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Motivation
Coordination of the Systems
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Systems are complementary.
Both are active to some extent at the same time – not
alternating.
What happens during anger?
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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
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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
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Origins vary depending on the
neurotransmitter involved:
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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
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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.
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Mimic effects of sympathetic ANS activation.
Drug Effects (Cont.)
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Stimulants block catecholamine reuptake and
stimulate release of DA (dopamine),
intensifying effects of DA and NE.
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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?
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That which gives energy and direction to
behavior.
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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
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Hypothalamic regulation has three
components:
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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
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Eating food produces glycogens and
triglycerides (stored as fat) which are broken
down to provide energy for cell metabolism.
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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.
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Storage of glucose keeps this from happening.
Setpoint Hypothesis of Eating
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Adiposity (fat storage) may be a regulator of eating
behavior.
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The brain directs metabolic processes to maintain its fat
store.
Insulin signals the state of fat stores to the brain.
Adiposity affects insulin secretion.
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Lean people are more sensitive to insulin so more
carbohydrate is used and does not become fat.
Appetite Control
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Starvation – intake of energy consistently fails
to meet the body’s needs.
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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
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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.
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Insulin acts like leptin to regulate feeding.
Satiety Factors
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Stretch receptors signal “fullness” to prevent
overfilling of the stomach.
Digestive hormones secreted in the gut signal
satiety.
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Manipulation of these hormones can change
eating behaviors and weight in mice.
Psychological Factors
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Learned associations with time and place.
Socialization and rituals associated with food
(e.g., eating at a party).
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People eat more when in social situations.
Preferences and taste
Dopamine Stimulates Cravings
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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
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Serotonin levels increase as the result of
eating, resulting in mood elevation.
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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
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Anorexia Nervosa – deliberate starvation due
to psychological factors.
Insufficient body weight
 Distorted body image, food obsession
 Anorexics have normal appetite
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Bulimia Nervosa – food binging followed by
purging with laxatives or vomiting.
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Normal body weight, typically
Obesity
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Based on height and weight, a body mass index above
30 (above 25 is overweight).
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Causes:
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http://www.caloriecontrol.org/bmi.html
Different metabolic rate
Larger adipocytes
More vulnerable to food cues, finicky
Recidivism after dieting = 90+% in all forms of
treatment.
Thirst
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Two physiological signals stimulate drinking
behavior:
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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.
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Lack of vasopressin results in diabetes insipidus.
Temperature Regulation
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Two controls:
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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
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Occurs when immune response causes heatgain mechanisms to increase body
temperature.
Elevated temperature:
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Activates antibody-producing cells
Increases the rate at which white blood cells
move to sites of infection.
Directly affect some viruses but not all.