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BIO 132BIO 132
NeurophysiologyNeurophysiology
Lecture 35Lecture 35
MotivationMotivation
Lecture Goals:Lecture Goals:
 Understanding the underlying mechanismsUnderstanding the underlying mechanisms
affecting ru...
 Motivation – the driving force behind behaviorMotivation – the driving force behind behavior
 The brain area(s) respons...
 Hunger: the motivation to eatHunger: the motivation to eat
 Hunger is affected by more than one homeostaticHunger is af...
 Goal of long-term feeding behavior: MaintainGoal of long-term feeding behavior: Maintain
long-term energy stores (fat).l...
 Experimentally, rats were given food to eat wheneverExperimentally, rats were given food to eat whenever
they wanted (th...
 Caloric intake = caloric expenditure Normal weightCaloric intake = caloric expenditure Normal weight
 Caloric intake > ...
 First proposed in 1953, theFirst proposed in 1953, the lipostaticlipostatic
hypothesishypothesis states that the brain m...
 Evidence of a hormone from the fat (1960s):Evidence of a hormone from the fat (1960s):
 Parabiosis (the fusing of two a...
 It was apparent that the blood carried someIt was apparent that the blood carried some
signal to the brain from the fat ...
 Once isolated an synthesized, leptin could beOnce isolated an synthesized, leptin could be
injected into obese mice (ob/...
 It was known since the 1940s that destruction of theIt was known since the 1940s that destruction of the
hypothalamus le...
 Once leptin binds to receptors in the arcuate nucleus,Once leptin binds to receptors in the arcuate nucleus,
activated n...
 Other hypothalamic neurons projecting to the pituitaryOther hypothalamic neurons projecting to the pituitary
release cor...
Effects of Leptin
ventrical
Arcuate nucleus
Lateral zonePeriventricular
zone
nutrients
Fat
leptin
αMSH
CART
Pituitary
Feed...
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Lecture 35 (Motivation)

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Transcript of "Lecture 35 (Motivation)"

  1. 1. BIO 132BIO 132 NeurophysiologyNeurophysiology Lecture 35Lecture 35 MotivationMotivation
  2. 2. Lecture Goals:Lecture Goals:  Understanding the underlying mechanismsUnderstanding the underlying mechanisms affecting rudimentary motivations (hunger,affecting rudimentary motivations (hunger, thirst, warmth, etc).thirst, warmth, etc).  Appreciating the common elements behind theAppreciating the common elements behind the feedback loops controlling hunger, thirst, andfeedback loops controlling hunger, thirst, and temperature regulation.temperature regulation.
  3. 3.  Motivation – the driving force behind behaviorMotivation – the driving force behind behavior  The brain area(s) responsible for keeping trackThe brain area(s) responsible for keeping track and deciding on what the current behaviorand deciding on what the current behavior should be is still unknown.should be is still unknown.  Many motivations arise from internalMany motivations arise from internal homeostatic feedback loops.homeostatic feedback loops. Motivation Current Goal Sit in class Get food Urinate Listen to music Sit in class Motivations Behavior
  4. 4.  Hunger: the motivation to eatHunger: the motivation to eat  Hunger is affected by more than one homeostaticHunger is affected by more than one homeostatic feedback loop.feedback loop.  Maintenance of blood glucose levels (short-term feedingMaintenance of blood glucose levels (short-term feeding behavior)behavior)  Maintenance of fat stores (long-term feeding behavior)Maintenance of fat stores (long-term feeding behavior)  Hunger can also be affected by things other than homeostaticHunger can also be affected by things other than homeostatic feedback loops such as mood (bored, sad, happy, anxious,feedback loops such as mood (bored, sad, happy, anxious, etc).etc). Hunger
  5. 5.  Goal of long-term feeding behavior: MaintainGoal of long-term feeding behavior: Maintain long-term energy stores (fat).long-term energy stores (fat).  Fat has twice the energy (per weight) as glucoseFat has twice the energy (per weight) as glucose and doesn’t require excess water storage likeand doesn’t require excess water storage like glucose (fat isn’t osmotically active).glucose (fat isn’t osmotically active).  The body has a set-point for the amount of fat itThe body has a set-point for the amount of fat it would like stored on the body.would like stored on the body. Long-term Feeding Behavior
  6. 6.  Experimentally, rats were given food to eat wheneverExperimentally, rats were given food to eat whenever they wanted (they wanted (ad libitumad libitum), but at two time periods of the), but at two time periods of the experiment were deprived of food and forced fed.experiment were deprived of food and forced fed. Maintenance of Fat Stores Time (days) Bodyweight(g) fasted force-fed set-point
  7. 7.  Caloric intake = caloric expenditure Normal weightCaloric intake = caloric expenditure Normal weight  Caloric intake > caloric expenditure Gain weightCaloric intake > caloric expenditure Gain weight  Caloric intake < caloric expenditure Lose weightCaloric intake < caloric expenditure Lose weight Energy Balance
  8. 8.  First proposed in 1953, theFirst proposed in 1953, the lipostaticlipostatic hypothesishypothesis states that the brain monitors fatstates that the brain monitors fat levels and maintains them at some fixed set-levels and maintains them at some fixed set- point amount.point amount.  The lipostatic hypothesis requires that the fatThe lipostatic hypothesis requires that the fat communicate with the brain in some way.communicate with the brain in some way.  First suspected was some blood-borne chemincal (aFirst suspected was some blood-borne chemincal (a hormone).hormone). Lipostatic Hypothesis
  9. 9.  Evidence of a hormone from the fat (1960s):Evidence of a hormone from the fat (1960s):  Parabiosis (the fusing of two animals so that theyParabiosis (the fusing of two animals so that they share the same blood) of a genetically obese mouseshare the same blood) of a genetically obese mouse to a normal mouse caused the obese mouse toto a normal mouse caused the obese mouse to become thin (normal weight).become thin (normal weight). Hormone from Fat Obese Normal Surgically fused (share blood)
  10. 10.  It was apparent that the blood carried someIt was apparent that the blood carried some signal to the brain from the fat that allowed thesignal to the brain from the fat that allowed the brain to monitor the levels of fat.brain to monitor the levels of fat.  The hormone went undiscovered until 1994.The hormone went undiscovered until 1994.  The gene that made genetically obese miceThe gene that made genetically obese mice (ob/ob) was finally isolated and its product(ob/ob) was finally isolated and its product synethesized.synethesized.  The product of the gene was namedThe product of the gene was named leptinleptin Hormone from Fat
  11. 11.  Once isolated an synthesized, leptin could beOnce isolated an synthesized, leptin could be injected into obese mice (ob/ob) that cannoneinjected into obese mice (ob/ob) that cannone make leptin themselves, and the mice wouldmake leptin themselves, and the mice would become thin (normal weight).become thin (normal weight). Hormone from Fat - Leptin Obese (ob/ob) Normal leptin
  12. 12.  It was known since the 1940s that destruction of theIt was known since the 1940s that destruction of the hypothalamus led to abnormal food intake.hypothalamus led to abnormal food intake.  Leptin was theorized to have its effect on theLeptin was theorized to have its effect on the hypothalamus.hypothalamus.  It is now known that leptin binds toIt is now known that leptin binds to ααMSH and CARTMSH and CART receptors in the arcuate nucleus of the hypthalamus.receptors in the arcuate nucleus of the hypthalamus.  ααMSH stands for alpha-melanocyte-stimulating hormone.MSH stands for alpha-melanocyte-stimulating hormone.  CART stands for cocaine-and amphetamine-regulatedCART stands for cocaine-and amphetamine-regulated transcript.transcript. * You do not need to memorize these names, just the abbreviations.* You do not need to memorize these names, just the abbreviations. How Does Leptin Work?
  13. 13.  Once leptin binds to receptors in the arcuate nucleus,Once leptin binds to receptors in the arcuate nucleus, activated neurons project to the periventricular and theactivated neurons project to the periventricular and the lateral zones.lateral zones.  The periventricular zone activates both the sympatheticThe periventricular zone activates both the sympathetic NS and neurons projecting to the pituitary gland.NS and neurons projecting to the pituitary gland.  Activated SNS causes in increase in metabolism (burningActivated SNS causes in increase in metabolism (burning calories).calories).  Hypothalamic neurons projecting to the pituitary releaseHypothalamic neurons projecting to the pituitary release thyroid releasing hormone (TRH) which causes the release ofthyroid releasing hormone (TRH) which causes the release of thyroid stimulating hormone (TSH) from secretory cells inthyroid stimulating hormone (TSH) from secretory cells in the anterior pituitary, causing the release of thyroid hormonethe anterior pituitary, causing the release of thyroid hormone from the thyroid gland, increasing metabolism.from the thyroid gland, increasing metabolism. Effects of Leptin on the Arcuate Nucleus
  14. 14.  Other hypothalamic neurons projecting to the pituitaryOther hypothalamic neurons projecting to the pituitary release corticotropin releasing hormone (CRH) which causesrelease corticotropin releasing hormone (CRH) which causes the release of adrenocorticotropic hormone (ACTH) fromthe release of adrenocorticotropic hormone (ACTH) from secretory cells of the pituitary, causing the release of cortisolsecretory cells of the pituitary, causing the release of cortisol from the adrenal gland which increases metabolism.from the adrenal gland which increases metabolism.  The lateral zone activates neurons that decrease theThe lateral zone activates neurons that decrease the motivation to eat by decreasing hunger and increasingmotivation to eat by decreasing hunger and increasing the feeling of satiety. This decreases caloric intake.the feeling of satiety. This decreases caloric intake. Effects of Leptin on the Arcuate Nucleus
  15. 15. Effects of Leptin ventrical Arcuate nucleus Lateral zonePeriventricular zone nutrients Fat leptin αMSH CART Pituitary Feeding behavior TRH TSH thyroid hormone CRH ACTH cortisol Metabolic rate Satiety Hunger Caloric intake SNS inhibit
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