Motivation Flashcards
1
Q
Drive-reduction theory
A
- Drive = unpleasant state of arousal or tension caused by a need.
- This drive impels the organism to engage in behaviour that will satisfy the need and reduce the tension.
- Maintenance of homeostasis: deviation of a parameter from the normal values leads to corrective action associated with motivation (instinct, drive)
- important for survival → e.g. water and temperature levels
- social homeostasis = maintaining or regaining contact with “special others”: partner, child, parents
2
Q
Short-term regulation
A
- Hypothalamus monitors storage and use of carbohydrates (glucostatic theory; Mayer, 1955)
- Cells need sugar for energy
- Sugar cannot get into most cells directly → insulin
- When eat carbs
- → glucose in blood → signal to pancreas to release insulin → glucose enters cell
-
Glucose
- (1) used by cells as energy
- (2) stored excess as glycogen in liver and muscles
- When glucose gets low, pancreas signals to liver and muscle cells to release glucagon into bloodstream
3
Q
Digestion phases
A
- Cephalic phase: the gastric secretion that occurs even before food enters the oral cavity. It results from the visual, olfactory, and auditory inputs to the brain induce anticipatory responses to prepare the gastrointestinal tract for the meal.
- Gastric phase: period in which swallowed food and semi-digested protein ( peptides and amino acids ) activate gastric activity.
- Substrate phase: Stomach chemical secretion ceases once the intestinal phase of digestion begins.
4
Q
Diabetes and insulin
A
- In diabetes Insulin levels remain constantly low
- Blood glucose is too high
- People and animals with diabetes eat more than normal because their cells are starving
- But they may excrete most of their glucose and lose weight
5
Q
Insulin and hunger
A
If insulin stays high, the body continues to move blood glucose into cells: glucose drops.
- Despite high insulin, hunger increases
- In autumn, animals that hibernate have higher insulin
- Humans have been shown to eat more in autumn (de Castro, 2000)
6
Q
Ghrelin
A
- Other short-term regulator hormone
- Increase in ghrelin → increase in appetite
- Decrease in ghrelin → decrease in appetite → stomach expansion
- Swallowing a balloon can cause eating smaller meals (Cannon & Washburn, 1912)
7
Q
Long-term regulation
A
- Hypothalamus monitors storage and metabolism of fat (lipostatic theory; Kennedy, 1953)
- Leptin = “satiety hormone” → long-term compensation for daily “mistakes”
- Set-point body fat
- the body weight of adults is relatively constant
- deviations from the set-point produce compensatory adjustments in eating
- Leptin released by fat cells
- Leptin is detected in hypothalamus
- Leptin↑ enhanced satiety
- Leptin↓ reduced satiety
8
Q
Leptin/genes studies
A
-
Ingalls et al., 1950
- Genetically modified ob/ob mice brain reacts as if the body has no fat → higher food intake; conserves energy
- Injection of leptin reverses these symptoms i.e. weight loss
-
Coleman, 2010
- Ob/ob parabiosed to normal mice
- Joined surgically, develop single shared physiological system
- As if missing hormone was replaced
- Feeding behaviour and obesity greatly reduced
9
Q
Lipostatic hypothesis limitations
A
- Almost all over-weight people produce plenty of leptin (Considine et al., 1996)
- → Less sensitive to it
- → Decreased sensitivity also seen in pregnancy and hibernation (where increased intake makes sense)
- Following overeating, damages part of neurons of hypothalamus → decrease sensitivity (Ernst et al., 2009)
- Undo effect with physical exercise, helps repair cells (Ropelle et al., 2010).
10
Q
Lateral hypothalamus
A
- Hunger centre
- Many axons containing dopamine pass through lateral hypothalamus
- Axons can alter taste sensation (when it detects hunger, makes food taste better)
- Increases sensory response to taste, smell, sight of food (Critchley & Rolls, 1996)
- Increases secretion of hormones à increase insulin
- Helps digestion secretions (van den Pol, 1999)
- Hunger or motivation centre?
- Lesions cause aphagia (absence of eating) – as if food were distasteful -
- and adipsia (absence of drinking)
- But also, general lack of responsiveness to sensory input (not only food /drink)
11
Q
Ventromedial hypothalamus
A
- Satiety centre
- Lesion causes:
- Overeating
- Eat normal sized meals more often (Hoebel & Hernandez, 1993)
- Increased stomach muscle contractions and secretions, stomachs empty faster than normal
- Damage increases insulin production (King, Smith & Frohman, 1984)
- Satiety centre or a change in metabolic rate?
- Initial interpretation: lesioned animals become obese because they overeat
- new interpretation:
- bilateral VMH lesions → increased blood insulin levels → increased lipogenesis → decreased breakdown of lipids
- Ingested calories are converted into fat at a high rate → rat needs to eat more to ensure that enough calories are in the blood for immediate energy requirements → more hunger
12
Q
Incentive theories
A
- We are not only driven to eat by energy deficits, but also because we crave it (like sex and drugs)
- We take advantage of good food when it is available
- We are drawn to eat by the anticipated pleasure of eating → positive incentive value
- The incentives are dependent on:
- hunger / satiety level
- external environment
- learning
- individual differences in listening to interoceptive signals about hunger and being influenced by the environment or other internal states
13
Q
Appetitive phase
A
- Mesolimbic dopaminergic pathway → dopamine is sent to the amygdala
- Destruction of this pathway makes animals lack motivation to seek food i.e. they like it but they don’t want it
- Important for reward prediction/learning
- You need to want something to achieve it - this phase is crucial
14
Q
Consummatory phase
A
- Once goal is found
- Nucleus Accumbens is linked to liking the food and signals the termination of the appetitive phase
- Controls reward and avoids punishment i.e. shapes likes/dislikes of food
15
Q
Food and mood
A
- Food elicits strong dopamine and serotonin bursts → Reinforcement and hedonic effect
- Serotonin is derived from tryptophan (linked to carbohydrates).
- Serotonin suppresses appetite
- Abnormalities linked to eating
disorders (linked to depression)
- Depression ≠ obesity (McIntyre et al., 2006):
- 19% of depressed people are obese
- 15% of non-depressed people are obese
