the limbic brain Flashcards

1
Q

How does the body use energy?

A

Three primary ways:
Basal Metabolism (BMR): 55% of energy is used to maintain body heat and other resting functions.
Digestion of Food: 33% of energy is used to process food.
Active Behavioral Processes: 12-13% of energy is used for non-resting behaviors.
**Stored energy: **Remaining energy is typically stored as reserves.

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2
Q

What is the Kleiber function for calculating Basal Metabolic Rate (BMR)?

A

Kleiber’s formula: Kcal/day = 70 × weight^0.75
Purpose: Estimates the energy expenditure based on body weight.

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3
Q

What are the primary nutrients and their energy values?

A

Carbohydrates: ~4 kcal per gram. Converted to glucose, the primary energy source. Stored as glycogen in liver and muscles.
Amino Acids (Proteins): ~4 kcal per gram. Basic building blocks of cells. 9 out of 20 amino acids are essential (cannot be produced by the body).
Lipids (Fats): ~9 kcal per gram. Long-term energy storage and source of glucose.
Vitamins and Minerals: Essential for bodily functions but do not provide energy. Needed for digestion, homeostasis, and cell building.

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4
Q

What is glucose’s role in the body?

A

Primary fuel: Glucose is the main source of energy for the body, derived from carbohydrates.

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5
Q

What is the role of appetite in maintaining homeostasis?

A

Variable: The body needs to maintain balance in variables like glucose or body fat.
Set-point: The desired level of a specific variable (e.g., blood glucose or body fat).
Sensor: Measures the levels of variables.
**Effector mechanisms: **Control feeding behavior, metabolism, etc.

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6
Q

What is the glucostat theory?

A

Theory (Mayer, 1954): Blood glucose levels are a primary variable that needs to be at equilibrium.
**Outcome of low glucose: **Drive to eat (to restore glucose levels).

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7
Q

What is the lipostatic theory?

A

Theory: Eating is regulated by a hypothetical body-fat set-point.
Homeostasis: The body maintains a certain level of fat for long-term energy storage.

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8
Q

What is the dual-centre hypothesis?

A

Ventromedial Hypothalamus (VMH): Lesions cause increased feeding and weight. VMH is proposed as the satiety (stop eating) center.
Lateral Hypothalamus (LH): Lesions cause reduced feeding and weight. LH is proposed as the hunger (start eating) center.

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9
Q

What are the problems with the dual-centre hypothesis?

A

James Olds’ experiments: Self-stimulation of LH did not just lead to eating but also other behaviors (e.g., drinking, fighting, mating).
Elliot Valenstein: LH stimulation leads to various behaviors, not just eating, suggesting LH is involved in motivated behaviors, not just hunger.

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10
Q

What hormones are involved in hunger and satiety signals?

A

Hunger signals (e.g., Ghrelin, Orexin): Peptide hormones from the gut, adipose tissue, and hypothalamus that increase hunger.
Satiety signals (e.g., CCK, PYY, Leptin):
Cholecystokinin (CCK): Released in response to fat and inhibits feeding.
Peptide YY (PYY): Released after food intake and inhibits eating.
Leptin: Produced by adipose tissue, interacts with receptors in the hypothalamus to reduce hunger.

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11
Q

What is the role of Leptin in satiety?

A

Leptin: Produced by fat cells, signals the brain to reduce hunger.
Deficiency: Leads to obesity, as seen in leptin-deficient mice.
Action: Binds to receptors in the hypothalamus, particularly in the ventromedial nucleus, to regulate appetite.

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12
Q

What is appetite as a motivational system?

A

**Homeostatic system: **Competing hunger and satiety signals regulate eating behavior.
Hunger signals: Lateral Hypothalamus, Ghrelin, Orexin.
Satiety signals: Ventromedial Hypothalamus, CCK, PYY, Leptin.

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13
Q

Does motivation to eat always depend on homeostatic mechanisms?

A

Non-homeostatic factors: Learned associations, taste, smell, and anticipation can drive eating even when not hungry or full.
**Anticipatory eating: **For example, babies may eat before a long night’s sleep even if not hungry.

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14
Q

What is anticipatory eating in rats?

A

Study finding: Rats eat and drink before lights go off (before sleep), even if not hungry. This is driven by an internal clock rather than by hunger.

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15
Q

What is cue-potentiated feeding?

A

Pavlovian conditioning: A cue (CS+) paired with food delivery can trigger overeating, even when the animal is satiated.
Brain involvement: The amygdala influences hypothalamic processes related to hunger.

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16
Q

How do learned associations influence appetite?

A

Learned cues: Food-specific cues (visual or auditory) can trigger feeding behavior in humans and animals, even when not hungry.
Study (Birch et al., 1989): Food-related cues enhanced eating in children.

17
Q

What is the role of the mesolimbic dopamine system in eating behavior?

A

Study findings: Rats that are deprived of food show pleasure responses to sweet solutions, which is dopamine-mediated.
**Dopamine’s role: **Dopamine promotes the “wanting” of food, though not necessarily the “liking.”

18
Q

What is the dissociation between liking and wanting in eating behavior?

A

**Liking: **Mediated by opioid, GABA, and cannabinoid systems in the nucleus accumbens.
Wanting: Mediated by dopamine in the mesolimbic system.
**Study findings: **Genetically altered mice with high dopamine levels “want” more food, but do not “like” it more.

19
Q

What brain areas are involved in motivation to eat and drink?

A

Limbic system: Includes the cingulate cortex, hippocampus, amygdala, and nucleus accumbens, which integrate homeostatic and non-homeostatic signals for feeding, drinking, and temperature regulation.

20
Q

What is the motivation summary in relation to appetite?

A

Homeostatic mechanisms: Maintain temperature, hydration, and nutrient levels.
Hypothalamus: Critical in regulating homeostasis.
Limbic system: Non-homeostatic influences (e.g., learning, emotion) on feeding behavior.