Notes for A2 Psychology Unit 3 Eating Behaviour The Role of Neural Mechanisms

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 showedlong-term deficits in their eating behaviour.

Conclusion: Damage to the hypothalamus impairs feeding responses, but the LN maynot have as much of an effect as previously thought.

Evaluation: This research is useful as it shows that the localisation of brain function ismore complex than originally thought. However, this was an exploratory study to test whether NMDA was an effective toxin for use on the hypothalamus and wasn't originally intended to investigate hunger. Therefore all the relevant variables may not have been controlled, reducing the reliability of the results.

The role of ghrelin:

• Ghrelin is a hormone secreted from the mucous membrane of an empty stomach.
• Contributes to eating behaviour by inhibiting signals to the brain that indicate satiety.
• When food is eaten secretion of ghrelin stops.
• Lutter et al (2008) found that, in mice, hunger, stress and anxiety are associated with ghrelin.

The role of glucose (glucostatic theory):

• Blood glucose (sugar) levels are monitored by sensors in the liver and hypothalamus.
• The body consumes energy in the form of glucose.
• A decline in blood glucose levels triggers a drive to eat in order to replenish these glucose levels and maintain energy homeostasis.
• Whilst a drop in glucose concentration increases feelings of hunger, increases in glucose are related to feelings of satiety.

Problems with glucostatic theory:

• Blood glucose levels decline slightly a few minutes before eating but reverse just prior to eating. This happens even if no food is then eaten. This suggests that it is the brain initiating a dip in blood sugar levels prior to eating.
• A number of physiological changes are associated with eating, not just glucose levels. E.g. Woods et al (2000) found, in experiments on rats, that body temperature also fluctuates.
• Fats are also used for energy homeostasis, so it is likely that consumption of food is influenced by a number of factors, including glucose levels.

Neural mechanisms controlling eating - evaluation:

• Meal times and food types are more likely to be determined by social factors than by biology.
• Hunger is not the only thing to initiate eating - just thinking about food generates activity in the food-related parts of the brain and therefore changes eating behaviour.
• Pleasure centres in the brain also influence eating, with both the anticipation and onset of eating associated with increased dopamine activity (a neurotransmitter associated with mood).
• Learning is a very important factor - animals can learn to produce neurotransmitters and hormones that help regulate food intake at times of day when food is expected.

Neural mechanisms controlling satiation:

When we eat, this eventually generates several body signals that cause us to feel full and stop eating.

The role of leptin (lipostatic theory):

Leptin is a hormone secreted by fat cells (adipocytes) which cause a decrease in appetite and energy expenditure. It is released in direct proportion to the amount of fat stored in fats cells and as such is an adipose (fat) signal to the brain. Leptin does not directly affect satiety but moderates other satiety signals.

Increase in adipocytes leads to secretion of more leptin, influencing satiety signals and thus making us feel full sooner whereas a loss of adipocytes (e.g. because of dieting) results in a decline in leptin levels, reducing satiety signals and increasing our interest in food.

Research evidence:

• Mice with genetic mutations in the leptin gene (ob/ob mice) or leptin receptors (db/db mice) do not readily reach satiety, consume excessive amounts of food and become extremely obese (Zhang et al, 1994).
• The VMH (considered a satiety centre) is particularly sensitive to leptin. Damage to the VMH can cause hyperphagia and obesity (Mayer and Thomas, 1967).

The role of other mechanisms involved in satiation:

• Vagal sensory nerves - Act as `stretch receptors` in the stomach. As stomach wall stretches from eating, nerves send signals of fulness to the brain. However, hunger is still felt by people with stomachs removed.
• Cholecystokinin (CCK) - A substance released into the bloodstream by the intestine in response to food. CCK stimulates signals to the brain, inhibiting food intake.
• Insulin - A hormone secreted by the pancreas that enables tissues to remove glucose from the blood. Insufficient insulin leads to hyperphagia and an inhibition of satiety but not obesity, as without insulin the body cannot store fat.
• Ventromedial hypothalamus (VMH) - Produces feelings of being full (satiation). Damage to the VMH results in overeating (hyperphagia).