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Neural mechanisms 2012

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The document discusses the neural mechanisms involved in controlling eating behavior and satiation. It describes the dual feeding system in the hypothalamus, with the lateral hypothalamus (LH) acting as the "on" switch that triggers hunger and feeding behaviors, and the ventromedial hypothalamus (VMH) acting as the "off" switch that induces satiety and inhibits further eating. Glucose levels, ghrelin, neuropeptide Y (NPY), and leptin are identified as important biological factors that influence these hypothalamic centers and control feelings of hunger and fullness.

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Biological explanations of eating behaviour Specification: The role of neural mechanisms involved in controlling eating and satiation
How do we know when it is time to eat? • Hunger is activated by both environmental and biological factors. This topic looks at biological mechanisms involved in eating. •What makes us feel hungry? •What tells us to stop eating when we are full?
Neural mechanisms in eating and satiation Involves mechanisms that detect both the Homeostasis state of the internal environment (e.g. Level of nutrients) and correct the situation to Humans, along with all restore that environment to its optimal state mammals are Our eating behaviour is a prime example of homeostatic animals, this internal balance in that it is clear from (we are designed to run our research that we have a “Feeding” centre bodies in a constant state in the brain activated when we are hungry of balance) and a “Satiety” centre activated when we are full. The body has evolved two separate systems The Dual Feeding System! (both involving the hypothalamus) Turning eating OFF Turning eating ON - Ventromedial - Lateral hypothalamus hypothalamus
The control of eating and satiation Among humans, glucose levels play the most important part in producing feelings of hunger Decreasing glucose and Rising glucose and the the Lateral Hypothalamus Ventromedial Hypothalamus 1. A decline in glucose levels 1. A rise in glucose levels in the in the blood activates the blood activate the VMH Lateral Hypothalamus. 2. Feeling of satiation (fullness) 2. Feelings of hunger 3. Individual searches for and This inhibits further feeding then consumes food - Glucose levels rise again **Hunger increases as glucose levels decrease** **Satiation (fullness) increases as glucose levels increase**
LH + NPY seem to control eating behaviour In the 1950’s... • Researchers found that damage to the LH in rats caused aphagia It was (a failure to eat when hungry) concluded • Stimulation of the LH caused the therefore that the LH was the animal to want to feed „ON‟ switch for eating Neuropeptide Y (NPY) was also behaviour found to be important in turning eating on. Repeated injections of NPY caused obesity in a matter of days - When injected into the (Stanley 1986) hypothalamus of rats, NPY caused them to start feeding, even when they were full!
What does this suggest about the neural mechanisms of the LH in controlling eating behaviour? * It suggests that the LH is the main feeding centre in rats and that the LH triggers feeding in response to signals from the body. * It also suggests that NPY is also important in triggering the feeding response. * The LH and NPY therefore turn feeding ON! (not off)
AO1 – Neural mechanisms involved in the control of eating.... High levels of LH NPY Ghrelin Cause Hunger All switch eating ON
AO2: An evaluation of the role of the LH in eating behaviour Damage to the LH causes deficits in other aspects of behaviour (e.g. Thirst and sex). Therefore LH does not only control hunger. More recent research has shown that eating behaviour is controlled by neural circuits that run through the brain, not just the hypothalamus This shows that although LH undoubtedly plays an important role in the control of eating behaviour, it may not, as previously thought, be the brain’s sole feeding centre Sakurai et al, 1998
AO2: An evaluation of the role of Neuropeptide Y in eating behaviour Recent research on NPY has cast doubt on whether its normal function is to influence feeding behaviour Marie et al (2005) genetically manipulated mice so that they did not make NPY. They found no subsequent decrease in their feeding behaviour This suggests that the hunger stimulated by the injections of NPY may actually thea result of the experimental artefact, in This shows that be relationship between NPY and feeding that the floodremains given to the ratsmeans the we do not behaviour of NPY unclear. Which during that experimental manipulations about brain mechanisms which know everything “as yet” could cause behaviour not like control feeding behaviour. that caused by normal amounts of the neurotransmitter
Hormone - Ghrelin • Ghrelin is a hormone that is released from an empty stomach • The amount of ghrelin released is directly proportional to the emptiness of the stomach i.e. As the time from the last meal increases and we feel hungrier, so ghrelin secretion is increased Ghrelin is the hunger signal
Research into the role of A03? Ghrelin IDEAs? F – Cummings al (2004) Cummings et found that ghrelin levels fell immediately after eating lunch and then – To investigate changes in blood ghrelin A slowly began to rise, peaking as participants levels over time between meals requested their evening meal. In 5/6 P participants ghrelin levels were closely eat – 6 male participants were allowed to correlated to their self-report feelings of lunch, ghrelin levels were monitored via hunger C blood samples taken every 5 minutesthat – The researchers concluded therefore until the participant reflects stomach emptiness ghrelin directly requested their evening meal. Participants assessed their degree and are closely related to subjective feelings of hunger. every 30 minutes hunger Ghrelin therefore has a key role in appetite signalling in humans
Evaluation Ghrelin Further research conducted by Cummings (2006) has found that injections of ghrelin increases food intake in both animals and humans This provides biological evidence of the link between the hormone ghrelin and the beginning of eating, satiety and overeating. Cummings Cummings Cummings Cummings (2004) (2004) (2006) (2004) Ps were isolated Sample Ethical Correlation? from time & Bias? Issues social cues
Approaches: Biological Debates: Deterministic Ignores other explanations (e.g. evolutionary explanation) Also, don‟t forget..AO3.. How Issues: - Extrapolation Reductionist Ethical issues
Question exercise Outline the role of neural mechanisms involved in controlling eating behaviour (8 marks)
Mind map Make sure you construct a mind map to organise the AO1; AO2; AO3 and IDEAs for the role of neural mechanisms involved in eating behaviours
The Ventromedial Hypothalamus • Researchers discovered that damage to the VMH caused rats to overeat leading to a condition called It was hyperphagia. concluded therefore that • Stimulation of the VMH inhibits the VMH was feeding the „OFF‟ switch for A02 - However... eating Damage to the nerves passing behaviour through the VMH causes damage A02 to another part of the The PVN also hypothalamus, the paraventricular detects the specific nucleus (PVN) – it is thought that foods our body needs (may be damage to the PVN alone causes responsible for hyperphagia cravings)
Evaluation Ventromedial Hypothalamus Extensive research has supported the finding that lesions/damage to the VMH results in hyperphagia and obesity Shows that the VMH plays an important part in signalling to an individual when it’s necessary for them to cease eating Hetherington & Ranson conducted research and reported that lesions to the VMH caused rats to become dramatically obese Supporting the idea that if the VMH (satiety centre) is destroyed it can lead to uncontrolled eating
Evaluation Ventromedial Hypothalamus Gold (1973) found lesions/damage to the VMH alone did not result in hyperphagia and only produced over eating when other areas (such as the PVN) was also damaged Suggesting that the VMH doesn’t appear to control hunger/satiety alone The However... reliability of Further research has failed to replicate Gold’s Gold’s findings, demonstrating that research can be animals with VMH lesions ate questioned substantially more and gained more weight compared to those with lesions in other brain areas
The role of Leptin • Leptin is a fat hormone • It is secreted into the blood stream to signal to the brain (via the hypothalamus) that calorie storage is high. • Basically telling the brain that the body has sufficient fat stored The body releases more leptin as more fat is stored – how should the body respond to this? STOP EATING!
Therefore..Low levels of Leptin also cause us to feel hungry * When people don’t eat enough food, fat is used up, the fat cells cease to secrete leptin. * Leptin levels in the blood fall – the hypothalamus detects the drop in leptin levels and generates a feeling of hunger to increase eating. In summary.........
AO2: An evaluation of the role of Leptin in eating behaviour Support for the role of leptin in eating behaviour comes from conducting experiments using ‘ob’ mice (a stain of mice that are genetically obese). Studies have demonstrated that these mice are missing the gene that produces leptin. They therefore eat continually. (remember, low levels of leptin are thought to cause hunger) Furthermore, injections of leptin into the ob mice stop them eating so much and their weight eventually returns to normal This shows that there appears to be a strong link in the relationship between low levels of leptin and over-eating
AO2: An evaluation of the role of Leptin in eating behaviour However, some humans who are overweight have a leptin deficiency but most actually have increased levels of leptin!
Approaches: Biological Debates: Deterministic Ignores other explanations (e.g. evolutionary explanation) Also, don‟t forget..AO3.. How Issues: - Extrapolation Reductionist Ethical issues
General Evaluation The role of neural mechanisms are still unclear, exactly how ghrelin and leptin reach their targets in the brain is not fully clear, both are large peptides what do not cross the blood brain barrier easily Influence of biological rhythms, research has shown that rats become more active and start to eat soon after darkness descends. This and similar rhythms are controlled by another area of the hypothalamus (the SCN) IDEA - Alternative approach – what other factors influence your hunger levels everyday?
Diagram of the Dual Centre Model of Feeding Feelings of hunger - feeding starts Food intake, rise in LH feeding glucose levels centre is and a activated decrease in ghrelin Signals of decline in nutrients VMH satiety (decrease of centre glucose, satisfied increase of ghrelin Satiety, feeling of fullness (feeding stops)

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Neural mechanisms 2012

  • 1. Biological explanations of eating behaviour Specification: The role of neural mechanisms involved in controlling eating and satiation
  • 2. How do we know when it is time to eat? • Hunger is activated by both environmental and biological factors. This topic looks at biological mechanisms involved in eating. •What makes us feel hungry? •What tells us to stop eating when we are full?
  • 3. Neural mechanisms in eating and satiation Involves mechanisms that detect both the Homeostasis state of the internal environment (e.g. Level of nutrients) and correct the situation to Humans, along with all restore that environment to its optimal state mammals are Our eating behaviour is a prime example of homeostatic animals, this internal balance in that it is clear from (we are designed to run our research that we have a “Feeding” centre bodies in a constant state in the brain activated when we are hungry of balance) and a “Satiety” centre activated when we are full. The body has evolved two separate systems The Dual Feeding System! (both involving the hypothalamus) Turning eating OFF Turning eating ON - Ventromedial - Lateral hypothalamus hypothalamus
  • 4. The control of eating and satiation Among humans, glucose levels play the most important part in producing feelings of hunger Decreasing glucose and Rising glucose and the the Lateral Hypothalamus Ventromedial Hypothalamus 1. A decline in glucose levels 1. A rise in glucose levels in the in the blood activates the blood activate the VMH Lateral Hypothalamus. 2. Feeling of satiation (fullness) 2. Feelings of hunger 3. Individual searches for and This inhibits further feeding then consumes food - Glucose levels rise again **Hunger increases as glucose levels decrease** **Satiation (fullness) increases as glucose levels increase**
  • 5. LH + NPY seem to control eating behaviour In the 1950’s... • Researchers found that damage to the LH in rats caused aphagia It was (a failure to eat when hungry) concluded • Stimulation of the LH caused the therefore that the LH was the animal to want to feed „ON‟ switch for eating Neuropeptide Y (NPY) was also behaviour found to be important in turning eating on. Repeated injections of NPY caused obesity in a matter of days - When injected into the (Stanley 1986) hypothalamus of rats, NPY caused them to start feeding, even when they were full!
  • 6. What does this suggest about the neural mechanisms of the LH in controlling eating behaviour? * It suggests that the LH is the main feeding centre in rats and that the LH triggers feeding in response to signals from the body. * It also suggests that NPY is also important in triggering the feeding response. * The LH and NPY therefore turn feeding ON! (not off)
  • 7. AO1 – Neural mechanisms involved in the control of eating.... High levels of LH NPY Ghrelin Cause Hunger All switch eating ON
  • 8. AO2: An evaluation of the role of the LH in eating behaviour Damage to the LH causes deficits in other aspects of behaviour (e.g. Thirst and sex). Therefore LH does not only control hunger. More recent research has shown that eating behaviour is controlled by neural circuits that run through the brain, not just the hypothalamus This shows that although LH undoubtedly plays an important role in the control of eating behaviour, it may not, as previously thought, be the brain’s sole feeding centre Sakurai et al, 1998
  • 9. AO2: An evaluation of the role of Neuropeptide Y in eating behaviour Recent research on NPY has cast doubt on whether its normal function is to influence feeding behaviour Marie et al (2005) genetically manipulated mice so that they did not make NPY. They found no subsequent decrease in their feeding behaviour This suggests that the hunger stimulated by the injections of NPY may actually thea result of the experimental artefact, in This shows that be relationship between NPY and feeding that the floodremains given to the ratsmeans the we do not behaviour of NPY unclear. Which during that experimental manipulations about brain mechanisms which know everything “as yet” could cause behaviour not like control feeding behaviour. that caused by normal amounts of the neurotransmitter
  • 10. Hormone - Ghrelin • Ghrelin is a hormone that is released from an empty stomach • The amount of ghrelin released is directly proportional to the emptiness of the stomach i.e. As the time from the last meal increases and we feel hungrier, so ghrelin secretion is increased Ghrelin is the hunger signal
  • 11. Research into the role of A03? Ghrelin IDEAs? F – Cummings al (2004) Cummings et found that ghrelin levels fell immediately after eating lunch and then – To investigate changes in blood ghrelin A slowly began to rise, peaking as participants levels over time between meals requested their evening meal. In 5/6 P participants ghrelin levels were closely eat – 6 male participants were allowed to correlated to their self-report feelings of lunch, ghrelin levels were monitored via hunger C blood samples taken every 5 minutesthat – The researchers concluded therefore until the participant reflects stomach emptiness ghrelin directly requested their evening meal. Participants assessed their degree and are closely related to subjective feelings of hunger. every 30 minutes hunger Ghrelin therefore has a key role in appetite signalling in humans
  • 12. Evaluation Ghrelin Further research conducted by Cummings (2006) has found that injections of ghrelin increases food intake in both animals and humans This provides biological evidence of the link between the hormone ghrelin and the beginning of eating, satiety and overeating. Cummings Cummings Cummings Cummings (2004) (2004) (2006) (2004) Ps were isolated Sample Ethical Correlation? from time & Bias? Issues social cues
  • 13. Approaches: Biological Debates: Deterministic Ignores other explanations (e.g. evolutionary explanation) Also, don‟t forget..AO3.. How Issues: - Extrapolation Reductionist Ethical issues
  • 14. Question exercise Outline the role of neural mechanisms involved in controlling eating behaviour (8 marks)
  • 15. Mind map Make sure you construct a mind map to organise the AO1; AO2; AO3 and IDEAs for the role of neural mechanisms involved in eating behaviours
  • 16. The Ventromedial Hypothalamus • Researchers discovered that damage to the VMH caused rats to overeat leading to a condition called It was hyperphagia. concluded therefore that • Stimulation of the VMH inhibits the VMH was feeding the „OFF‟ switch for A02 - However... eating Damage to the nerves passing behaviour through the VMH causes damage A02 to another part of the The PVN also hypothalamus, the paraventricular detects the specific nucleus (PVN) – it is thought that foods our body needs (may be damage to the PVN alone causes responsible for hyperphagia cravings)
  • 17. Evaluation Ventromedial Hypothalamus Extensive research has supported the finding that lesions/damage to the VMH results in hyperphagia and obesity Shows that the VMH plays an important part in signalling to an individual when it’s necessary for them to cease eating Hetherington & Ranson conducted research and reported that lesions to the VMH caused rats to become dramatically obese Supporting the idea that if the VMH (satiety centre) is destroyed it can lead to uncontrolled eating
  • 18. Evaluation Ventromedial Hypothalamus Gold (1973) found lesions/damage to the VMH alone did not result in hyperphagia and only produced over eating when other areas (such as the PVN) was also damaged Suggesting that the VMH doesn’t appear to control hunger/satiety alone The However... reliability of Further research has failed to replicate Gold’s Gold’s findings, demonstrating that research can be animals with VMH lesions ate questioned substantially more and gained more weight compared to those with lesions in other brain areas
  • 19. The role of Leptin • Leptin is a fat hormone • It is secreted into the blood stream to signal to the brain (via the hypothalamus) that calorie storage is high. • Basically telling the brain that the body has sufficient fat stored The body releases more leptin as more fat is stored – how should the body respond to this? STOP EATING!
  • 20. Therefore..Low levels of Leptin also cause us to feel hungry * When people don’t eat enough food, fat is used up, the fat cells cease to secrete leptin. * Leptin levels in the blood fall – the hypothalamus detects the drop in leptin levels and generates a feeling of hunger to increase eating. In summary.........
  • 21. AO2: An evaluation of the role of Leptin in eating behaviour Support for the role of leptin in eating behaviour comes from conducting experiments using ‘ob’ mice (a stain of mice that are genetically obese). Studies have demonstrated that these mice are missing the gene that produces leptin. They therefore eat continually. (remember, low levels of leptin are thought to cause hunger) Furthermore, injections of leptin into the ob mice stop them eating so much and their weight eventually returns to normal This shows that there appears to be a strong link in the relationship between low levels of leptin and over-eating
  • 22. AO2: An evaluation of the role of Leptin in eating behaviour However, some humans who are overweight have a leptin deficiency but most actually have increased levels of leptin!
  • 23. Approaches: Biological Debates: Deterministic Ignores other explanations (e.g. evolutionary explanation) Also, don‟t forget..AO3.. How Issues: - Extrapolation Reductionist Ethical issues
  • 24. General Evaluation The role of neural mechanisms are still unclear, exactly how ghrelin and leptin reach their targets in the brain is not fully clear, both are large peptides what do not cross the blood brain barrier easily Influence of biological rhythms, research has shown that rats become more active and start to eat soon after darkness descends. This and similar rhythms are controlled by another area of the hypothalamus (the SCN) IDEA - Alternative approach – what other factors influence your hunger levels everyday?
  • 25. Diagram of the Dual Centre Model of Feeding Feelings of hunger - feeding starts Food intake, rise in LH feeding glucose levels centre is and a activated decrease in ghrelin Signals of decline in nutrients VMH satiety (decrease of centre glucose, satisfied increase of ghrelin Satiety, feeling of fullness (feeding stops)