Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
22 Cards in this Set
- Front
- Back
- 3rd side (hint)
|
Which model explains the neural mechanisms involved in controlling eating behaviour? |
Dual Centre Model |
DCM |
|
|
name the 2 areas the hypothalamus can be split into |
Ventral Medial Hypothalamus Lateral Hypothalamus |
VMH LH |
|
|
which of these areas stimulates eating behaviour and inhibiting eating behanviour |
VMH - Inhibits (Satiety Centre) LH - Hunger (Feeding Centre) |
|
|
|
is hunger experienced when blood glucose levels rise or fall? |
fall |
|
|
|
this feeling of hunger then activates the.. |
Lateral Hypothalamus |
|
|
|
after feeding, blood glucose levels rise again, this activate the.. |
ventral medial hypothalamus - inhibits eating |
|
|
|
Name the 2 neurotransmitters that act as signal for inhibiting food intake |
Bombesin Serotonin |
B_______ S______ |
|
|
how does bombesin work? |
binds to receptors in the hypothalamus to suppress hunger and reduce food intake |
receptors/ food intake |
|
|
how does serotonin work? |
produced in response to increased glucose levels and inhibits intake of carbohydrates |
carbs |
|
|
which hormone is released into the blood stream by fat tissue? |
Leptin |
L |
|
|
what does leptin do once released? |
binds to the receptors in the hypothalamus to reduce eating behaviour |
hypothalamus |
|
|
name a hormone that acts as a signal for eating |
Ghrelin |
G________ |
|
|
how does ghrelin work and where is it produced? |
produced by the stomach and pancreas; travles in the bloodstream to active nuerons in the lateral hypothalamus causing them to release nuerotransmitters to increase feeding and feels of huger |
gut LH |
|
|
Eval.. Hetherington & Ranson |
lesioned the VMH in rats which cause them to become morbidly obese. Evidence suggests that the VMH is responsible to reducing food intake as when it was damaged, eating becomes completely uninhibited |
lesions of the VMH |
|
|
Eval.. Anand and Brobeck |
lesioned the LH in rats, this resulted in them not eating and starving themselves. This evidence suggests that the LH is responsible for increasing food intake as when it was damaged food intake completely stopped |
lesions of the LH |
|
|
eval.. however with lesions |
one problem with lesion experiments is that its very difficult to localise the specific areas of dmage to the brian, makes conclusions difficult as cannot be confident where the damage is. this is demonstrated by recent research that has shown that hunger is controlled by neural circuits that run throughout the brain and not just by the hypothalamus |
other neural circuits |
|
|
eval.. carlson 2007 |
used genetically modified mice to provide support for the role of leptin in signalling the hypothalamus to inhibit eating behaviour mice that are made to lack leptin show that they rapidly become obese (ob mice) injections of leptin restore normal body weight= supporting role of leptin |
leptin in mice |
|
|
however of animal research |
caution must be taken when generalising the findings to humans due to different underlying physiological factors. e.g religious festivals of fasting such as Ramadan is a cultural influence likely to outweigh neural signals to feed |
Ramadan |
|
|
Evidence fo the role of ghrelin actign as a signal for the hypothalamus Cummings et al |
measured blood levels of ghrelin in 6 ppts between eating lunch and the time at which ppts usually ate their evening meal. They found that ghrelin levels fall after eating and then peaked again as ppts wantedtheir evening meal. suggests ghrelin levels are an important indicator of hunger, signalling the hypthalamus to trigger feelings of hunger |
|
|
|
IDA - practical application |
they provide insights for eating disorders such as anorexia or obesity. for example using gastric bands that limit food intake by reducing ghrelin production from the stomach and therefore reduce hunger signals to the hypothalamus, causing people to eat less. |
|
|
|
however.. of taking a purely biological approach to treating obesity |
is flawed as it suggests that leptin deficiencies may explain overeating as shown by the 'ob' mice. Research has shown that most people do not lack the key signals for fullness and have normal leptin levels. this shows that neural mechanisms for eating behaviour are complex and eating behaviour is not just as a result of biology. |
|
|
|
IDA deterministic de Castro |
a variety of factors that can affect eating behaviour; mood/dieting and so this approach is deterministic, it suggest that feeding is under strict biological control. it must acknowledge cognitive/social processes as well de Castro shows that people eat more food when in the company of others |
|
