Understanding Motivation: Systems and Effects in Behavior Control

1. Motivation

2. Coordination of the Systems • Systems are complementary. • Both are active to some extent at the same time – not alternating. • What happens during anger? • Sympathetic arousal increases blood pressure. • Medulla detects that arousal and activates the parasympathetic to keep blood pressure within normal limits. • Hypertension occurs with deficient feedback.

3. Diffuse Modulatory Systems • A small set of diffuse modulatory neurons arise from the brain stem. • Each neuron has an axon that can influence more than 100,000 postsynaptic neurons spread widely across the brain. • Their synapses release neurotransmitter into the extracellular fluid, not into a confined synaptic cleft.

4. Origins of Diffuse Neurons • Origins vary depending on the neurotransmitter involved: • NE system – locus coeruleus (waking, arousal, attention, memory, anxiety, pain, mood). • 5-HT serotonin system – raphe nuclei (wakefulness, mood, emotional behavior). • DA system – substantia nigra & ventral tegmentum (reward). • ACh system – basal forebrain (unknown)

5. Effects of Drugs • Many abused drugs act directly on the modulatory systems. • Hallucinogens such as LSD – agonist for serotonin, decreasing activity of raphe nuclei. • Stimulants (cocaine, amphetamine) – affect DA and NE systems, causing increased alertness, self-confidence, euphoria. • Mimic effects of sympathetic ANS activation.

6. Drug Effects (Cont.) • Stimulants block catecholamine reuptake and stimulate release of DA (dopamine), intensifying effects of DA and NE. • This causes the stimulant effect. • Because cocaine and amphetamine affect the reward systems, drug-seeking behaviors are reinforced leading to addiction or psychological dependence.

7. What is Motivation? • That which gives energy and direction to behavior. • The driving force for behavior. • Motivation is necessary for behavior but does not guarantee it. • How we choose among competing goals is not well understood. • Survival-related behavior is best understood.

8. Motivated Behavior • Hypothalamic regulation has three components: • Stimulation of the pituitary to release hormones into the bloodstream. • Neural signals to the sympathetic and parasympathetic ANS. • Somatic-motor response (behavior) to remedy the deficiency. • The psychological experience is “drive”

9. Maintaining an Energy Balance • Eating food produces glycogens and triglycerides (stored as fat) which are broken down to provide energy for cell metabolism. • Glucose is used by neurons, but not fatty acids and ketones (used by all other cells). • Without adequate glucose, a person will lose consciousness and quickly die. • Storage of glucose keeps this from happening.

10. Setpoint Hypothesis of Eating • Adiposity (fat storage) may be a regulator of eating behavior. • The brain directs metabolic processes to maintain its fat store. • Insulin signals the state of fat stores to the brain. • Adiposity affects insulin secretion. • Lean people are more sensitive to insulin so more carbohydrate is used and does not become fat.

11. Appetite Control • Starvation – intake of energy consistently fails to meet the body’s needs. • Adiposity (fat) – intake consistently exceeds need • Motivation to eat arises from a complex interplay of physiological mechanisms. • Leptin levels act on the brain via peptides to inhibit or stimulate eating behavior and adjust metabolic activity.

12. Short-Term Regulation • The leptin-governed drive to eat is inhibited by satiety signals that occur during eating. • Gastric distension – how full the stomach feels – is signaled by mechanosensory receptors. • Intestines release CCK in response to stimulation, which inhibits appetite and releases insulin. • Insulin acts like leptin to regulate feeding.

13. Satiety Factors • Stretch receptors signal “fullness” to prevent overfilling of the stomach. • Digestive hormones secreted in the gut signal satiety. • Manipulation of these hormones can change eating behaviors and weight in mice.

14. Psychological Factors • Learned associations with time and place. • Socialization and rituals associated with food (e.g., eating at a party). • People eat more when in social situations. • Preferences and taste

15. Dopamine Stimulates Cravings • Originally, eating was thought to result in pleasure (release of dopamine in pleasure centers of brain). • However, dopamine-depleted rats behave as if eating is pleasurable but show decreased motivation to seek food. • Stimulation of dopamine pathways in hypothalamus appears to produce cravings, not pleasure.

16. Serotonin Links Food to Mood • Serotonin levels increase as the result of eating, resulting in mood elevation. • Derived from tryptophan which comes from carbohydrates. • Drugs that elevate serotonin are appetite suppressants. • Abnormalities in serotonin may contribute to eating disorders accompanied by depression.

17. Eating Disorders • Anorexia Nervosa – deliberate starvation due to psychological factors. • Insufficient body weight • Distorted body image, food obsession • Anorexics have normal appetite • Bulimia Nervosa – food binging followed by purging with laxatives or vomiting. • Normal body weight, typically

18. Obesity • Based on height and weight, a body mass index above 30 (above 25 is overweight). • http://www.caloriecontrol.org/bmi.html • Causes: • Different metabolic rate • Larger adipocytes • More vulnerable to food cues, finicky • Recidivism after dieting = 90+% in all forms of treatment.

19. Thirst • Two physiological signals stimulate drinking behavior: • Decrease in blood volume • Increase in the concentration of dissolved substances in the blood. • Vasopressin acts on the kidneys to increase water retention and inhibit urine production. • Lack of vasopressin results in diabetes insipidus.

20. Temperature Regulation • Two controls: • Sensors from skin • Blood temperature (at hypothalamus) • Heat-gain mechanisms increase blood temperature (goose bumps). • Heat-loss mechanisms decrease it (shunt blood to skin, perspiration).

21. Purpose of Fever • Occurs when immune response causes heat-gain mechanisms to increase body temperature. • Elevated temperature: • Activates antibody-producing cells • Increases the rate at which white blood cells move to sites of infection. • Directly affect some viruses but not all.