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Chapter 11 - Emotional Behaviors
Terms in this set (58)
What are the major components of emotion?
Subjective psychological experience & Behavioral (physiological)
textbook: cognitions, feelings, actions, and physiological changes
sympathetic nervous system
readies the body for emergency fight-or-flight activities
James-Langue Theory of Emotion
When you feel an emotion, the autonomic arousal and skeletal actions come first. What you experience as an emotion is the label you give to your responses: You feel afraid because you ran away, and you feel angry because you attack.
James-Lange Theory says that emotion is the brain's perception of the brain's interpretation of bodily change produced by an emotion provoking event
□ see shark --> body changes --> fear
event -> appraisal -> action -> emotional feeling
What is the evidence for James-Langue Theory?
○ paralyzes muscles in the face, reducing lines and crows feet
○ binds to presynaptic Ach receptors and prevents the muscles from getting their ordinary sensory feedback
§ loss of regulation and control of the muscles
○ Normally, if we were to read a sad story, we would partly frown (measurement of muscles)
○ In some experiences, botox has been used to remove the frown lines
§ Under botox, the people are slower to read unhappy sentences than those who don't receive botox
§ removing the behavioral expression of emotion affects the processing of emotional information
○ In other experiences, where botox was used on all facial muscles
§ people will report a less intense emotional reaction to videos than those without botox
Body sensations can strengthen emotional feelings
Facial Feedback Hypothesis
There is a very large literature area that centers around the facial feedback hypothesis
- if you read a cartoon while you're biting a pencil that creates some of the facial expression that encourages laughing and smiling, people will rate the cartoons as funnier
- fMRI research where people are asked to imitate angry facial expressions and then measures amygdala activity
○ under botox, there's a reduction of amygdala regulation
Facial feedback is modulating the systems that regulate emotion
- if you reduce the physical change, you reduce the emotional experience
Pure Autonomic Failure
condition when output from the autonomic nervous system to the body fails
Someone would not react to stressful experiences with changes in heart rate, blood pressure, or sweating
These people report the same emotions as others and can identify what emotion a character in a story would be experiencing BUT they say they feel emotions less strongly and refer to the cognitive aspect of emotions.
Their decreased emotional feeling is consistent with predictions from the James-Langue theory
Textbook: eople with pure autonomic failure do not react to events with changes in heart rate or other autonomic failures. They report still having emotional experiences byt they do not feel them as strongly.
Cannon-Bard Theory of Emotion
- Cannon-Bard theory says that emotion is not a byproduct of bodily change
- emotion is an integrated response of the brain
○ you see in the environment some emotion provoking event, the bodily change and the subjective psychological experience are simultaneously and independently activated
The various components of emotion do not always occurs together. Also, apparently no emotion corresponds to activity in a single brian area. For thse and other reasons, many psychologists are uncertain that emotion is a natural cateogory.
Mixed Evidence between James-Langue and Cannon-Bard
Proponents of James-Lange theory studied paraplegics
- higher the damage, the less sensory input to the brain, the less able the brain is to produce a bodily change
- the higher the damage, the less emotion this group experienced
Proponents of Cannon-Bard
- studied same group
- same range of emotional experiences, but that the experiences were less intense
Evidence is mixed
Schacter-Singer 2 Factor Theory of Emotion
Modern theory of emotion
Schacter-Single 2 factor theory says that emotion involves the bodily change plus some cognitive interpretation of the brain where the brain labels what the emotion should be, and then you experience the subjective psychological experience
Emotion = bodily change + cognitive label
see shark --> body changes and label applied --> interpret and experience fear
Important of the different brain hemispheres in emotional behavior
Activation of the frontal and temporal areas of the left hemisphere is associated with approach and the behaviroal activation system. The corresponding areas of the right hemisphere are associated with withdrawal, decreased activity, and the behavioral inhibtion system
Ventromedial prefrontal cortex and emotion
Damage to the ventromedial prefrontal cortex in many cases impairs the ability to anticipate emotional consequences, alters responses to moral delimmas, and impairs decision making
Can cognition affect emotions? Schacter-Singer Experiement
Can cognition affect emotions?
- Experiment by Schacter and Singer
- told they were studying a new drug on vision (fictisious)
- first group received epinephrine (arousal) (told what would happen)
- second group was told the drug would make them itchy
- third drug said the drug had no side effects
- while they were in the waiting room, there was a confederate acting crazy or "euphoric"
- 20 minutes later asked to rate how happy they are
The groups that were misinformed rated themselves as being more happy than the other control groups
- the logic of this experiment was that the misinformed groups rated themselves as being happier because them misinterpreted the arousal caused by the drug to the waiting room
- those that got the drug in the control group attributed their arousal to the drug
- Another finding was that the group that was informed rated themselves as slightly less happy than those who received placebo
Cognition can affect emotion
The forebrain areas surrounding the thalamus; regarded as critical for emotion
Limbic system is a forebrain system that includes the amygdala
- there are different pathways for fear/emotion
○ fast pathway (fear)
§ some sensory danger or fear event
§ routed through the thalamus, the fast pathway goes to the amygdala and then directly downstream to control muscles and cause movement for defense
§ attributed to fear
○ slower pathway (anger, resentment, joy)
§ sensory information comes in, routed through the thalamus, but then projects through the hippocampus, frontal cortex, then amygdala, then downstream
- different circuits for different emotions
Fast pathway is most consistent with the Cannon-Bard theory
- nearly simultaneous
Slow pathway is more consistent with the Schacter & Singer theory
- cognitive appraisal
Evidence of the Papez Circuit
Papez circuits is an early forerunner to the limbic system
Anatomist who was interested in whether there was a circuit in the brain that regulated emotion
- Papez would do brain autopsies on people and animals that had have significant emotional disturbance
- he would sometimes intentionally inject rabies virus into the vat/rat brain in exploratory studies
○ track where it spread throughout the brain and where it accumulated
○ brain sites important to emotion
- proposed a main circuit involved in structures that might be regulating emotion
- Kluver & Bucy syndrome
○ many primates will experience an innate fear of creepy, slimy, crawly things
○ when they damaged the hippocampus and amygdala, the animals would experience a loss of natural fear
○ there were motivational changes (eating and sexuality)
- Paul Maclean coined the term the "Limbic System" and added the amygdala
○ hypothalamus (moticated behavior), hipocampus, amgdala, olfactory bulb
In what physiological way, if any, does one type of emotion differ from one another?
No type of emotion has a unique pattern of physiological activity, wither in the autonomic nercous system or in the brain
What evidence challenges the idea that we identify people's emotions by their facial expressions?
Given a photo of a spontaneous facial expression, people usually see more than one emotion and often don't see the emotion described by the person whose face was shown. People recognize expressions from their own culture better than those from other cultures. Also, in everyday life we identify someone's emotion by a combination of cues, including posture, context, gestures, and tone of voice.
Stress and Health
There's a psychological basis to the ideas that stress can lead to increased risk of ulcers
- suggested a psychological state of stress can be associated with physiological damage
- avoidance learning task (rodent placed in running wheel and every once in a while it would be amplified by shock)
○ can escape by running, if they keep running the shock won't turn on
- conducted an experiment where one group of rats would be in an avoidance condition and another group would have no ability to control the design (called Yoked control group - gets the shock that the first group controls)
○ in the no avoidance group (stress condition) they develop more ulcers in repeated session
the cause of the ulcers was not the stress of the no avoidance shock per say
- during unavoidable shock sessions, there's a lot of sympathetic nervous system activation
- increase in heartrate, reduction in parasympathetic control
During the shock sessions, the shock is present
When the session is over, there was a parasympathetic rebound when the stressor was removed
- this increase in stomach enzyme secretion associated with parasympathetic engagement was what caused the ulcers
Aggressive behavior relates to both genetic and environmental influences. Most evidence supports the hypothesis that a gene decreasing the activity of monoamine oxidase increases aggressive behavior mainly among people who had abusive experiences in childhood.
Testosterone/cortisol's effects on Aggression
Testosterone increases the probability of aggressive or assertive behavior, and cortisol decreases it.
HPA axis (hypothalamic-pituitary-adrenal axis) and the Immune System
The HPA axis also linked stress and health
- HPA axis is language to describe the neural relationship between the hypothalamus, pituitary, and adrenal gland
○ hypothalamus releases releasing factors that then targets the pituitary land that releases tropic hormones that targets the adrenal cortex that releases its own hormone (cortisol)
- Yerkes Dodson law of arousal
○ a little bit of stress enhances your performance and immune system function
○ long-term stress is detrimental to performance and immune system function
○ inverted U in the relationship of arousal and performance
When we encounted an environmental stressor, it activated the amygdala and therefore the HPA axis
- HPA releases the stress hormone
High levels of cortisol are negative to the immune system
The functional idea is that one of the consequences of cortisol increase is to enhance metabolism and increase blood sugar
- if there's danger, you need more energy to deal with it
- but, that process of HPA engagement and rising cortisol levels has a metabolic cost (one on the immune system)
immune system struggles with long term stressors
- renders person more vulnerable to other kinds of assault
Stress immediately activates the sympathetic nervous system and more slowly activates the hypothalamus-pituitary-adrenal cotrex axis. The adrenal cortex releases cortisol, which increases metabolism.
Stress activates the immune system, helping to fight viruses and bacteria. The immune system releaes cytokines, which stimulate the hypothalamus by releasing prostaglandins, which cross the blood-brain barrier. THe hypothalamus reacts by activities to compat illness, including sleepiness, fever, and lack of appetite and energy.
Because stress causes release of cytokines, it can also lead to lethargy and other symptoms that resemble those of illness.
HPA Axis & The Hippocampus
Cortisol level also affects the brain, particularly the hippocampus
- high levels are toxic to hippocampal neurons
- loss of hippocampal neurons results in further increases in cortisol production
- one explanation for why long-term stress can be detrimental to memory and encoding
The high cortisol levels associated with prolonged stress damages cells in the hippocampus, thereby impairing memory.
Fear and the Amygdala
When we talk about fear, we are talking about multiple different responses of the brain and body to a particular event in the environment
- regulated by projections by the amygdala
○ changes in HR and BP
○ release of stress hormones
○ fear -potentiation of the startle reflex
The amygdala is very complex and has different subsystems in it (multiple nuclei)
- the lateral nucleus received incoming sensory information from the environment
- basolateral nucleus projects to the PAG (gateway or output to different aspects of a fear response, integrative sight for fear learning)
- central nucleus is the major output pathway
Each regulates or controlling a different aspect of a fear response
fear: "fear state"
neuroscience = brain activation
collateral activation of downstream pathways in addition to critical fear stimulation parts of the brain (amygdala)
We know the amygdala is important in regulating and producing fear behaviors.
Responses strongly to fear stimuli and other stimuli that oevoke strong emotional processing; most strongly when the processing is effortful
Effects of amygdala damage on
Fail to focus their attention of stimuli with important emotional content
Impairs recognition of fear expressions largely because of lack of attention to the eyes
A "fear state" is a state of activation related to these different active pathways
Fear-potentiated startle is an experimental model that is used to study the neural basis of fear, anxiety, and stress
- a lot of focus on the use of experimental paradigm is trying to understand the neurotransmitter systems involved with fear that would allow the better development of treatments of fear disorders or the anatomical origin locations of fear behavior
You're watching a scary movie and a friend taps you on the shoulder during a non-eventful part of the movie
- different than when the scene is ramping up for something scary (suspense)
- fear potentiates our behavioral reactivity (notion of fear potentiated startle)
○ fear potentiates startle reactions
also acoustic-mediated startle reactions
Researchers measure enhancement of the startle reflex as an indication of anxiety or learned fear.
Fear Potentiated Startle Rat Experiment
Fear learning phase: experience a tone and then low shock amplitude foot shocks
- the rat or rodent sits on a scale that can measure force displacement
Test phase 1: a startle eliciting probe will give off a loud blast of white noise (causing muscular flinch, which is measured)
Test phase 2: tone + noise startles
Fear potentiated response creates a larger force displacement with the tone + noise if the learning had occurred that connects the tone with a shock
- If during the training phase, you never connect the tone and shock, you don't see effects of the fear potentiated startle
The acoustic flinch is mediated by a simple neural circuit (ear, thalamus, hindbrain, spinal motor neurons)
- somehow the neural circuitry responsible for learning the flinch is modulating the neural circuitry across the circuit that causes the flinch
- what is the nature of that modulation/neural basis of learning?
Damage to the amygdala (or glutamate antagonists delivered to amygdala) will block or impair fear potentiated startle
Is the amygdala the site of the subjective experience in addtion to regulating the behavior?
The amygdala might have a role in the subjective, psychological experience as well.
- convergent evidence that it does both
- also is critical in the subjective experience of fear
In animal models, damage to the amygdala will decrease fear behaviors and vice versa.
Some people who suffer from epilepsy (particularly in the medial temporal lobe, under which is the amygdala) can report before the seizure begins, they feel unspecific and unexplainable fear and anxiety.
There is a rare disease names Urbach-Weithe Disease that involves bilateral degeneration of the amygdala
tends to not affect overlying tissues (selective degeneration)
a naturally occurring lesion of amygdala
social cognitive changes associated with this disorder, poor at identifying emotional content from facial expressions
Amygdala and Autism
Asperger's is on the autism spectrum
deficits in empathy are commonly describes as symptoms of autism
some research has implicated the amygdala in playing a role in some of the social-cognitive deficits in autism
Eye-blink - record magnitude of blink response with electrodes
blink = startle reaction to burst of air
FPS paradigm researchers conducted a fear potentiated startle experience with humans one group had Asperger's similar to rat experience the control group rapidly acquired fear potential startle (non-Asperger's group) and there was a deficit in the ability to acquire this social cognitive learning in people with Asperger's
What is the difference between fear and anxiety?
Anxiety is more chronic, less specific, lack of a stimulus triggering it than fear
Fear is "now" oriented
Anxiety is "future" oriented and doesn't shut off as quickly.
As with fear, in anxiety the amygdala has bee suggested to play a role (will be qualified)
focus has been on treatment, development of drug therapies
What is the role of the GABA receptor?
Drugs that act at the GABA receptor tend to have anxiolytics properties
There are many GABA receptors concentrated in the amygdala
Activation of those receptors is how the brain regulates its own fear (Inhibitory)
At the center of the GABA receptor is a chloride channel. When it opens, it permits chloride ions (Cl-) to cross the membrane into the neuron, hyperpolarizing the cell or at least counteracting any sodium entering the cell through excitatory synapses. That is, the GABA synapse is inhibitory.
What are anxiolytic drugs?
Anxiolytic drugs reduce anxiety
3 classes - Barbiturates, Meprobomate, Benzodiazepines
Most of these drugs facilitating binding at GABA receptors (inhibitory neurotransmitter receptor) and affect how will GABA binds to its receptors
for most, GABA has to be present for the drug to have any effect
The most common anxiolytic (anti-anxiety) dug are the benzodiazepines. They bind to the GABA receptor, which includes a site and binds GABA as well as sites that modify the sensitivity of the GABA site.
Barbiturates (lots of them)
oldest and most dangerous
neural inhibitors (sedatives) meaning they suppress neural activity
Barbiturates are highly addictive and dangerous
- all drugs (transmitters) have more than one affect on the brain
- barbiturates have an anxiolytic effect and a neural sedative effect (neural inhibition)
○ all drugs develop tolerance (stops having the same effect at the same dosage)
○ There is differential development of tolerance based on the different effects
- The anxiety reducing properties develops tolerance, but the sedative effect does not experience tolerance
○ when the dosage in increased, the risk of overdose increases
○ more dangerous levels of neural inhibition leading to a high incidence of overdose
Therapeutic Index (TI)
One way in which you can quantify how dangerous a drug is = the therapeutic index (TI)
- takes a ration of 2 values
○ LD50 dose - the dose that is lethal in 50% of subjects (mg/kg)
○ ED50 dose - the dose that's effective to some measurement in the model
○ the TI is a ratio of the LD50 dose over the ED50 dose for a drug
- In humans, the TD (toxic dose) is taken instead of lethal dose
If you're developing a drug, you would want a high TI ratio because you want the effective dose to be smaller than the lethal/dangerous dose
- you want a big difference between the effective dose and the dangerous dose
Barbiturates have a low TI as tolerance develops
when the effective dose goes up, it quickly approaches the dangerous dose
Meprobamate is a non-barbituruate that has a similar reaction
- anxiolytic qualities
- led to a significant reduction in shock therapy in the 50s
- The Rolling Stones wrote a song called "Mother's little helper" about meprobamate
- During WWII, women entered the workforce but would return to homemakers when their husbands returned
○ increase in depression and anxiety
○ over prescription of this drug
- **different from other barbiturates because GABA doesn't have to be present to reduce anxiety
○ can have a more direct form of effect
○ still similar problems
Benzodiazepines are the "better" barbiturates
- safer and have a high therapeutic index (TI), at least 20:1
Rohypnol (Roofies) are a benzodiazepines and can produce drowsiness, confusion, visual disturbances
- when mixed with alcohol, effects are more profound and can be lethal
How do drugs affect GABA transmission?
The dugs bind to specialized receptors on the receptor component of an ionophore
- multiple binding sites
- binds to GABA associated receptors
- most anxiolytic drugs don't have a direct effect when they bind
○ changes how well GABA itself binds (affinity or length of time GABA binds)
§ the drug binding wouldn't do anything if GABA wasn't present
○ the exception is meprobamate, which can have a direct influence on the cell
Alloseric binding site
The drug binds to an allosteric binding site (other than the GABA neurotransmitter itself) but causes subtle conformational change in the receptor for GABA that makes it easier or harder for GABA to bind
If someone becomes tolerant to one drug because they've taken it many times, they can show tolerance to other drugs they've never taken before (cross-tolerance)
- barbiturates, benzodiazepines, and alcohol all show cross-tolerance because they all act on the GABA transmission
- overdose with a barbiturate with a low TI would have a higher chance of overdose due to their cross-tolerance because they need a higher effective dose
Drugs that have a similar mechanism of action in the brain tend to show cross-tolerance
- combining any two drugs that show cross tolerance can become very dangerous because the person will need a higher dose of one and then the effects of those drugs are both producing GABA inhibition
○ affect breathing, heartrate, etc.
Neural inhibitions has been implicated in clinical fear disorders
- panic disorder (panic attack) causes strong engagement in the sympathetic nervous system
○ overstimulated, over-aroused
○ there's evidence that people who suffer from panic disorder have structures in their brain that don't allow benzo binding as well as others
- hypothesis for fear disorders is there is something wrong with the GABA inhibition systems
○ our ability to deal with normal life stressors requires that our brain modulates stress and anxiety and fear
○ normal inhibitory mechanisms are required to modulate fear on a daily basis
Rodent Studies on anxiety
Rodent model of anxiety - rodents are pro-social and like to spend time with eeach other
- normal animals will spend a lit of time interacting
- an animal in a fear space will be socially isolated (measure of social anxiety)
- chronically blocked GABA receptors with a dug
- exposed the animals to a social interaction test
- the control spent a lot of time interacting socially
- animals with blocked GABA receptors socially isolated themselves
An example of the idea that the GAB receptors plays a role in regulating normal levels of stress and engaging in social behavior
The idea is that changes in GABA binding underlying anxiety disorders
- an underactive GABA system might sensitize the amygdala to responding to environmental stress
- low levels of stress in the environment can produce an exaggerated reaction
GABA inhibition not working
- increased fear & anxiety disinhibiting the amygdala
Drugs allow the brain to reset the threshold of GABA inhibition
- some of the drugs reset the brain to being more normally responsive to the transmitters
- allowing the brain to better self regulate the threshold for amygdala inhibition
Light Enhanced Startle
Fear-potentiated startle is learned fear
Light-enhanced started is used to study unlearned fear or anxiety
Light enhanced startle paradigm
- many rodents are nocturnal
- if you go into a brightly lit open space, you are at a higher risk of predation
- the animal sits on the same platform as fear-potentiated startle
○ sound presented, muscle flinch
○ in other trials this is done in the presence of a bright light
○ typical finding is that the light potentiate the startle reflex
- people show the opposite
○ dark-enhanced startle
It has been powerful in asking if there are different forms of fear mediated by different systems (transmitter systems)
- light enhanced startle implicates the bed nucleus of the stria teminalis
○ near the amygdala, outside of it
○ receives input from the PVN (hypothalamus)
paraventricular nucleus of the hypothalamus (stress hormones)
How are fear potentiated startle and light enhanced startle dissociated?
anatomically & pharmacologically
Lesioning the amygdala knocks out fear potentiated startle and not light enhanced startle (double association)
Lesioning the bed nucleus of the stria terminalis, light potentiation startle is knocked out and fear potentiated startle in unaffected.
Michael Davis at Emory injected a glutamate antagonist (NBQX) into the amygdala or into the bed nucleus of the stria terminalis and asked how it affected fear-potentiated startle vs light-enhanced startle.
When injected into amygdala, fear potentiated startle doesn't happen.
When he injected the same drug into the bed nucleus, fear potentiated startle does occur.
He conducted the same experiment with the light-enhanced startle.
When you inactivate the bed nucleus, light potentiated startle is impaired but fear potentiated startle is not.
These two phenomena are caused by different things.
Lesioning the amygdala knocks out fear potentiated startle and not light enhanced startle (double association)
Lesioning the bed nucleus of the stria terminalis, light potentiation startle is knocked out and fear potentiated startle in unaffected.
Learned fear (FPS) and unlearned anxiety (LES) are anatomically and pharmacologically dissociated.
Corticotrophic Releasing Hormone (CRH)
If the bed nucleus is important for anxiety, what regulates it?
If CRH effect on the BNST (and not amygdala) is what mediates anxiety, CRH itself should produce anxiety or continue to produce anxiety even if the amygdala is lesioned.
When the bed nucleus is lesioned, the CRH should not produce anxiety.
Measuring baseline flinching under influence of CRH
In control, CRH produced anxiety.
When amygdala was lesioned, (bnst in tact) CRH increases anxiety.
When BNST is lesioned and amygdala is attached, it no longer produces anxiety.
What this implies is that CRH increases anxiety by the bed nucleus
- unlearned anxiety is mediated particularly by CRH at the bnst and the amygdala responsible fear plays a very limited role
We know that MDMA receptors (glutamate) are critical for forming new memories in the brain
Behaviorally, in learning experiments (fear experiments), we know that MDMA receptors are critical in animals' ability to form these associations
Acquisition is learning something
- if you produce the tone by itself, there will be some fear response (without the shock)
- That is called an extinction trial because if you do that enough times, fear will gradually reduce
We know that learning requires the MDMA receptors, but what about loss of learning?
Fear potentiated startle does extinguish
- a test trial for fear potentiated startle is a no shock trial (by definition), which makes it an extinction trial
How to enhance the effectiveness of fear loss treatments
From some research, some MDMA receptors (important for memory formation) are also important for extinction
- e.g. D-cycloserine (MDMA agonist, partial agonist)
○ bind but not super well
○ during extinction, a control group extinguishes but the animals that receive D-cycloserine extinguish faster
○ could enhance the effect of fear loss therapy
Light enhanced startle doesn't extinguish. What does this tell us?
What it suggests is that fear potentiates startle and light enhanced startle and dissociated anatomically and behaviorally
- they don't follow the same rules
- if fear potentiated startle is a measure of learned fear, this can be overridden by learned fear
- unlearned anxiety is unlikely to extinguish (innately driven)
Amygdala is not the whole story in fear regulation
What does that imply - the treatment modality should be very different
What is the role of the BNST in depression?
animal model of depression - forced swim test or "porsolt swim test"
- very good swimmers, but don't like being wet
- sometimes, rats will dive down
- at some point, they give up and almost start floating
- the give-up response is not due to motor fatigue
○ a behavioral measure of depression
how much time in the give-up postion is one meaure of depression in these models
behavioral measure of depressive behavior are important in developing treatments of depression
In one experiment, they exposed animals to cobalt chloride which temporarily deactivates the bed nucleus system
- depression-like behavior was decreased when the bnst was inactivated
Maybe the bed nucleus plays a critical role in the anxiety associated with depression
- overactivity in the bed nucleus is mediating the anxiety associated with depression
- side effect is inability to cope with everyday stressors
What are the conceptual ways to think about fear in the brain?
entral fear generator view (Fanselow)
○ fear (subjective, psychological) plus physiological responses to a fear stimulus are both mediated by a central fear generator in the brain
○ for Fanselow = amygdala causes upstream and downstream activations
§ cognitive, physiological, behavioral as different outputs
2-system fear framework (Joseph LeDoux)
○ the fear is not mediated by the same system as physiological responses and behavioral changes
○ activation of the amygdala will produce behavioral responses and physiological change (defensive reactions)
○ not responsible for subjective psychological fear (role of the cortex)
Debate over the role of the amygdala
broad conceptual stuff (evolution of thinking about the fear system in the brain)
- post Darwinian
○ subjective fear was proposed as being an innate mental state inherited from animal ancestors
- 1900s and increase in brain structures (modern neuroscience variant)
○ subjective fear is mediated by sub cortical subsystems in the brain
○ subcortical circuit in the amygdala (highly conserved across vertebrates)
- neuro-behaviorist approach
○ difficult to define intangible constructs (what do we mean by fear) so now we define these constructs in terms of something we all agree on - behavior
○ If we want to understand how fear works in the brain, we have to stop talking about subjective, psychological gear
○ we can agrees on physiological responses (heartrate, blood flow, etc.)
○ we can take as an indicator of fear the physiological changes and behaviors changes
○ neuroscientists have been using these defensive reactions as an indicator of fear
neural-behavioral approach is the central fear generator view (we can measure some indicators of fear and it doesn't matter which of the outputs we measure because we would be tapping into the same brain mechanism for measuring fear because they all original from the same structure)
Why does LaDoux argue that the neuro-behavior approach is incorrect?
La Doux is arguing that this is not correct (you're only measuring the defensive reactions) and subjective, psychological fear is important for indivudals that have anxiety and depressive disorders
- we are not making progress
How does Fanseloe argue that 2 system fear is problematic?
if we adopt the 2 system view, we have to throw away over 100 years of neuroscience advances based on animal models (you cannot measure subjective, psychological fear in animals)
you have to throw away all research to date that measures fear behaviors and psychological responses in humans (part of the defensive system)
the only option that is left is to study subjective responses in people (problem of bias, verbal report)
Contradictory experimental evidence
LaDoux 2 systems view
- suggests that if patients with amygdala damage can still experience fear, that would imply that the amygdala is not part of the fear system (some other system)
central fear generator
- the najority and the best evidence available suggests that when the amygdala is damaged, it does affet fear
- the case of S.M. --> UW disease
○ explicitly tried to scare her (thought it was all funny)
○ one haunted house is called the Waverly Hill Sanitarium, reported arousal but thought that it was funny
What is the role of serotonin in aggression?
Low levels of serotonin has been associated with higher levels of aggression
- human data is almost always correlational when identifying cause and effect relationships
- animal models can be directly manipulated/measured
Experimental data suggesting a link between serotonin and aggression
(also can influence more complex social structures)
Vervet monkeys have a complex social structure
- the most aggressive animals tend to have lower serotonin levels
- more aggressive animals tend to have higher social ranks
- if someone is over the top aggressive, they can be ostracized and kicked out
Dominance hierarchy can be altered by manipulating 5-HY levels (serotonin antagonists)
- rank goes up
How can you measure serotonin levels in the brain?
- invasive, direct measurement though a hole in the skill
- measure a metabolite that indicates how much serotonin is being produced and broken down
○ tryptophan --> serotonin --> 5-hydroxy-indole-acetic acid (metabolite)
○ can be measured from urine, if there's a lot of the metabolite, it reflects a high rate of serotonin turnover (assume there are high levels of serotonin in the brain)
§ whenever you measure something that's not what you really want to measure, don't fool yourself because you're making an inference
Rodent Models & Receptor Knock-out (Aggression and 5-HT)
experiment involving different types of mice and rats, the most aggressive strains tend to have low levels of 5-HT
knockout animals' serotonin receptors tend to be more aggressive
- administering serotinin deosn't really happen
- stronger in males
Rodent Models and Social Isolation (Aggression & 5-HT)
if they're reared as social isolates (aggression induction model)
- sex dependent affect (stronger in males)
- lower levels of serotonin
Humans and Social Isolation
Measuring the metabolite is an indicator of serotonin turnover
- there's evidence that it is lower in violent criminals for crimes against humanity
- we put criminals in social isolation, which increases aggression as well
- repeat violence offence is more likely the lower the metabolite levels are
- in suicidal individuals, you can think of a suicide attack as an act of aggression toward the self
- some clinically depressed individuals have lower metabolite levels
- prozac is a selective srotonin reuptake inhibitor
- in suicide, it's been demonstrated that the metabolic level is a funciton of the number of times that a depressed individual has attempted suicide
- the more frequent the attempt, the lower the metabolite levels
Role of Diet in Aggression
countries where corn is a stable element of the diet have higher homicide rates (violent crimes)
- hypothesis is populations with corn-based diets have lower metabolite levels
- corn has reduced tryptophan (precurser to serotinin)
○ brain doesn't make as much serotonin
- corn is high in phenylalanine (disrupts the tryptophan transporter that bring it acorss the blood brain border) even when it is available
○ reduction in 5-HT synthesis
Aggression & Predation
At the very beginning of the course, we talked about one way that neuroscience has tried to understand behavior (tracing neural circuits)
Using optogenetic to activate very specific circuits in the brain (tracing pathways)
- an integration of genetics, molecular biology, and optic laser technology
- there's a gene called opsin that codes for the redopsin protein that's in the eye
○ rodopsin named for rod opsin, helps with night vision and periphery, light reactive photopigment (don't need to know too many details)
○ ion channels will open or close when rodopsin are activated, but there's a messenger system cascade
- it was discovered in green algea that there was a rhodopsin that involed a light reactive ion channel
○ microbial directly transduces light to electricity (light strikes, it directly opens the ion chnnels), but it's not like this in vertebrate rhodopsin
- this was important because it suggested that maybe we could use these light reactive ion channels to turn on neural circuits in the brain
integrative control of predatory hunting
- many evolutionary biologists consider a milestone in an evolutionary advantage
- there are 2 output pathways from the central pathways of the amygala
○ prey pursuit (locomotion)
○ prey capture (attach and bite)
Infected these pathways the opsin, implanted fiberoptic cables into the brain region and this induced prey pursuit and/or prey capture in rodents.
How optogenetics works
a neuron is infected with the opsin gene with a viral vector and virus is exposed to the cell and is infected with the virus and has the gene
- protein expressed as a light-reactive ion channel
- light activates or inhibits the neuron
There are different kinds of opsin genes
- once these light reactive ion channels are expressed in the brain, you can shine light in the brain that turn on/off pathways
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