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1. NEURAL MECHANISMS IN EATING AND SATIATION 2. Keywords to learn <ul><li>Satiation </li></ul><ul><li>Aphagia…
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  • 1. NEURAL MECHANISMS IN EATING AND SATIATION
  • 2. Keywords to learn <ul><li>Satiation </li></ul><ul><li>Aphagia </li></ul><ul><li>Leptin </li></ul><ul><li>Hyperphagia </li></ul><ul><li>Neuropeptide Y </li></ul><ul><li>Lateral hypothalamus </li></ul><ul><li>Ventromedial hypothalamus </li></ul><ul><li>Paraventricular nucleus </li></ul><ul><li>Amygdala </li></ul><ul><li>Inferior frontal cortex </li></ul>
  • 3. Homeostasis <ul><li>Involves mechanisms that can detect and correct. </li></ul><ul><li>Detect – check whether the body has enough nutrients (internal environment) </li></ul><ul><li>Correct – restore the body to its optimal state. </li></ul><ul><li>Body evolved 2 separate systems in order to cope with the time lag between restoring equilibrium and body registering their effect. </li></ul><ul><li>Turning eating on and turning eating off! </li></ul>
  • 4. GLUCOSE LEVELS Decrease in glucose levels As glucose levels decrease hunger levels increase Increase in glucose levels means satiation reached. Activates this area – feel hungry. Individual searches for food and eats Increase in glucose levels Activates this area – feeling of satiation – inhibits further feeding
  • 5. Research with mice – Zhang et al (1994) <ul><li>Some mice receive two copies of the gene for obesity ( ob ) </li></ul><ul><li>Ob/ob mice have a tendency to overeat – foods high in fat or sugar. </li></ul><ul><li>Have defective genes for the protein leptin </li></ul><ul><li>LEPTIN – normally produced by fat tissue and secreted into the bloodstream where it travels to the brain and other tissues, causing fat loss and decreased appetite </li></ul><ul><li>In ob/ob mice leptin is not produced </li></ul>Injecting ob/ob mice with leptin causes them to dramatically lose weight. Leptin injected Future – treatment for obese patients – still in research
  • 6. Homeostasis - evaluation – commentary AO2 <ul><li>Limited view as being adaptive – for it should anticipate and prevent energy deficits </li></ul><ul><li>this explanation just reacts to being hungry </li></ul><ul><li>Systems would have evolved to not only maintain bodily resources but to maintain levels above – so it acts as a buffer against future lack of food </li></ul>
  • 7. AO2 – role of LH <ul><li>Damage to LH causes other problems/deficits such as thirst and sex rather than just hunger </li></ul><ul><li>More recent research has shown that eating behaviour is controlled by neural circuits that run throughout the brain not just the hypothalamus </li></ul><ul><li>Sakurai et al (1998) – LH not the brains eating centre </li></ul>
  • 8. Lateral hypothalamus <ul><li>Researchers discovered damage to LH in rats caused aphagia </li></ul><ul><li>Aphagia – absence of eating (ie hunger) </li></ul><ul><li>Stimulation of LH – elicits feeding behaviour – ON switch for eating </li></ul><ul><li>Neuropeptide Y (NPY) – neurotransmitter found in the hypothalamus </li></ul><ul><li>When NPY injected into hypothalamus of rats it caused them to begin feeding even when satiated (Wickens 2000). </li></ul><ul><li>Repeated injections of NPY produced obesity in just a few days (Stanley et al 1986) </li></ul>
  • 9. Evaluation – AO2 <ul><li>Is NPY’s normal function to influence feeding behaviour </li></ul><ul><li>Marie et al (2005) genetically manipulated mice so they did not make NPY. </li></ul><ul><li>They found no subsequent decrease in their feeding behaviour, suggesting that hunger stimulated by injections of NPY may be an experimental artefact in that the flood of NPY stimulates other areas – ie it is something else </li></ul><ul><li>Yang et al 2008 – research into obesity. </li></ul>
  • 10. AO2 – NPY – real world application obesity <ul><li>Yang et al 2008 </li></ul>
  • 11. Role of ventromedial hypothalamus <ul><li>Damage to VMH causes rats to overeat – condition called hyperphagia </li></ul><ul><li>Stimulation of this area inhibits feeding </li></ul><ul><li>VMH signals – stop eating as glucose receptors in this area </li></ul><ul><li>Damage to nerve fibres passing through VMH possibly damages the paraventricular nucleus (PVN) </li></ul><ul><li>It is this damage to the PVN that causes hyperphagia (Gold 1973) </li></ul><ul><li>PVN also detects specific foods our body needs – feel cravings! </li></ul>
  • 12. Hetherington and Ranson (1942) The VMH Rat Made lesions on an area of the ventromedial nucleus (part of the hypothalamus) in rats. Caused the rats to overeat and be dramatically obese. This lesion destroyed a centre that is vital for the control of feeding behaviour. Its destruction led to an increase in feeding and body weight. It was assumed that this was a satiety centre – which is normally activated when the animal is full at the end of the meal. Satiety – the feeling or state of being fully satisfied. Satiety centre’s function is to stop feeding
  • 13. AO2 – evaluation VMH <ul><li>Designation of the VMH as ‘satiety centre’ but it could be other factors </li></ul><ul><li>Gold 1973 – lesions to VMH alone does not result in hyperphagia and only produced overeating when included other areas such as the paraventricular nucleus (PVN) </li></ul><ul><li>However, research has failed to replicate Gold’s findings </li></ul><ul><li>Animals gained substantially more weight with VMH lesions more than lesions else where </li></ul>
  • 14. Neural control of cognitive factors <ul><li>Thinking about food makes us hungry </li></ul><ul><li>Images, memories, sights and smells </li></ul><ul><li>Amygdala and inferior frontal cortex </li></ul>
  • 15. Selection of foods from previous experience Rolls & Rolls (1973) surgically removing amygdala in rats would cause the animals to consume both familiar and novel (unfamiliar) foods indiscriminately – whereas amygdala-intact rats would intially avoid novel foods and consume only the familiar foods. ROLE OF AMYGDALA ROLE OF INFERIOR FRONTAL CORTEX Receives messages from the olfactory bulb (smell area of brain). As odours influence the taste of foods – damage to this area should decrease eating – in response to smell and taste. (Kolb and Whishaw 2006). Kluver-Bucy syndrome – damage to inferior frontal cortex and amygdala could explain feeding abnormalities – patients show increased appetite, indiscriminate eating and trying to eat non food items. Research on effects of damage to these brain areas suggest that food cues don’t have same effect as non damaged patients. (But these patients do have other problem areas as well, also Kluver Bucy syndrome also damaged areas in anterior temporal lobes. AO2 Zald & Pardo (1997) – physiological evidence supporting amygdala – olfactory stimuli.
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