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Lecture 6

Lecture 6 - Eating

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Emis Akbari

PSY398H5S – Motivational Systems Lecture 6 – February 14, 2013 Eating Introduction  When reached satiety – we get aversive, nauseating  Smell invlolved ; the rewarding incentive stimuli becomes extremely aversive. Its different with other behv such as SM, MB What motivates us to eat?  Metabolism is the ultimate in self perserfvfation, mmotivation and evolutoin of brain in motivation “...The biological systems of weight regulation promote consumption well above [our] immediate needs... excess energy can be stored to protect from future famine.” (de Ridder and van den Bos 2006 Appetite 47) Energy Balance/Homeostasis  Acquisition not continuous – we eat (more than we need) and the enxpend, get hungry, eat…. Anabolism vs. Catabolism  Anabolism: is the set of metabolic pathway that construct molecules from smaller units. Anabolism is powered by catabolism  Catabolism: is the set of metabolic pathways that breaks down molecules into smaller units and release energy Hormones & Peptides Involved in Feeding  Glucose is a primary source of energy for the brain, and hence its availability influence psychological processes. When glucose is low psychological processes requiring mental effort (e.g. Self-control, effortful decision-making) are impaired (ENERGY)  Ketone bodies are three compounds that are produced as by-products when fatty acids are broken down for energy in the liver. Two of the three are used as a source of energy in the heart and brain while the third (acetone) is a waste product excreted from the body. In the brain, they are a vital source of energy during fasting.  Glycogen serves as a form of energy storage in animals, and fungi. In humans, glycogen is made and stored primarily in the cells of the liver and the muscles (STORED ENERGY)  Insulin is a peptide hormone produced in the pancreas and is central to regulating carbohydrates and fat metabolism in the body. Insulin causes cells in the liver, skeletal muscles and fat tissue to take up glucose from the blood  Glucagon is a peptide hormone secreted by the pancreas that raises blood glucose levels. Its effect is opposite that of insulin, which lowers blood glucose levels.The pancreas releases glucagon when blood sugar (glucose) levels fall too low. Glucagon causes the liver to convert stored glycogen into glucose, which is released into the bloodstream.  Neuropeptide Y (NPY) is an activator of food intake and increases motivation to eat. Found in the PVN (paraventricular nucleus)  CRH (Corticotropin Releasing Hormone) is an acute reduction of food intake  Cholecystokinin (CCK) signals satiety and is released during feeding – digestion PSY398H5S – Motivational Systems Lecture 6 – February 14, 2013  Leptin plays a key role in regulating energy intake and energy expenditure, including appetite/hunger and metabolism. It is one of the most important adipose- derived hormones. Receptors in the VMN and Arcuate Nucleus. Shuts down food intake  Ghrelin is a hunger-stimulating peptide and hormone that is produced mainly by the stomach and pancreas Ghrelin  Stimulates eating by acting on the hypothalamus has been targeted as an anti-obese drug, and potentially a vaccine against obesity!  inc before we eat, peak when we decide to eat, aft eating dec  Completely dictated by eating  Acts on hyp  Block G and is not realeased then no signal for hunger Leptin knockout mice • Mutant mice without leptin or leptin receptor are grossly obese • lack of leptin or its receptor causes morbid obesity in humans • OB is the leptin gene, DB is the leptin receptor gene Well Fed Fasting  1 when glucose levels drop  Glycogen -> glucose glycogen..  When hungry, body is not releasing leptin Dual-center Hypothesis? • Hunger center – Lateral Hypothalamus stimulates eating (lesions lead to complete anorexia) • Satiety Center – Ventromedial Hypothalamus inhibits eating • when u eat, blood glucose levl inc which acts on VMH (same as female sex) – satiety – stops eating – then glucose dec – which acts on LH which is the hunger center which stimulates to eating • Anorexia – lesion of LH PSY398H5S – Motivational Systems Lecture 6 – February 14, 2013 Dual – Hypothesis?  But this is no longer believed to be the case – “animals with VMH lesions do not become fat because they eat too much, but instead they overeat because they are becoming obese”  BECAUSE VMH lesions might actually INHIBIT lypolysis, while ENCOURAGING excessive energy storage – so there’s lots of fat, but none of it can be used by the animal.  ALSO, LH lesions also disrupt ALL motivated behaviors, such as sexual behavior, not just feeding o vMN lesions inhibit glycolysis while encouraging excess storage …the energy is just stored and not available for immediate effects so they eat more ( cant use stored energy) o LH is not specific to eating but any motivated ebhv  CCK released by mechanical disruption (we stop eating when pants are tight) which sends signal thru vagus nerve. Thru the Vnerves it synapse in the brain stem (coming from ST signals)  Hyp affected by long term signals (leptin) (ARC, PVN  ST and Lt sig are merging I nthe brain  -Perception of pleasure associated with consumption of palatable food involves neuronal activation in the Nac and striatum, which through activation of opiate peptide receptors disinhibits the lateral hypothalamic area and thereby stimulates feeding.  VTA – NAC – inhibitory pathway from NAC to areas involed in food PSY398H5S – Motivational Systems Lecture 6 – February 14, 2013  Reward pathway once over activated shuts down the brain areas imp in eating so something that was rewarding will not be rewarding anymore Summary: Brain Areas  Many brain areas involved:  Brain stem: Nucleus tractus solitarius (NTS) receives satiety signals from vagus nerve and other afferents  Midbrain: ventral tegmental area (VTA) passes information to nucleus accumbens (NAc) and striatum about reward value of food  Forebrain:  Hypothalamus receives adiposity signals (leptin, insulin)  NAc and striatum assign/assess reward value of food  There are many compensatory mechanisms which act if one area has a deficit – making it difficult to un
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