NEURAL MECHANISMS INVOLVED IN CONTROLLING EATING BEHAVIOUR

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Miller's Rat Study

This rat was part of an experiment by Miller. It had a portion of its brain removed; the ventromedial hypothalamus, a brain structure thought to be related to the control of eating.

After the surgery, the VMH rat with constant access to tasty food will eat until it's twice normal weight. The fat rat demonstrates excessive eating known as hyperphagia. 

Rats also had their lateral hypothalamus removed that the rats seemed to stop eating - also known as aphagia.

Damage to the lateral hypothalamus caused the absence of eating and stimulation to the lateral hypothalamus elicits eating behaviour.

Damage to the ventromedial hypothalamus caused overeating and stimulation to the ventromedial hypothalamus inhibited eating.

Miller concluded that the lateral hypothalamus was the 'feeding centre' and the ventromedial hypothalamus was the 'satiety centre'. The findings seemed to support a model called the Dual Control Model of Feeding which was based on a homeostatic view of hunger and satiety.

THE DUAL-CONTROL MODEL OF FEEDING

  • A decline in glucose activates the lateral hypothalamus (LH).
  • Activity within the LH gives a rise to hunger.
  • Hunger motivates the search for and consumption of food.
  • Food is broken dow to release glucose.
  • Glucose activated the VMH.
  • Activation of the VMH causes a feeling of satiety.
  • Satiety inhibits further feeding.

Evaluation:

 To reflect this idea, the damaged VMH rats are said to be in either a dynamic or static phase of weight gain. It's clear that the simple Dual-Control theory cannot explain these results. The damaged VMH rats were able to reach satiety despite the absence of their satiety centre, this shouldn't be the case according to the model. We can't extrapolate the results either, due to the fact that the study was conducted on rats.

Researchers started to delve deeper into this idea. Teitelbaum found that the damaged VMH rats were lazier at obstaining food than the normal rats, especially those in the static phase. They were also fussier about eating, eg. if the food had quinine added to make it tase bitter or if the food was stale. This suggests that once they get fat, they get fussy. It also suggests that damage to the VMH does not increase motivation, but if the satiety centre is also damaged so you are nevver full, you should be motivated to eat anything you could. 

This observation of behaviour in fat rats seems to correspond to ovese humans, they eat fewer peanuts if they have to shell them.

Research also foud similar things when the LH was damaged - initially this decreased eating, but again this effect was not permanent - recovery occured.

The dual control theory cannot explain the long term effects of damagge to the different parts of the hypothalamus.

SET POINT THEORY

Keeley and Powley coined the term 'set point' to refer to a level of fat in the body that is kept at a certain level. Fat cells are elastic. If animals are given access to adequate…

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