Neural Mechanisms Explanation of Aggression
Discuss the role of neural mechanisms involved in controlling eating and satiation. 8+16 or 4+8
1. The body is regulated by homeostatic mechanisms; concerning food intake this is dependent on glucose levels. Decrease in glucose levels means hunger levels increase, whereas an increase in glucose levels means satiation is reached.
2. Research has revealed two significant eating centres in the hypothalamus; the lateral hypothalamus (LH) and the ventro-medial hypothalamus (VMH). Research from the 1940s onwards has showed that lesioning tiny areas in the LH in rats, dogs and other mammals led to aphagia (lack of interest in food and eating), the animals seemingly unaware they were starving.
3. When we are full the Ventro Medial Nucleus (VMN) of the hypothalamus is activated which inhibits eating and satiety is reached. Blood glucose levels drop again after eating and the Lateral hypothalamus is activated (which initiates feeding) and we become hungry and the process starts again. Damage to the VMH in animals caused overeating (hyperphagia).
4. There are several neurotransmitters in the body which are also involved in eating regulation. Ghrelin is a hormone which is released when the stomach is empty so it triggers eating. The second most important hormone is leptin and this is released from adipocytes, and the more fat a person has the more leptin is released and it acts as a satiety signal so stops food intake. Leptin reduces the release of Neuropeptide Tyrosine (NPY), an amine that influences hunger stimulation: normal leptin levels reduce the production of NPY, in turn reducing hunger and eating.
5. Licinio et al (2004) observed three morbidly obese adults from a Turkish family with a genetic deficiency in leptin to demonstrate that when given leptin supplements, their body weight and eating reduced to a ‘normal’ level, thus supporting the importance of leptin in controlling eating and satiety.
6. Matochik et al (2005) also studied Effect of Leptin
1. The body is regulated by homeostatic mechanisms; concerning food intake this is dependent on glucose levels. Decrease in glucose levels means hunger levels increase, whereas an increase in glucose levels means satiation is reached.
2. Research has revealed two significant eating centres in the hypothalamus; the lateral hypothalamus (LH) and the ventro-medial hypothalamus (VMH). Research from the 1940s onwards has showed that lesioning tiny areas in the LH in rats, dogs and other mammals led to aphagia (lack of interest in food and eating), the animals seemingly unaware they were starving.
3. When we are full the Ventro Medial Nucleus (VMN) of the hypothalamus is activated which inhibits eating and satiety is reached. Blood glucose levels drop again after eating and the Lateral hypothalamus is activated (which initiates feeding) and we become hungry and the process starts again. Damage to the VMH in animals caused overeating (hyperphagia).
4. There are several neurotransmitters in the body which are also involved in eating regulation. Ghrelin is a hormone which is released when the stomach is empty so it triggers eating. The second most important hormone is leptin and this is released from adipocytes, and the more fat a person has the more leptin is released and it acts as a satiety signal so stops food intake. Leptin reduces the release of Neuropeptide Tyrosine (NPY), an amine that influences hunger stimulation: normal leptin levels reduce the production of NPY, in turn reducing hunger and eating.
5. Licinio et al (2004) observed three morbidly obese adults from a Turkish family with a genetic deficiency in leptin to demonstrate that when given leptin supplements, their body weight and eating reduced to a ‘normal’ level, thus supporting the importance of leptin in controlling eating and satiety.
6. Matochik et al (2005) also studied Effect of Leptin