AQA A2 Psychology Unit 3 Eating Behaviour: The Role of Neural Mechanisms Involved In Controlling Eating And Satiation Notes


A2 Psychology Unit 3 Eating Behaviour: The Role Of Neural Mechanisms Involved In Controlling Eating And Satiation Notes

What You Need To Know:

  • The role of neural mechanisms involved in controlling eating and satiation.

The Role Of Neural Mechanisms Involved In Controlling Eating And Satiation:

We eat in order to function and survive. When and how much we eat is largely determined by our metabolism (the rate at which the body uses energy). Several physiological mechanisms try to maintain this energy homeostasis (balance).

Set point theory of homeostasis:

  • Our body weight is regulated to a biologically determined `target`.
  • If we eat too little or too much, homeostatic mechanisms alter our metabolism and appetite accordingly, in order to return us to our original weight.
  • It becomes difficult for homeostatic mechanisms to do this if we persistently over-eat or under-eat and so we may settle on a new weight.

Neural mechanisms controlling eating:

The main area of the brain involved in the regulation of appetite is the hypothalamus.

The role of the hypothalamus:

  • The Lateral hypothalamus (LH) also known as Lateral Nucleus (LN) produces the experience of hunger which leads to eating. The damage to the LH results in dramatic reductions in food intake (aphagia).
  • The Ventromedial hypothalamus (VMH) also known as Ventromedial Nucleus (VMN) produces feelings of being full (satiation. The damage to VMH results in overeating (hyperphagia).
  • The Paraventricular nucleus (PVN) integrates signals that influence metabolic and digestive processes. The increased levels of Neuropeptide Y (NPY) in the PVN promote increased food intake and weight.

Baylis et al (1996) - VMN lesioning in rats.

Method: Two symmetrical lesions (injuries) were made in the VMN of eight male and five female rats. Their body weight was later compared with age-matched controls.

Results: The rats with lesions in their VMN had become obese, while the control rats had not.

Conclusion: Lesions in the VMN cause hyperphagia (overeating) and obesity, so the VMN must play a role in satiation.

Evaluation: This was a very small sample using only one breed of rat, so the findings can't be generalised. Also, other tissues surrounding the VMN might have been damaged when the lesions were created, so it might not necessarily just be the VMN that is involved.

Winn et al (1980) - LN lesioning in rats.

Method: The toxin NMDA was used to make leisons in the LN of rats. A small dose (lesions in LN only) and a large dose (lesions spread to adjacent areas) condition was used, and there was also a control group.

Results: Rats that had the small dose of NMDA showed no changes in their eating behaviour after a brief recovery period. However, rats that had the large dose showed long-term deficits in their eating behaviour.

Conclusion: Damage to the hypothalamus impairs feeding responses, but the


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