Lecture 30: Emotion, Risk, and Reward

skin conductance response

Skin conductance response is a product of electrodermal activity

Activation of eccrine sweat glands – controlled solely by the sympathetic nervous system – increases electrical conductance of the skin surface

Characteristic onset latency and peak latency

Measures emotional arousal

Identifies stimulus-evoked arousal responses that arise subconsciously

James-Lange feedback theory

feedback circuit whereby sensory stimuli lead to autonomic physiological

responses, which then produce a conscious feeling

Cannon-Bard theory of emotion

parallel processing circuit whereby

sensory stimuli are directed to the

cortex to produce a conscious feeling, and to the hypothalamus to produce an autonomic physiological response

Functional lateralization

Callosotomy performed to alleviate epileptic seizures

Image projected onto right

visual field: Patient can identify the

object using both verbal and

non-verbal cues

Image projected onto left

visual field: Patient is unable to identify

the object verbally, but able to identify the object non-verbally

If the projected image has emotional significance, the patient experiences altered emotions even though they

cannot recognize the image

Asymmetric smiles

Facial expressions are often more quickly and fully expressed by the left facial musculature than the right

Since the left lower face is controlled by the right hemisphere, most individuals are emotionally “left-faced” in the same sense that most individuals are right-handed

Duchenne smile

Emotion-driven contraction of the

orbicularis oculi, together with the zygomaticus major

It is initiated by motor areas in the anterior cingulate cortex

Cingulate motor cortex mediates non-conscious emotion-driven facial movements

Emotion can produce motor activity

independent of somatomotor cortex

Fear acquisition

Dissociation between fear learning and declarative memory

Simple forms of fear conditioning can be dissociated from declarative memory

Fearful stimuli can be conditioned subliminally, without conscious awareness in healthy individuals

Subconscious fear

amygdala becomes active in response to fearful stimuli even if the subject is unaware of the fearful stimulus

During a binocular rivalry task in which subjects are presented with houses,

neutral faces, and fearful faces, the amygdala exhibits greater activity for fearful than for neutral faces even when the subject reports seeing only the house

Posttraumatic Stress Disorder

Deficits of fear extinction

When a stimulus that previously predicted a threat becomes “safe,” PTSD patients continue to exhibit

greater skin conductance response to the now-safe stimulus

greater amygdala activation during the extinction test, as well as hypoactivation of the vmPFC

This pattern is indicative of persistent hyperreactivity to threats, and difficulty engaging executive control circuits to suppress acquired fears when they are no longer appropriate to express

Normal fear extinction depends on the vmPFC

damage to vmPFC

lack the somatic marker predicting risky actions, leading to non-optimal choices and poor decision-making

Supports James-Lange Theory

Interoception

conscious or subconscious cortical representation of the body’s physiological state

Activity of the insular cortex correlates with a subject’s ability to detect their own heartbeat

Damage to insular cortex impairs the ability to recognize certain emotions, especially disgust

Emotional effects on attentional blink

amygdala appears able to override the attentional blink, allowing emotional stimuli to reach awareness more readily

Individuals with bilateral damage to the amygdala do not exhibit this emotional facilitation

stress and consolidation

Those who experienced the cold stress had better recall of emotionally-charged image

Dopaminergic projections from the VTA

Dopaminergic neurons of the VTA have

projections to the septal nuclei and nucleus accumbens via the mesolimbic pathway, and to diffuse cortical areas via the mesocortical pathway

Several lines of evidence link these dopaminergic projections to reward processing

drugs of abuse

Nearly all drugs of abuse exert their addictive influence through alterations of the mesolimbic pathway

These drugs either cause VTA neurons to release more DA, block the reuptake of DA, or indirectly modulate the activity of neurons in the VTA or nucleus accumbens

gambling addiction

nucleus accumbens activates to winning plays but also in response to near-misses (right)

brain responds in a way that reinforces the problem behavior even when the reward is not delivered

The magnitude of activation is greater in individuals with gambling problems

Parkinson’s patients who are treated with dopamine agonists have a higher risk of developing gambling problems

These patients can also exhibit other uncontrolled compulsions and addictive behaviors

Dopamine

activity of dopamine neurons encode

errors in reward prediction

Events that are “better than expected” cause high activity in VTA neurons

Events that are “worse than expected” inhibit activity in VTA neurons

Events that occur “as expected” produce no change in activity, even if the event still provides hedonic reward