Eating Behaviour and Disorders

  1. Information from which four areas must be integrated for feeding behaviour to occur?
    • Gut
    • Liver
    • Taste
    • Homeostatic mechanisms
  2. Ultimately feeding behaviour must come under the control of the ___.
  3. What is the term which means that ingestive behaviours occur in all species?
    Phylogenetically ancient
  4. The fact that feeding behaviours are phylogenetically ancient means that ___ must be located in the most ancient parts of the brain.
    Feeding centres
  5. Which major source of information terminates as it enters the brain?
    Vagus nerve
  6. Which area in the brain stem is the key centre for control of appetitie?
  7. The vagus nerve which carries information from peripheral organs involved in feeding and taste pathways terminates in the ___.
    Brain stem
  8. Which two methodologies can be used to study eating behaviour?
    Lesions and electrical stimulation
  9. Lesions is where brain regions are damaged or destroyed using microelectrode or neurotoxin. The purpose is to see what ___ can no longer be performed.
  10. Which method involves placing an electrode into a brain region to see what behaviour is exhibited?
    Electrical stimulation
  11. What method involves infusing a neurotransmitter, drug (agonist) or antagonist through a capillary tube to a specific region to observe behaviour?
  12. Which method involves withdrawal of cerebrospinal fluid via a cannula, to then analyse it to see what neurotransmitters are active in a particular area during a particular behaviour?
  13. Which method involves injections of radioactive labelled neurotransmitters or drugs, and imaging (PET scan) of areas in which it binds?
    Radiologand binding
  14. Which two subregions of the hypothalamus are important in feeding?
    • Ventromedial Nucleus (VMH)
    • Lateral Hypothalamus (LH)
  15. Which subregion of the hypothalamus controls satiety?
    Ventromedial Nucleus (VMH)
  16. Lesions to the Ventromedial Nucles (VMH) produces overeating and ____.
  17. Hetherington & Ranson (1942) found that electrical stimulation of the Ventromedial Nucleus (VMH) _____ eating.
  18. The Lateral Hypothalamus control ___.
  19. Lesions to the Lateral Hypothalamus (LH) ___ eating and drinking.
  20. Anand and Brobeck (1951) found that electrical stimulation of the Lateral Hypothalamus (LH) ___ eating and drinking.
  21. Animals with lesions to the Ventromedial Nucleus (VMH) were also ___ feeders.
  22. The fact that animals with VMH lesions would not overeat if quinine (bitter taste) was added to their diet indicates that they have not lost all control of ___.
  23. Animals with lesions of the Ventromedial Nucleus (VMH) mainly overconsume ___.
    Carbohydtrates (CHO)
  24. The fact that there is an increase in the parasympathetic activity of the vagus in animals with lesions of the VMH suggests that they are unable to get energy from stores and overeat as a result. This also says that there may have been accidental damage to the ___ system.
  25. The fact the Sclafani (1975) only made knife cuts around the VMH still produced overeating suggests that the VMH may not be central to the control of ___.
  26. Later lesion studies found that axons form the Paraventricular Nuclesu (PVN) to the brain stem had also been damaged, therefore the conclusion is that the PVN is also involved in the control of ___.
  27. Where fo the vagus and taste pathways terminsate?
    Nucleus of the Solitary Tract
  28. Azons connect both the ___ and the ___ to the Nucleus of the Solitary Tract.
    Ventromedial Nucleus, Paraventricular Nucleus (therefore damage to these pathways could explain the complex VMH syndrome).
  29. Lesions to the ___ abolished eating.
    Lateral Hypothalamus (LH)
  30. Leisons to the Lateral Hypothalamus also caused behavioural impairments (small movement deficits) due to damage of the ___ which pass through this area.
    Nigrostriatal bundle
  31. One problem of the damage to the ___ as a result of LH lesions is that it could not be established whether the animal was not eating due to being unable to move physically or it did not need as much food due to expending less energy.
    Nigrostriatal bundle
  32. To investigate the role of damage to the nigrostriatal bundle, lesions were made with specific neurotoxins whoch would damage cell bodies but not ___ passing through food areas.
  33. Recent research has focused upon the ___ and in particular CHO appetite.
    Paraventricular (PVN)
  34. Which neurotransmitter stimulates CHO intake in the PVN?
  35. Which neurotransmitter inhibits CHO intake in the PVN?
  36. Microdialysis showed an increse in ___ levels before the onset of a CHO meal on waking, suggesting that levels rise just before feeding.
    Norepinephrine (NE)
  37. Infusions of ___ into the Paraventicular Nucleus stimulates eating, particularly carbohydrates.
    Norepinephrine (NE)
  38. Infusions of NE Antagonist drug into the PVN causes ___.
  39. The precise area of the inhibitory function of the neurotransmitter ___ is not known.
    Serotonin (5-HT)
  40. Microdialysis shows that ___ is released in the PVN following a meal.
    Serotonin (5-HT)
  41. Infusion of Serotonin (5-HT) into the Paraventricular Nucleus or Ventromedial Nucleus suppresses ___ intake.
    Carbohydrate (CHO)
  42. Fenfluramine, a Serotonin (5-HT) agonist is used to treat ___.
  43. Which neurotransmitter is a very potent appetite stimulant which can be infused into the Lateral Hypothalamus (LH)?
    Neuropeptide Y (NPY)
  44. Drugs which block ___ infused into the hypothalamus suppress eating.
    Neuropeptide Y (NPY)
  45. Neurones that secrete Neuropeptide Y (NPY) are found in the ___.
    Arcuate Nucleus (part of hypothalamus added to group controlling food intake when found out).
  46. The Arcuate Nucleus sends projections to the ___ and other regions of the hypothalamus.
    Paraventricular Nucleus (PVN)
  47. For many years, investigators believed that which two regions controlled hunger and satiety?
    • Laterl Hypothalamus (LH)
    • Ventromedial Hypothalamus (VMH)
  48. The ___ receives signals from the tongue, stomach, small intestine and liver and sends the information on to many regions of the forebrain.
    Nucleus of the Solitary Tract (NST)
  49. The release of ___ in the Lateral Hypothalamus induces ravenous eating.
    Neuropeptide Y
  50. Rodin et al (1989) found that unhappiness and depression appearto be the ___ of obesity.
  51. There is some evidence that ___weakens physiological controls of appetite e.g. praise for eating all we are given (Birch et al 1987).
  52. ___ have shown evidence for genetic factors having an effect on obesity.
    Twin studies
  53. Adoption studies have shown that family envionment has ___effect on weight.
  54. Which studies illustrated how it is beneficial to store energy which is released in times of famine?
    • Gibbs et al (1996) Nauru islanders
    • Pima Indians (Mexico to Arizona)
  55. The Nauru islander and Pima Indians studies suggest that there is an underlying ___ cause of obsity.
  56. Researchers have looked for a signal released by fat tissue to inform the brain how much fat reserve we have. This is thought to ___ body weight.
  57. The role of fat was thought to be a ___ feedback mechanism to turn off appetite.
  58. What is the name of the gentically engineered obese mouse with a low metabolism which develops diabetes in adulthood?
    The Ob Mouse
  59. Ob mice lack which gene?
    The Ob gene
  60. The ob gene normally produces which protein?
  61. Leptin is usually produced by ___.
    Fat cells
  62. Lack of ___ is the cause of obesity in the ob mouse.
  63. Injections of leptin in ob mice increases ___ rate which increases activity and decreases eating, leading to a normal body weight.
  64. Where does Leptin produce its effects?
    The brain
  65. Infusion of leptin into the brain ___ eating and productin of Neuropeptide Y (NPY) in the arcuate nucleus.
  66. Ob mice that were mutated not to produce NPY were not obese (mid weight) suggesting NPY activity is not the only function of ___.
  67. An explanation for obese individuals having more body fat, and hence more leptin could be that they are less ___ to leptin.
  68. Leptin is transported into the brain by an ___.
    Active system
  69. An explanation for obesity could be that the ___ system is defective and therefore less letptin enters the brain.
  70. Caro et al (1996) found that obese people have ___% more leptin in the blood but only ___% more in cerebrospinal fluid, indicating that there does appear to be proportionally less entering the brain.
    318, 30
  71. There is some evidence that some individuals show a decrease in leptin production caused by a ___ gene but this is very rare.
  72. How many families did Farooqui et al (2001) find had mutations causing obesity?
  73. In aged rats there is shown to be a ___% reduction in leptin receptors, which could explain why individuals often gain weight with age.
  74. What is found in breast milk which suggests that early neonatal environment can influence later obesity?
  75. Stocker & Cawthorne (2008) found that if young animals are given leptin during the period of feeding from the mother, they are ___ likely to become obese.
Card Set
Eating Behaviour and Disorders
Eating Behaviour and Disorders