lesions included the PVN
  • However, recent studies do not support this
• Now PVN has another function = detect specific foods our body needs which may account for cravings

• Lutter - hunger and eating may not be purely under neural control
  • body produces extra quantities of ghrelin in response to stress
• Ghrelin also boosts appetite - increased comfort eating
• blocking the body's response to ghrelin may help people with a tendency to comfort eat, lose weight