AO1 Neural machanism in eating behaviour

Homeostasis involves mechanisms which detect the state of the internal environment and correct the situation to restore that environment to its optimal state. Hoever, there is a significant time lag between mechanisms operating to restore equilibrium and the body registering their effect. For example, by the time a person has eaten enough to restore energy levels, only a small amount of food has been digested. Therefoere the receptors responsible for detecting nutrient levels have insufficient 'data' to turn off eating.

There are two seperate systems in the body for turning eating on and off. In humans, glucose levels play an important role in producing feeling of huner. Hunger increases and glucose levels decrease. A decline in glucse in the blood activates a brain area called the lateral hypothalamus, resulting in feelings of hunger. The person then eats food, causing the glucose levels to rise again, and this activates the ventromedial hypothalamus and leads to feelings of satiety. This in turn inhibits further feeding.

The role of the lateral hypothalamus LH was discovered when researchers discovered that damage to the LH in rats caused a condition called aphagia (greek for the absence of eating) and that stimulation of the LH caused feeding behaviour. These two findings led researchers to conclude that they had found the 'on' switch for eating. A neurotransmitter found in the hypothalamus called neuropeptide Y (NPY) is particularly important in turning on eating. When injected into the hypothalamus of rats, NPY causes them to immediately begin feeding, even when satiated. (Wickens)

The role of the ventomedial hypothalamus (VMH) was discovered when researchers observed that damage to the VMH caused a condition called hyperagia (greek for over eating) in rats. Similarly, stimulation of the VMH inhibits feeding. Reseachers concluded that the VMH signals 'stop eating' as a result of the many glucose receptors in the area.