Emotions

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Emotions
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I. What is an emotion?

• What do you think???

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II. What are the 6 basic emotions?

• Sadness
• Happiness
• Anger
• Disgust
• Surprise
• Fear

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III. How do we define emotions?

• We often describe our emotions by the
  physiological sensations we experience at the
  time of the emotions.
• E.g., if you feel fear, you may describe this
  fear response by describing how fast your heart
  is racing.

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Why use physiology to describe emotions?

• Our bodies undergo significant changes while we
  are experiencing different emotions. We can use
  this information to describe what were feeling.
• Theories of emotion incorporate both
  parasympathetic sympathetic NS responses in
  defining emotions.

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IV. Theories of emotion

• 1. James-Lange theory of emotion argues we
  experience physiological sensations in response
  to an event our perception of these changes
  defines the emotion.
• (E.g., We feel sad because we cry, we feel angry
  because hour heart races!!!)
• Problem Similar patterns of autonomic activity
  are produced for different emotions (fear,
  anger).
• For example, how do you tell the difference
  between anxiety anger? The pattern of activity
  is similar, but the emotions are distinctly
  different.

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2. Cannon-Bard Theory

• Cognitive aspect of emotion is independent
• from physiological aspects of emotion.
• Problem Theoretically, changes in the intensity
  of autonomic arousal should have no effect on
  emotional experience, but they do.
• E.g., While spinal cord injury patients report
  being able to experience emotions, they report
  the emotions are perceived less intensely than
  before the injuries.

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3. Schachter and Singers Theory of Emotions

• Argues we experience a given emotion based on our
  cognitive appraisal (label) of our physiological
  sensations.
• Were interested in determinants of anger, fear,
  euphoria. They explored interdependence between
• External environment
• Internal events (e.g., adrenaline)
• Subjective feelings

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Schachter Singers Classic Study

• Four groups of Ss participated in the study.
• Three groups of Ss were given a shot of
  epinephrine (activates sympathetic arousal for
  20-30 min.), whereas the fourth group was given a
  placebo injection.
• All Ss were told they received suproxin, a
  harmless drug.

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Experimental groups in Schacter Singer study
(1962)

• Group 1 Epinephrine informed- were told side
  effects of drug (those relating to epinephrine
  such as increased HR).
• Group 2 Epinephrine uninformed- those told
  nothing of possible side effects.
• Group 3 Epinephrine Misinformed- those
  misinformed of possible side effects (e.g., numb
  feed, headache).

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Changing the social context of emotion.

• Following injections instructions, each subject
  was placed in a situation that was designed to
  promote either euphoria or anger.
• Note Ss in the misinformed group did not
  particular in the anger condition (see next
  slide).

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Creating euphoria or anger

• Anger conditionSs were placed in a room with an
  angry confederate required to fill out a
  questionnaire. The angry confederate was surly,
  used obscenities, was generally annoying.
• Euphoria condition-Ss were placed in a room with
  a happy confederate who did silly things
  (building paper planes, throwing wads of paper,
  jumping up on desk, etc.)

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Results of study

• Euphoria Anger
• Placebo Euphoria Anger
• E-informed Little emotion Little emotion
• E-uninformed Euphoria Anger
• E-misinformed Euphoria XXX

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Summary of Results

• 1. Ss who knew they were feeling the effects of
  the drug, showed less intense emotional
  responses in both conditions. They didnt
  attribute their physiological activity to the
  situation, but to the drug.
• 2. Ss who were either uninformed or misinformed
  appeared to rely on the contextual cues from the
  situation (euphoric or angry) to label their
  physiological sensations hence emotions.

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Serious Flaw of Schacter Singer Study

• Ss who were given placebo injections instead of
  epinephrine, showed about as much euphoria in the
  euphoria condition as much anger in the anger
  condition as did Ss given epinephrine.
• If epinephrine had nothing to do with the results
  of the study, then the data dont support the
  theory. The jury is still out on this one!!!

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V. Violent or attacking behavior

• The emotion of anger elicits a sympathetic
  response that increases the organisms likelihood
  of attack.
• In animals (nonhuman human) attacking behavior
  will either be calculated or affective.
• Affective attacking- Cats threatened by other
  cats shriek hiss, show piloerection, increased
  posture.
• Non-affective attacking- A cat attacking
• a mouse, will attack kill the mouse in
• a smooth swift fashion.

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Why do we usually attack others?

• We attack usually because of pain or a
  perceived threat.
• E.g., Hamsters in home cage will attack intruding
  hamsters (over territorial issues).
• Hamster will be likely to attack intruder for up
  to 30 min. following intrusion.
• Biologically this is linked with increased
  activity in the corticomedial area of the
  amygdala.

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Does genetics play a role in whether attacking
behavior will occur?

• Yes!!! Studies of twins adopted kids show that
  genetics contributes to aggressive behavior
  (antisocial, criminal).
• Adopted kids most likely to engage in
  aggressive behaviors-- had biological parents
  with criminal records AND adoptive parents with
  marital discord, depression, substance abuse,
  etc.
• A biological predisposition or a troubled
• adoptive family by itself produced only
• moderate effects (Cadoret et al., 1995).

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Do hormones play a role in aggressive behaviors?

• Yes!!!
• Most violent or attacking behavior occurs in
  males (in humans nonhumans), implicating
  testosterone in aggressive behavior.

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Evidence that testosterone is linked with
aggression

• 1. Castrated males males during
  non-reproductive seasons fight significantly less
  than males higher in testosterone.
• 2. Men arrested for committing violent crimes
  have higher testosterone levels than men
  committing non-violent crimes.
• 3. Highest incidence of violence is in men 15-25
  years of age, when testosterone is at highest
  level.

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Neurophysiological basis of aggression

• Stimulation of an animals corticomedial amygdala
  will increase the probability of attack against
  an intruder.
• Stimulation of the ventromedial nucleus of the
  hypothalamus also leads to violent behavior.
• (Rabies is caused by a virus that attacks the
  brain especially the temporal lobe (amygdala)).
• Stimulating the amygdala may lead to aggressive
  responses (cats), whereas removing it leads to
  tameness placidity (monkeys).

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VI. Fear, enhanced fears, and the Amygdala

• All animals humans have a startle reflex to
  loud noises.
• This is an unlearned fear, but can be
  conditioned.
• We jump or react more vigorously to
• loud noise when we are already tense
• (walking to car in dark).

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Startle Response

• We can measure enhancement of startle reflex to
  index fear or anxiety.
• A baseline measure of startle is first obtained.
  This is done by measuring an organisms response
  to a loud noise.
• Then an external stimulus (light) is repeatedly
  paired with a shock or loud noise.
• This will enhance or increase the startle reflex.
  

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What does the amygdala do during startle?

• Output from the amygdala goes to the hypothalamus
  which controls autonomic fear responses.
• Projections are then sent to the pons to control
  the reflex.
• Evidence animals with damage to the amygdala
  will show reduced or no learning of enhanced
  fears (and social relationships will be
  impaired).

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Frontal cortex and emotions

• The frontal lobes may play a role in regulating
  our emotions in given social contexts.
• Left frontal activation appears to be related to
  behavioral approach. Emotions regulated by this
  area may be anger, joy, happiness.
• Right frontal activation appears to be related to
  behavioral withdrawal. Emotions regulated by
  this area may be fear, sadness, depression.