Task 2 The emotionally motivated brain Flashcards

1
Q

What is affective neuroscience?

A

science concerned with neural basis of emotion
- functional neuroimaging
- behavioural experiments
- electrophysiological recordings
- animal and human lesion studies

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2
Q

James-Lange Theories of emotion (1920)

A

different patterns of bodily changes code different emotions –> emotions are no more than experience of sets of of bodily changes in response to emotive stimuli

–> emphasis placed on embodiment of emotions: changes in body can alter the experienced intensity of emotions

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3
Q

Cannon-Bard theory (1927)

A
  • criticism of James-Lange theory: decorticated cats make sudden, inappropriate and ill-directed anger attacks
  • if emotions were perception of bodily change: should be entirely dependent on having intact sensory and motor cortices but removal of cortices did not eliminate emotions

–> Cannon and Bard proposed first substantive theory of brain mechanisms of emotion
- Hypothalamus: brain region involved in emotional response to stimuli
- responses are inhibited by evolutionary more recent neocortical regions

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4
Q

Papez circuit (1937)

A

Papez proposed scheme for central neural circuitry of emotion

  • sensory input into thalamus diverges into upstream (thought) and downstream (feeling)

Thought stream:
- transmitted from thalamus to sensory cortex
- continues through cingulum to hippocampus
- through fornix to mammilary bodies of hypothalamus
- from hypothalamus via mammillothalamic track back to thalamus

Feeling stream:
- transmitted from thalamus to mammilary bodies (generation of emotion)
- via anterior thalamus upwareds to cingulate cortex

–> emotions = function of activity in cingulate cortex and can be generated through either stream

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5
Q

Mac Lean’s model

A
  • elaboration on Papez and Cannon and Bard
  • based on findings that bilateral removal of temporal lobes in monkeys led to loss of emotional reactivity, increased exploratory behaviour, hypersexuality –> key role for temporal lobe structures in emotion

essential idea: emotional experiences involve integration of sensations with information from the body
- visceral brain (old mammalian brain) –> introduced limbic system

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6
Q

role of amygdala in emotion

A
  • amygdala is one of the most important structures for emotion: key role in processing social signals of emotion (fear) in emotional conditioning and emotional memory consolidation
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7
Q

role of PFC in emotion: PFC and reward processing

A
  • PFC regions work together with amygdala to learn and represent relationships between secondary reinforcers and primary reinforcers
  • neurons in PFC can detect changes in reward value of learned stimuli and change responses accordingly
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8
Q

role of PFC in emotion: PFC and bodily signals

A

vmPFC could play key role for bodily feedback in emotion
- somatic markers: physiological reactions (shifts in autonomic nervous system activity) that tag previous emotionally significant events
- patients with vmPFC lesions cannot use somatic markers

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9
Q

role of PFC in emotion: PFC and top-down regulation

A
  • PFC and ACC send bias signals to other brain parts to guide behaviour towards most adaptive current goals
    –> behavioural choices are influenced by immediate affective consequences
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10
Q

role of ACC in emotion

A
  • point of integration of visceral, attentional, and emotional information involved in regulation of affect and other forms of top-down control
    –> key substrate of conscious emotion experience and of central representation of autonomic arousal

Affective and dorsal ACC
- ventral (affective) subdivision of ACC is routinely activated in imaging studies following emotional stimuli –> might monitor conflict between the functional state of organism and new information that has potential affective or motivational consequences

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11
Q

role of hypothalamus in emotion

A
  • electrical stimulation of hypothalamus in cats leads to “affective defense reaction” –> increased HR, alertness
    –> simple train of electrical impulse can bring about emotional responses

–> hypothalamus seems to be part of an extensive reward network in the brain (PFC, amygdala, ventral striatum)

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12
Q

Main idea two-system model:

A

suggests that there are two parallel neural pathways involved in processing of emotions
- low road: subcortically and unconscious
- high road: cortical and conscious

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13
Q

low road

A
  • fast and direct pathway that bypasses conscious awareness –> involves subcortical brain structures
  • rapid transmission occurs via direct pathway from thalamus to amygdala (thalamo-amygdala pathway –> enables swift, automatic processing of threat stimulus without conscious deliberation
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14
Q

high road

A
  • slower, more elaborate pathway
  • involves cortical processing and conscious awareness
  • initial low road activation –> sensory information reaches sensory cortex (further processing analysis and evaluation) –> amygdala (thalamo-cortico-amygdala pathway –> feelings)
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15
Q

Involvement of pathways in anxiety disorders

A
  • anxiety becomes pathological when frequency and intensity of experienced fear does not match actual occurrence of threats
  • anxiety = uncertainty about threat
  • often involves hyperactivation/dysregulation of BNST (bed nucleus of stria terminalis : response for processing uncertain threats –> BNST activation activates circuits that are responsible for conscious experiences of fear
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16
Q

LeDoux model: Is amygdala centre of explicit emotional experience?

A

No:
- involvement of other brain regions (Cortex) in generation of explicit emotional experience –> amygdala is primarily involved in rapid and unconscious processing of emotional information (fear and threat detection)

17
Q

LeDoux

A

from view of amygdala as fear system to view: animals have brain threat detectors for defense repsonses but not fear as psychological emotion and required brain systems

18
Q

Why does fear not cause threat responses

A
  • fear is higher-order cognitive process: involves conscious awareness
  • threat responses: more primitive, automatic responses occurring at subcortical level –> fear is not the cause of threat responses but result of interpretation of threatening stimuli
19
Q

Why can subjects without amygdala still feel fear?

A
  • amygdala: primary hub for fear processing
  • alternative neural pathways (high road) can also elicit fear responses (e.g., cortical areas can respond to previously learned fear-inducing stimuli)
20
Q

Experiment Holzschneider and Mulert: Setup

A
  • symptom provocation paradigm: elicited fear responses in PTSD patients and controls by contrasting negative emotional condition vs. neutral/pos. condition
21
Q

Experiment Holzschneider and Mulert: findings

A
  • fMRI shows hyperactivity in amygdala, medial PFC, and ACC during symptom provocation –> related to experienced symptoms of fear
  • reduction of hippocampal activity
22
Q

Experiment Holzschneider and Mulert: interpretation

A
  • aversive conditioning network: amygdala, insula (emotion processing for subjective feelings and interoceptive awareness), and ACC (approach, avoidance, fear learning)
  • aversive conditioning network is dysregulated in PTSD patients: increased amygdala responsiveness
  • in healthy controls: higher-order cortical structures have regulating effect on amygdala –> inhibits expression of fear as reaction to stimulus
23
Q

How to explain higher amygdala responsiveness to neg. stimuli in anxiety disorder patients

A
  • after conditioning: presentation of conditioned stimulus evokes brain activity in aversive conditioning network
  • in anxiety disorder patients: network is dysregulated
    –> hyperactivity in amygdala: persistently elevated fear response
    –> hypoactivity in frontal regions: reduced potential for top-down control and regulation of fear response
    –> reduced activity in hippocampus: reduced ability in identifying safe contexts