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Neural mechanisms 2012

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Neural mechanisms 2012

  1. 1. Biologicalexplanations of eating behaviourSpecification:The role of neuralmechanisms involved incontrolling eating andsatiation
  2. 2. How do we know when it is time to eat?• Hunger is activated by bothenvironmental and biologicalfactors.This topic looks at biologicalmechanisms involved ineating.•What makes us feel hungry?•What tells us to stop eatingwhen we are full?
  3. 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. 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 thethe Lateral Hypothalamus Ventromedial Hypothalamus1. 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 hunger3. 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. 5. LH + NPY seem to control eating behaviourIn 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 eatingNeuropeptide Y (NPY) was also behaviourfound to be important in turningeating on. Repeated injections of NPY caused obesity in a matter of days- When injected into the (Stanley 1986)hypothalamus of rats, NPY causedthem to start feeding, even when theywere full!
  6. 6. What does this suggest about theneural mechanisms of the LH in controlling eating behaviour?* It suggests that the LH is the main feeding centrein rats and that the LH triggers feeding in responseto signals from the body.* It also suggests that NPY is also important intriggering the feeding response.* The LH and NPY therefore turn feeding ON! (notoff)
  7. 7. AO1 – Neural mechanismsinvolved in the control of eating.... High levels of LH NPY Ghrelin Cause Hunger All switch eating ON
  8. 8. AO2: An evaluation of the role of the LH in eating behaviourDamage to the LH causes deficits in other aspects ofbehaviour (e.g. Thirst and sex). Therefore LH does not onlycontrol hunger. More recent research has shown that eating behaviour is controlled by neural circuits that run through the brain, not just the hypothalamusThis 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. 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 behaviourMarie et al (2005) genetically manipulated mice so that they did not make NPY. They found no subsequent decrease in their feeding behaviourThis suggests that the hunger stimulated by the injections ofNPY may actually thea result of the experimental artefact, in This shows that be relationship between NPY and feedingthat the floodremains given to the ratsmeans the we do not behaviour of NPY unclear. Which during thatexperimental 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. 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 stomachi.e. As the time from the last meal increases and we feel hungrier, so ghrelin secretion is increased Ghrelin is the hunger signal
  11. 11. Research into the role ofA03? Ghrelin IDEAs?F – Cummings al (2004)Cummings et found that ghrelin levels fell immediately after eating lunch and then – To investigate changes in blood ghrelinA slowly began to rise, peaking as participants levels over time between meals requested their evening meal. In 5/6P 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 hungerC 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. 12. Evaluation Ghrelin Further research conducted by Cummings (2006) has foundthat injections of ghrelin increases food intake in both animals and humansThis provides biological evidence of the link between thehormone ghrelin and the beginning of eating, satiety andovereating. Cummings Cummings Cummings Cummings (2004) (2004) (2006) (2004) Ps were isolated Sample Ethical Correlation? from time & Bias? Issues social cues
  13. 13. Approaches: Biological Debates: DeterministicIgnores other explanations (e.g.evolutionary explanation) Also, don‟t forget..AO3.. How Issues: - Extrapolation Reductionist Ethical issues
  14. 14. Question exerciseOutline the role of neuralmechanisms involved incontrolling eating behaviour(8 marks)
  15. 15. Mind mapMake sure you construct amind map to organise theAO1; AO2; AO3 and IDEAsfor the role of neuralmechanisms involved ineating behaviours
  16. 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 forA02 - However... eatingDamage 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. 17. EvaluationVentromedial Hypothalamus Extensive research has supported the finding that lesions/damage to the VMH results in hyperphagia and obesityShows that the VMH plays an important part in signalling toan 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 obeseSupporting the idea that if the VMH (satiety centre) isdestroyed it can lead to uncontrolled eating
  18. 18. EvaluationVentromedial HypothalamusGold (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 damagedSuggesting that the VMH doesn’t appear to controlhunger/satiety alone The However... reliability ofFurther 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 moreweight compared to those with lesions in other brain areas
  19. 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. 20. Therefore..Low levels of Leptin also cause us to feel hungry* When people don’t eat enough food, fat is usedup, the fat cells cease to secrete leptin.* Leptin levels in the blood fall – thehypothalamus detects the drop in leptin levelsand generates a feeling of hunger to increaseeating. In summary.........
  21. 21. AO2: An evaluation of the role ofLeptin in eating behaviourSupport for the role of leptin in eating behaviour comes fromconducting experiments using ‘ob’ mice (a stain of mice thatare genetically obese).Studies have demonstrated that these mice are missing thegene 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. 22. AO2: An evaluation of the role ofLeptin in eating behaviour However, some humans who are overweight have a leptin deficiency but most actually have increased levels of leptin!
  23. 23. Approaches: Biological Debates: DeterministicIgnores other explanations (e.g.evolutionary explanation) Also, don‟t forget..AO3.. How Issues: - Extrapolation Reductionist Ethical issues
  24. 24. General EvaluationThe 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 easilyInfluence 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. 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)

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