Neural Mechanisms involved in eating behaviour

The Dual Control Model of Feeding

• A decline in glucose activate the Lateral Hypothalamus.
• Activity within the LH gives rise to hunger.
• Hunger motivates the search for ad consumption of food.
• Food is broken down to release glucose.
• Glucose activates the Ventromedial Hypothalamus.
• Activation of the VMH causes a feeling of satiety.
• Satiety inhibits further feeding.

EVALUATION: Research showed that the effects of damaging the VMH were not permenant. After initial increase, body weight stabilised. Damaged rates were in either a DYNAMIC OR STATIC phase of weight gain. It is 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 extrapilate the results either.

Teitelbaum found that damaged VMH rats were lazier at obtaining food than normal rats, especially those in the static phase. They were also fussier about eating. This suggests that once they get fat, they get fussy. It also suggests that damage to the VMH doees not increase motivation, but if the satiety centre is also damaged so you are never full, you should be motivated to eat and eat anything you could.

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

THE DUAL CONTROL THEEORY CAN'T EXPLAIN THE LONG TERM EFFECTS OF DAMAGE TO TH DIFFERENT PARTS OF THE HYPOTHALAMUS.

Set Point Theory

Key and Powley came up with the term 'set point' to refer to a level of fat in the body that is kept a certain leve. Fat cells are elastic. If animals are given access to adequate supplies of food and left alone, the fat cells stay in constant size. This indicates some sort of regulatory process. Eg. if we eat too much or too little we have homeostatic mechanisms that alter our metabolism and appetite to return us to our original weights.

Fat is the most energy dense substance in the body and the set point theory suggests we need to regulate our level of fat to regulate the storage of energy. The natural or ideal level of fat in your body is the set point. The set point determines what level of fat the body will return to.

It was now assumed that the damaged VMH rat had a defect in fat regulation: a high set point, caused by damage to their VMH.

According to set point theory:

• LH damage reduces the set point for body weight, rats with damage maintain body weight at a new lower level.
• VMH damage increases the set point for body weight, so rats with damage maintain body weight at a higher level.

Rats were starved so that they lost body weight before recieving LH damage. According to set point theory, the LH damage should have little or no effect on these rats because starvation would reduce the body weight so that it was…