Discoveries made in the 1940s and 1950s focused the attention of researchers interested in ingestive behaviour on two regions of the hypothalamus: the lateral area and the ventromedial area. For many years investigators believed that these two regions controlled hunger and satiety, respectively, one was the accelerator and one was the brake. The basic findings were these. After the lateral hypothalamus was destroyed, animals stopped eating or drinking (Anand and Brobeck, 1951). Electrical stimulation of the same region would produce eating, drinking, or both behaviours. Conversely, lesions of the ventromedial hypothalamus produced overeating that led to gross obesity, whereas electrical stimulation suppressed eating (Hetherington and Ranson, 1942). .
However, Stricker and Zigmond (1976), reviewed the evidence and concluded that behvioural effects (catatonic behaviour of rats) of lateral hypothalamic lesions, including eating suppression, were produced by damage to axons that pass through the region, known to play a role in the control of movement. Also injections activate two populations of neurons located in the lateral hypothalamus that stimulate hunger and decrease metabolic rate. The neurons secrete two different peptide neurotransmitters; melanin-concentrating hormone (MCH) and orexin. Injections of either one into the lateral ventricles or various regions of the brain induce eating. In addition if rats are deprived of food mRNA levels for MCH and orexin increase in the lateral hypothalamus (Qu et al., 1996). .
The axons of MCH and orexin neurons travel to a variety of brain structures known to be involved in motivation and movement, including the neocortex, reticular formation and thalamus. These neurons also have connections with neurons in the spinal cord that control the autonomic nervous system, which can explain how they can affect the body's metabolic rate (Nambu et al., 1999).
