Motivation

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.

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.

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)

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.

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.

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.

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”

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.

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.

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.

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.

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.

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

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.

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.

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

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.

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.

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).

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.