Neural mechs in EB

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  • Created by: imanilara
  • Created on: 06-06-16 15:09

Glucostat theory - LH+VMH AO1

Hunger and satiety controlled by hypo:

Blood glucose levs decrease- LH activated= feelings of hunger+leading to behaviours searching for food=increasing blood glucose lev. 
When too high- Ventromedial hypo activated= feelings of satiety +prevention of further eating behaviour. 
THIS IS HOMEOSTASIS BY NEGATIVE FEEDBACK= deviation from the norm in internal conditions is reversed back to the optimum state. 

LH: feeding centre- In 1950s, researchers found that by damaging the LH in rats= aphagia (absence of eating) , stimulation= eating behaviour. Led researchers to believe LH was on-switch 4 eating. 

VMH: satiety centre- researchers found that damage to the VMH in rats caused hyperphagia (overeating)+stimulation decreases feeding. Also lots of glucose receptors in VMH. Led researchers to believe that VMH is off switch for eating. Damage to the nerves entering the vMH damages the paraventricular nucleus too which is believed to cause hyperphagia. 

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Neurotransmitters theory AO1

Another theory looks at the role of NT's, in the ways that particular hormones interact w neural circuits. 

Neuropeptide Y- NPY

  • NT found in hypothalamus
  • If injected into hypo, immeediate feeding even when rats are satiated (Wickens 2000)
  • Repeated injections cause obesity in just a few days (Stanley 1980s)


  • hormone released by the empty stomach signals hypo to stimulate feeding 
  • hormone acts on the feeding centre in the hypo in the LH 
  • Cummings et al (2004) measured Ghrelin levels between 5mins after lunch and the time the p's asked for their evening meals - found positive correlation between ghrelin levs and degree of hunger 
  • Cummings also found that injections led to increase in body weight, food intake, and found evidence that hormone stimulates the hypothalamus 
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A STRENGTH of these theories..plenty of evidence supporting the role of the hypothalamus, NPY+Ghrelin in feeding and satiety some of which are mentioned above. All given evidence suggesting LH is feeding centre and VMH satiety centre. 

Role of the LH:

  • Weakness- damage to the LH causes deficits in other aspects of behviour, eg thirst and sex, and its sole purpose is not the on-switch for feeding 
  • Recent research indicates that NEURAL CIRCUITS throughout brain stimulated in EB- not just hypo
  • they now questions whether LH is feeding centre - may be dominant but not only brain structure involved 
    Role of VMH:
  • Most studies show that compared to other lesions in the brain, most weight gain when lesions in VMH.- STRENGTH
  • Some research casts doubt as to whether VMH is satiety centre - mixed findings- Gold 1973-  lesions in VMH did not cause hyperphagia however subsequent studies have failed to get same results- lack of replicability- not reliable as a theory
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AO2 NT's

Role of NPY:

Recent research casts doubt- normal role of NPY is to control EB.

  • Marie et al 2005- produced knock out mice (without NPY gene) and found no decrease in feeding behviour 
  • suggested that feeding caused by NPy injections example of an experimental artefact- flooding system w much higher levs of NT than would happen naturally WEAKNESS
  • Interesting research on the effect on humans: Yang et al
  • NPY produced by abdominal fat- and so the more abdominal fat the mroe NPY produced as positive feedback - this could be an indication for hospitals now to see this risk and give obese patients drugs that switch off npy- ie the fatter you are the more you want to eat

Role of Ghrelin:

  • Lutter - other roles in controlling stress+ depression- could explain comfort eating- a real worl implication here that to stop comfort eating we should block body's response to ghrelin- this may stop its +ve effects on stress 
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Issue is that most research done on animals- this has to be the case bc ethical reasons - not ok to deliberately damage human brain. But from an ethical perspective we can question why it is ok to do this to rats- this is somewhat redundant since some of these studies carried out in 40s and 50s and unlikely to be repeated. 

More important q- emperical support - can findings of rat studies be extrapulated- animal model is a simplified system, meaning conc's drawn are reductionist- likely that in humans cognitive factors such as the dangers of overreating/undereating would play a part in controlling EB than in rats. Prefrontal cortex in humans involved in cognitions is much larger in humans than any other animal- no equivalent in rats? More complicated than rats and so relevance of animal studies questionable. 

Evol theory- in hunter-gatherer who supposedly had these homeostatic neural systems-they had to b adaptive. Not adaptive to only have feelings of hunger when glucose levs drop as they might not have the food- more adaptive to keep glucose above optimum to avoid running the risk- this is seen in our pref to high calorie foods. More than just a neural mech. 

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We may learn when to eat, when to stop and when to overeat and unereat by observing, identifying, - VICARIOUS REINFORCEMENT of their consequences+ then imitating to reap the same results via DIRECT REINFORCEMENT- more nurture side of debate 

however behaviourists to take into account biological preparedness- neural mechs may be involved in basic control of hunger/satiety- and so it could be an interaction between the two!!

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