Task 2 The emotionally motivated brain Flashcards
What is affective neuroscience?
science concerned with neural basis of emotion
- functional neuroimaging
- behavioural experiments
- electrophysiological recordings
- animal and human lesion studies
James-Lange Theories of emotion (1920)
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
Cannon-Bard theory (1927)
- 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
Papez circuit (1937)
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
Mac Lean’s model
- 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
role of amygdala in emotion
- 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
role of PFC in emotion: PFC and reward processing
- 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
role of PFC in emotion: PFC and bodily signals
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
role of PFC in emotion: PFC and top-down regulation
- 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
role of ACC in emotion
- 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
role of hypothalamus in emotion
- 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)
Main idea two-system model:
suggests that there are two parallel neural pathways involved in processing of emotions
- low road: subcortically and unconscious
- high road: cortical and conscious
low road
- 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
high road
- 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)
Involvement of pathways in anxiety disorders
- 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
LeDoux model: Is amygdala centre of explicit emotional experience?
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)
LeDoux
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
Why does fear not cause threat responses
- 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
Why can subjects without amygdala still feel fear?
- 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)
Experiment Holzschneider and Mulert: Setup
- symptom provocation paradigm: elicited fear responses in PTSD patients and controls by contrasting negative emotional condition vs. neutral/pos. condition
Experiment Holzschneider and Mulert: findings
- fMRI shows hyperactivity in amygdala, medial PFC, and ACC during symptom provocation –> related to experienced symptoms of fear
- reduction of hippocampal activity
Experiment Holzschneider and Mulert: interpretation
- 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
How to explain higher amygdala responsiveness to neg. stimuli in anxiety disorder patients
- 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
