Autonomic specificity
in line with James-Lange
= each distinct patterns of ANS activation lead to experience of different emotion
prove from recent research:
→over a dozen of distinct ANS pathways tht actitivate different regions of body
→different ways in which components of ANS could combine
Embodiement
higher order thought processes (emotion and cognition) are largely influenced by bodily processes
they are embedded in bodily representations
emotions and body are intertwined
Cannons Criticism on James
ANS response not specific enough to differentiate between emotions
Changes in bodily sensation to diffuse
Changes to small to be meaningful
ANS to slow to be source of emotion
ANS response appear also regardless of emotion (fe: fever)
We are not sensitive to all ANS responses
Bart and cannon hypothesis: NS in 3 levels
hindbrain, reflex pathways for simple functions such as movements
structures involved in emotion
cerebral cortex which controls and inhibtits lower levels
Prove:
children are not fully able to control emotions as cortex is not fully developed yet
no reduction of emotion occurs:
if viscera is served (part of brain where James thought emotion would arise) and if disconnection between guts and brain → Critique on James)
but if there is a disconnection between cortex and subcortical regions → emotion changes \n → his theory cortex inhibits subcortical regions
Cannon Bard Theory
Look at model in picture
Brain(thalamus) registers stimulus → produces the arousal and the emotion
bodily sensations co-occur with emotions, yet independent
autonomic specificity doesn't exist (one-arousal-fits-all model)
Facial action coding system (by Ekmann et al.)
=Muscle by muscle instruction to configure face in a specific emotion
-> while that ANS was measured
results
moving facial muscles change emotional experience
different autonomic reactions (galvanic skin response and increasing heart rate differ) to different negative emotions (fe between anger and sadness)
different autonomic reactions to different positive emotions
->supports Autonomic Specificity
Hohmann vs Bermond
Hohmann: participant with paralysis (as a result of spinal cord lesion)
reduced fear and anxiety
→evidence for Autonomic Specifity
Boermond: If Hoehmann is right then all emotions should be reduced
also observed participants with paralysis:
normal experience of sadness and happiness
heightened fear and anger
→Increase post in-jury and not decrease
experiment: adrenaline injections
some participants received info about effect on behavior some not
→ p who did not know about effect were influenced by behavior of accomplice of researcher who either behaved euphoric or angry
different contexts elicit different emotions
→ no support for Autonomic specificity
results not replicated
Schachter and Singer influence
→their model is used today
added to the interest in appraisal and in misattribution of arousal =when arousal does not have an obvious source people tend to label arousal accounting to situation
transfer of excitation= arousal can be transferred to other situations which can effect emotional experience in social world
Bodily sensation map
shows decreased and increased activity of body parts associated with an emotion
each map of body is associated with different emotion
Bodily reverberations
term introduced by James
they are product of:
ANS
endocrine system
immune system
(=including breathing, blood flow, heart palpitation, trembles, goosebumps, lacrimal glands that produce tears, and different muscle movements)
endocrine system
responsible for synthesis and distribution of hormones in body
(Pineal gland, Pituitary gland, Hypothalamus, Adrenal glands…)
Autonomic nervous system
ANS
cortex -> limbc system + hypothalamus -> ANSS and body parts -> send feedback
Regulate internal conditions of body: control digestion, blood flow, temperature, behaviour related to emotion (such as defensive behavior, aggression and sexual behavior
maintains homeostasis of body in order for individual to adapt to fluctuations of environment
originate from parts of spinal cord and are controlled by neurotransmitters
two parts of the system
2 Parts of the ANS
parasympathetic branch: responsible for restorative process -> makes us relax
→ reduce heart ,rate blood pressure...
+ activation of digestive processes
sympathetic branch: prepares individual for fight or flight response (physically demanding activities) increasing processes that provide energy for body:
→increasing heart rate, blood pressure and cardiac output
+ stops digestion
+decreases activity of immune system by reduding natural urotransmitters
HPA Axis
Hypothalamic-Pituitary-adrenal Axis →stress response system and part of endocrine system
Linked to fear but large individual differences
can have positive effects: increased focus performance generally
Cortisol
increases gluose production (needed for metabolically demanding action fight- flight)
increases heart rate and blood pressure-> blood supply to relevant muscles
suppresses immune system
Trier social stress task
P must perform a spontaneous speech in front of a critical audience ->stressful event
ACTH increase right afterwards and than bit later also cortisol increase (timeframe individually)-> proves that both are related to each other and to stressful task
elicts emotion fear -> recent study show that cortisol is more correlated to anger than fear
HPG axis
Hypthalamic-Pituritary-Goand-axis
testestorone
siehe pic
HPG vs HPA axis
siehe pic
Discovery of Neurochemicals by Galvani:
If electricity is passed onto dead frog legs they contract
Discovery of Neurochemicals: Loewi
First experiment
Electrical stimulation of a heart 1 → heart rate slows down
heart 2 (is in same fluid as heart 1) → heart rate also slows down
→ he hypothised this happens bcs of neurochemicals
Second experiment
stimulation of vagus nerve of donor heart
donor heart rate slows down
Remove fluid sample from donor heart
add it to recipient heart
Recipient heart rate slows down
Neurochemicals:
=located in different brain regions and related to behavior
Neurotransmitters
Communication between neurons
Norepinephrine, dopamine, serotonin, GABA
Hormons
Communication via blood circuit
take longer to act then neurotransmitters, but effects last longer
Adrenaline, cortisol, peptides
controlled by pituitary which is influenced by hypothalamus
neuromodulators
Signal enhancers/ diminishers
Most are peptides (like endogenous opiates) which modulate pain system
Serotonin
essential to emotional experience
Processing of affective info of faces
involved in processes that balance
Heuristic processes/fast thinking in subcortex
Deliberate procesess/ slow thinking in frontal lobes
->when serotonin levels are low fast and intuitive levels weigh more
Low levels of serotonin
antisocial tendencies (-> dysregulation of frontal lobes of aggressive tendencies)
Depression (frontal lobes not regulating negative emotions)
ASD
low levels of agreeableness and constraint high levels of neuroticism
Serotonin and Depression
SSRI increase serotonin levels in synaptic cleft by blocking its reuptake
→ less negattive affect im depression
early theories: insufficient serotonin might cause depression
Oxytocin
Hormone produced in hypothalmus
Oxytocin release has effect on
social processes: involved in lactation, maternal (mütterlich) bonding, sexual interaction, promotes social sensibilities to silent social cues and in Group prosocial behaviour
cognitive processes: social and olfactory memory, also emotional memoories (because it makes certain experiences more emotional)
neurendocrine: reduces activity of HPA axis→ less Cortisol produced if Oxitocin present, supresses hunger
autoregulation: autoexcitation during birth and suckling
emotional: reduces anxiety (by enhancing prefrontal circuits which inhibit limbic system) and increases pos. mood
might increase generoyity and empathy
Noreadrenaline/ Norepinephrine
= Neurotransmitter synthesised in Locus Coeruleus (LC)
→ 90% of neurons are noradrenergic
has widespread in projection: variety of processes
wakeful/sleep
attention
→ higher order area
pupil response: high LC activity pupils dilate, Less LC activity pupils constrict
arousal
→subordinate areas
noradrenaline cortical enhancer
Emotional arousal -> activation of LC -> increase noradrenaline -> noradrenaline modulates cortical circuits to enhance certain processes
Yerkes Dodson Curve
Low arousal on easy tasks -> no good performance
Low arousal on difficult task good performance
High arousal on easy task -Y good performance
High arousal on difficult tasks ->no good performance
Noreadrenaline and Emotion
Pupil size increases during arousal
cognitive effortful tasks also influence pupil size
Noradrenaline: signalling accumulation of evidence (=thinking about evidence for other persons felt emotion )
Pupil dilation reflect the confidence in decision and predicts decision about pos/neg emotion
MacLean
Forebrain and three distinct systems → “1 mind, 3 brains”
sensory impulses from body and outside world reach thalamus and are directed into 3 main pathways
each has a different evolotionary stage and species dependent functions
MacLean-Panksepp conjunction:
each distinct type of emotion is based on particular part of limbic system brain circuity
creating set of species characteristic brain systems and behaviors
limbic system
Centre of emotions
Includes thalamus, hippocampus and amygdala
Closely connected to hypothalamus controls,
Amygdala Fear Centre
Early theories brains centre of fear
helps to ensure survival
amygdala damage no behavioral & physiological response to threat
Amygdala sonstiges
depressive individuals have heightened amygdala activity
plays role in emotional memory and in assessing valence (goodness or badness of stimuli)
More intense stimuli-> higher activation of amygdala
emotional profile predicts intensity of amygdala activation in response to intense stimuli fe: looking at life in pos way -> greater activation to intense pos stimuli and
Amygdala anatomy
Basolateral amygdala
Basolateral amygdala
input - linked to prefrontal cortex
learning processes: treat conditioning (with Conditioned Stimulus - unconditioned stimulus associations) + stimulus outcome
Central Nucleus
output produce fear response:
ANS
startle (erschrecken) reactions
activation of neurotransmitter systems noradrenaline
arousal
amygdala functions
Emotions
Fear/Defensive processing
Pavlovian learning (dog) (stimulus-outcome)
Instrumental learning (reward) (stimulus-response)
→ Fear conditioning acoustic startle and skin conductance
Attention
Autonomic reactions
Social cognition
Emotions from faces, relevance
LeDoux Amygdala
detection of fear, but no role in concious experience of fear
Subjective responses (fear and anxiety are produced by higher-order brain circuits (prefrontal cortices)
Evidence: Damage to amygdala eliminates response, but not feeling of fear
+
emotional conditioning is possible: especially connections between negative stimuli is quickly made and slow to extinguish
before LeDoux the fear centre view of amgdala function
Le doux 2systems view of threat processing
LeDoux Rethink fear
Fear vs Anxiety
anxiety today
modern society requires active monitoring of potential harm
new threats: financial security, politics, meaning of life
(interplay of concious (LeDoux) underlies anxiety)
different meausurments to determine activity of ANS
galvanic skin response measurement: measures electrodermal skin response fe sweating
Facial action coding systems
Blood flow of different parts of the body or temperature throughout the body
ventral vagal complex/Â vagal branch
controlled by the ventral vagus nerve
part of parasympathetic nervous system
is involved in compassion and love
is unique to mammals and regulate facial muscle actions, head movements, vocalizations and heart rate declarations
activity of vagus nerve = vagal tone is measured by measuring relationship between heart rate and respiration (Atmung
compassion is associated with an elevated vagal tone
blushing
has highly social = showing reception (empfang) of a mistake to produce more positive responses in others
(Darwin:) product of self focused attention: while we are ashamed we direct our attention to the face, which causes blushing
(Larry et al.:) product negative self focused attention: we blush when we are object of undesirable attention
chills
goosebumps and piloerection (= contraction of small muscles surrounding hair )
triggered by awe-related experience or by experiences of horror
flash
non social response
associated with physical arousal, temperature changes or alcohol
regions involved in emotion
cortical
Prefrontal cortex
Visual cortex
(midline and) Anterior cingulate)
subcortical
Amygdala
hypothalamus
Periaqueductual gray
( hippocampus)
(Ventral striatum)
hindbrain
regulates basic physiological processes
medulla ->Â cardiovascular activity
Pons sleep breathing
cerebellum ->motor coordination and automatic movement
Forebrain
thalamus -> integrating sensory memory
hippocampus -> memory
hypothalamus -> biological functions/ emotionladen behavior (eating, sexual behaviour, aggression body temperature) +controls ANS via pituitary glands and controls hormonal system
Limbic system
Lateralization Approach/Withdrawl
looking at Emotion in term of approach or withdrawal
approach → left regions (language located here central to goal directed behavior)
withdrawal → right regions
Evidence:
perception of happy faces activates left side
perception of disgust activates right
anterior cingulate cortex
=brains alarm system
active during physical pain and activated in social pain (fe when socially rejected)
opiates used for physical pain can also relieve social pain
opiod and dopamine
nucleus accumbens and ventral tegmental area =dopamine rich networks)
Reward circuit: ventral stratium receives input from prefrontal cortex, amygdala, hippocampus than sends info to hypothalamus
→ dopamine essential to wanting
→opioid receptors essential for liking