Weeks 8-12 Flashcards
(266 cards)
1
Q
Examples of circadian rhythms
A
Body temp, cortisol levels, mood
2
Q
When do we dream
A
Mostly during REM, but also at other stages
3
Q
Is circadian rhythm exactly 24 hours
A
No, waking period will remain constant if in constant darkness. However there will be drift in when this occurs
4
Q
Zeitgeber
A
- Stimuli that adjust clock to normal day-night cycle
5
Q
Most common zeitgeber
A
Light.
6
Q
German sleep study showing that zeitgeber more important than clock
A
Study above looked at germany (one timezone)
West germany, sun goes up half an hour later than in east
- Although West and East germany have the same clock time, people in the West will wake up on average half an hour later than those in east
7
Q
Other factors beyond Zeitgeber which influence circadian rhythm
A
- Exercise
- Meals
- Temperature
Noise
8
Q
Are circadian rhythms stable?
A
No, the fluctuate during our lives. Young children sleep a lot, teenagers hardly sleep, old people sleep a lot etc. Midpoint is highest around 20 and then goes down (males tend to have higher midpoints between 20-40)
9
Q
EOG
A
- Electro-ocular gram
Measures activity of muscles that drive eye movements
10
Q
Relaxed awake stage
A
- A lot of activity in cortex
- Little bit of eye movements
Relaxed awake state (lie in bed before fall asleep)
- Little bit of eye movements
11
Q
Stage 1 sleep
A
- EEG signal dramatically decreases
- Lower cortical activity
Almost no eye movements
- Lower cortical activity
12
Q
Stage 2 sleep
A
Characterised by Sleep spindles and K-complex. Little eye movements still.
13
Q
Sleep spindle
A
Rapid activity in EEG - Information exchange between thalamus and cortex. Important for learning & memory. Sleep spindles related to overall intelligence. Interrupting spindle activity = people remember less
14
Q
K-Complex
A
Slower activity in EEG (still kinda rapid)
15
Q
Slow Wave sleep
A
- EEG becomes reasonably regular and much slower
16
Q
Second stage of Slow wave
A
- EEG is still regular and slow
Eye movements slightly increase
17
Q
REM sleep (paradoxical sleep)
A
- Rapid cortical activity - similar to being awake but less pronounced
RAPID movement of eyes, activity in eye muscles
18
Q
How is older adults sleep different from young peoples
A
- More fragmented
- More waking up
- More stage 1 sleep
Less slow wave sleep
19
Q
Where is the SCN located
A
Hypothalamus
20
Q
Suprachiasmatic nucleus
A
- Just above optic chiasm
- The most IMPORTANT clock we have in our brain
Almost 24/hour biological rhythm (if you take it out completely and put it in a median where it can survive, it will KEEP going throughout this 24 hour rhythm.
- The most IMPORTANT clock we have in our brain
21
Q
How does SCN workes SCN get info from
A
Gets information from the retina through the Retinohypothalamic tract
22
Q
Can ganglion cells respond to light and if so what does this mean.
A
Subgroup of ganglion cells that have their own light sensitive pigment. Mainly close to the nose (peripheral view)
23
Q
Ganglion cells sensitivity?
A
- Are slow to activate and extinguish (go on slowly but fade out very slowly too)
- When you take light away they will still keep firing
MOST sensitive to blue light
- When you take light away they will still keep firing
24
Q
What does more mRNA mean
A
More protein formed. Protein conc will follow mRNA conc
25
Clock
activates Per and Tim. Clock goes up, Per and Tim go up
26
PER and TIM
Both inhibit release of Clock
27
Per tim and clock in morning
- Per and Tim low
- Less inhibition of Clock
- Clock increases and therefore activates Per and Tim
Per and Tim conc increase
28
Per tim and clock in evening
- Per and Tim are very high
- More inhibition of Clock
- Clock decreases and therefore no longer activates Per and Tim
Therefore Per and Tim conc will decrease
29
Pineal Gland
- In middle of brain
Produces Melatonin
30
Melatonin
- Becomes active during the night
- Helps you stay asleep (not to fall asleep)
- Helps people suffering from jetlag
Antidepressants can selectively activate production of melatonin
31
Is melatonin active during the night in all species
YES! Even those that are nocturnal. Will stimulate awakeness instead (different effect on nocturnal animals)
32
How does caffeine effect melatonin
Inhibits production of melatonin through binding to receptors (agonist)
33
Why does regular consumption of caffeine no longer inhibit sleep
If you consume a lot of caffeine it can downregulate these receptors and therefore have a lesser effect
34
Reticular formation
- In the hindbrain
- Projects to almost all parts of the brain
- Ascending pathways Information goes up (to basal ganglia, cortex etc)
Descending pathways Down to cerebellum etc
35
What do Acetylcholine and glutamate promote
Promote wakefulness
- Excitatory neurotransmitters
Cause depolarisation, EPSP, post-synaptic neuron more likely to generate action potential
36
What does GABA promote
SLEEP! - Inhibitory neurotransmitter
- Through the action of Cl- ions
IPSP and therefore next neuron less likely to fire
37
Locus Coeruleus
- Largest conc of noradrenaline (norepinephrine) - increases alertness
- Activates sympathetic nervous system
Increase signal to noise ratio (ENHANCES signals DECREASE noise)
38
Histamine
increases alertness
39
Orexin
increases wakefulness
40
Why did older antihistamines induce sleepiness
as histamine is released from the hypothalamus to increase alertness (antihistamine = antialertness)
41
Narcolepsy
Due to genetic changes in Orexin. In humans, orexin is slightly changed in structure, therefore cannot bind to receptor and cannot stimulate alertness and therefore u have excessive sleepiness
42
How does sleep work
Increase in GABA activity. Decreased activity in the thalamus. As a result, sensory information does not reach the cortex, reducing our ability to respond to them.
43
Characteristics of GABA
- Since GABA neurons are often very small (interneurons) the effects of increased GABA can be very local. In other words, in some cases part of the brain may be sleeping while other parts are not can get very localised inhibition
44
Sleep walking
- Occurs more in children (5%) than adults (1.6%)
- Most of the brain is asleep but motor cortex is not, several other areas are also often awake
PFC not active
45
Lucid dreaming
- Being aware that you are dreaming
- Occurs regularly in 23% of people
Typically associated with frontal and temporal activity, while other parts are asleep (similar to sleepwalking in that sense) - usually frontal and temporal cortex will be awake (so you can monitor what happening) and motor cortex will be asleep
46
What can insomnia and hypersomnia cause
- Can cause multiple problems - aggression, irritability, accidents, psychiatric disorders
- Special case: Desynchronised circadian rhythms
47
Sleep apnea
- Difficulty in breathing while sleeping, leading to frequent awakening
- Increased sleepiness during the day and inattentiveness
- Increased risk of stroke, heart problems, and neuronal loss
- Deficits in learning, reasoning, attention, and impulse control
- Causes are multiple (genetics, hormones, obesity)
48
Why do we sleep
- Many different functions – energy conservation, cellular maintenance, synapse strengthening. Evolutionary, mainly to save energy when you can. Memory formation (hippocampus activity during sleep)
49
Functions of dreaming
Memory formation (esp. habit formation)
Cornea oxygeniation
50
Where does dreamlike activity start
Starts with activity in pons then geniculate then occipital cortex (PGO)
51
Activation-synthesis hypothesis
Bottom up - random activity in brain at lower level and dreaming is our higher level functions making sense of this
52
Neurocognitive hypothesis
top down - a lot of things that have happened during the day is still active in ur cortex and ur brain is trying to
53
Autonomic nervous system
crucial link between our brain and our internal organs
54
enteric nervous system
Intrinsic to the gastrointestinal system. Sometimes referred to as our second brain - much smaller than our brains but still have hundreds of millions of neurons. 95% of serotonin in our body is in second brain (only 5% in our actual brain)
55
Sympathetic
typically activating (“Fight or flight”)
56
Parasympathetic
typically restoring (“Rest and digest”)
57
The Sympathetic ANS:
Preganglionic fibers
have their cell body in the spinal cord and very short axons that terminate in the so-called sympathetic chain. Synapse very close to spinal cord
- Ganglia interconnected into the "sympathetic chain"
typically use acetylcholine as their neurotransmitter.
58
The Sympathetic ANS: Postganglionic fibers
- have their cell body in the sympathetic chain and have long axons that terminate onto the target organ. (need to go from spinal cord all the way to target organs = longer)
Typically use noradrenaline as their neurotransmitter
59
The parasympathetic ANS
Preganglionic fibers
very long axons
- Preganglionic fibers have their cell body in the hindbrain and sacral part of the spinal cord and very long axons that terminate close to the target organ.
- The preganglionic fibers typically use acetylcholine as their neurotransmitter.
- Either start very close to brain itself, or very far at terminal end
- Only two areas in spinal cord where preganglionic parasympathetic cells start from
60
The parasympathetic ANS: The postganglionic fibers
have their cell body in the ganglia close to the target organ with short axons.
The postganglionic fibers typically use acetylcholine as their neurotransmitter.
61
Sleep apnea
- Parasympathetic nervous system more activated
- Bronchial contraction
Less oxygen (usually not a problem but can be for those with sleep apnea)
62
HRV
intervals between individual beats
63
Higher HRV associated with
- Increased flexibility towards environmental response
- Better attentional control
Increased risk aversion
64
Low HRV (deficits in flexibility) associated with
- Schizophrenia
- MDD
- BP
- Addiction
- ADHD
- Addiction (POTENTIAL TOPIC ) - addiction focused solely on drug and no flexibility in anything else
- PTSD
- GAD
- ASP
65
Do any organs have only sympathetic influence?
Sweat gland, liver, adrenal gland have sympathetic influence and NOT parasympathetic influence
66
Evolutionary mismatch
modern environment is changing very fast (and challenges we face are very different from those our ancestors face) yet our brains are the same
67
The hungry judge case study
- Recorded ruling when they were hungry compared to when they just ate lunch
- Facourable rulings dropped from 65% to nearly 0% as time passed since last meal
- After food break, favourable decisions immediately jumped back
Shows how biological factors can influence our decision
68
biological monism
shows that mind & body are intrinsically connected - mind is manifestation of brain.
69
Examples of evolutionary mismatch
Sugar cravings and obesity, sedentary lifestyle, social media & social comparison, Fight-flight response and modern stress
70
Natural selection
The "survival" filter. To pass genes to next gen (ultimate goal) you first need to survive
Different survival and reproduction based on adaptive traits
71
What three things does natural selection require and what are examples of natural selection
variation, heritability, and selection. - Threat detection, disease avoidances, food preference
72
Sexual reproduction
The reproductive filter. Evolution through mate choice and competition. - May produce traits with survival costs
Different selection pressures on biological sexes
73
Honest signalling
- A trait or behaviour that reliably conveys info about an individuals quality
E.g., peacock tail conveys information that individual is in top condition
74
Why is honest signalling actually honest
- Costly to fake - only individuals with genuine traits can afford to display it
75
Courtship
Shows how reproduction is more important and ultimate goal over survival (pass on genes and have offspring)
76
Gene-Environment interaction
- Genes provide predispositions, environment triggers expression
77
What is phenotype
Phenotype = Genotype + Environment + Interaction
78
Relationship between environment and cultrue
Cultural variations reflect environmental challenges & there is genetic selection for cultural compatability
79
Rice vs wheat & cultrue
Rice - Labor intensive, requires cooporation (correlates with collectivist)
Wheat farming - more manageables, less intertependent (corellates with individualist)
80
SERT
Serotonin transporter - a protein that clears serotonin from synapse (needs to be removed so other neurotransmitters can have effect)
81
Two main variations of SERT and their resulting effect.
- Short (S)
- Tend to be more sensitive to environmental cues compared to those with long alleles
- Short --> Less SERT protein --> More Serotonin in synapse
-Long (L)
- Tend to be more sensitive to environmental cues compared to those with short
Long --> More SERT protein --> Less Serotonin in synapse
82
S vs L SERT Alleles
S-Allele : Higher environmental sensitivity (suit mood & norms, more adaptive in highly interdependent societies). L-Allele : Lower environmental sensitivity
83
Genetic Trade off - SERT
The SERT gene polymorphism illustrates how traits that increase risk for certain disorders (anxiety, depression, PTSD) however environmental niches favour different traits and therefore we still see high prevalence of SERT in collectivist cultures that really benefit from heightened environmental sensitivity.
84
Adaption vs Maldaption: Anxiety
Heightened threat detection → excessive fear/avoidance
85
Adaption vs Maldaption: ADHD
Adaptive in dynamic settings → disruptive in structured environments
85
Adaption vs Maldaption: Depression
Energy conservation → impaired functioning if prolonged
86
Gene-culture coevolution
Cultural practices can create selection pressures that favour certain genetic variants, which then reinforce cultural patterns.
87
Hormones
Influence the whole body and act over long time periods - can be released by gonads into BLOODSTREAM
88
Key hormones differentiating men and women
Androgens (male sex hormones = testosterone). Estrogens (female sex hormones = Estradiol)
89
Do females produce testosterone?
Yes, just a small amount. Relative difference that make estrogen more dominant in females (but females do produce both)
90
Neuropeptides
Released by neurons or the hypothalamus
- Can act as hormones, neuromodulators OR neurotransmitters. Effects are MODERATE (e.g., oxytocin increases during childbirth, prompting maternal care). Sometimes called neuromodulators. Have an indirect and pervasive effect
91
Neurotransmittrs
- Act at synapse in brain circuits controlling sexual arousal, motivation and reward
- Very fast-acting (milliseconds)
E.g., dopamine surges during mating related reward processing
92
Hormone: Size, speed, distance, function, examples
Small-large, slow, via bloodstream, regulate body/organs broadly, cortisol, estrogen
93
Neuropeptides: Size, speed, distance, function, examples
Medium, Moderate/slow, diffuse over wise brain areas, modulate brain activity & emotion, oxytocin, vasopressin
94
Neurotransmitters: Size, speed, distance, function, examples
Small, fast, locally at synapse, rapid signla transmission, Dopamine, GABA
95
2 effects hormonse can have:
Activating/organisitng
96
Activating effect of sex hormonse
- Direct influence on behaviour (in short time frame)
The resulting behaviour, in turn, will influence hormonal secretion
97
What would happen if you administered moderate dose of testosterone to a group of healthy adult females for 2 weeks
This shows an activating effect. Would see Aggression and dominance increases
- Argue more in a meeting
- Dominance seeking
- Increased focus on status and competition, not direct aggression
Trust in others decreases
- Testosterone reduces interpersonal trust in economic games
Spatial performance increases
- Improvement in mental rotation and spatial tasks
Sexual motivation & desire increases
- Testosterone patch has improves libido in surgically menopausal women
Emotion recognition decreases
- Lower ability to detect anger and threat
- Reduced ability to recognise angry faces or threat cues
98
99
Organising effect of sex hormones
- Guide early sexual differentiation
- Shape long-term patterns of behaviour
Set the stage for later activation by hormones during puberty and adulthood (e.g., responsiveness to testosterone or estrogen)
100
When do sexual organs differentiate
12th week of gestation
101
Activating vs organising
- Organising = building a house (permanent)
Activating = painting the walls (temporary & can change)
102
Effect of environmental hormone exposure
Endocrine-distrupting chemicals can interfere with natural hormone signalling during critical developmental windows - this can interfere with sexual differentiation
103
Phthalates
Block testosterone produced in the fetus
- Animal studies show altered sexual behaviours after exposure to phthalates
104
Do hormonse explain sexual orientation? What does?
Adult hormone levels DO NOT explain sexual orientation. - Potential prenatal factors (individuals exposed to certain stress/alcohol can increase cortisol and endorphins. Increased cortisol and endorphins lead to a decrease in testosterone levels IN RATS show preference for samesex/male rats show female typical behaviour
105
Intersex
- People with anatomies that are intermediate between male and female, or a mixture of both
Have XY chromosomes
106
Congenital Adrenal Hyperplasia (CAH)
- Overdevelopment of adrenal glands
- This leads to production of extra testosterone
- This extra testosterone can cause a genetic female to become partially masculinised
107
Function of adrenal glands
- Release cortisol & the androgen testosterone
108
Positive feedback mechanism adrenal cortex is involved in
When cortisol level increases. Sends negative feedback to hypothalamus and pituitary to ensure no overproduction.Cortisol level is low, Cannot inhibit hypothalamus and pituitary to slow adrenal clan
Adrenal gland therefore keeps working a produces lots of androgen
109
How to treat CAH
- Elevate level of cortisol
- Cortisol sends negative feedback to hypothalamus and pituitary
Adrenal gland therefore slows and androgen is lower produced
110
Girls born to mothers with a higher level of testosterone (PCOS) demonstrate what?
show an increased preference for "male" toys. This early exposure to high levels of testosterone also happens to girls with CAH and they also show preference for boy-typical toys
111
PCOS
1 in 10 females have PCOS
- 70% of females go undiagnosed
Most find out about condition when seeking fertility treatment
112
David Reimer
- Him and his twin brother had medical treatments and he damaged his genitalia permanently
- Medical advice given was to raise child as a female. He still had preference to play with boy typical boys and wear boy clothing. He - Suffered with depression his whole life
Commited suicide
113
Intersex psychological effects.
- Many intersex individuals are unhappy with the surgical procedures they were subjected to as babies. Such procedures can cause long-lasting emotional and psychological effects, including depression, anxiety, feelings of betrayal and isolation
114
Vasopressin
(monogamous hormone)
Territorial behaviour in males
115
Oxytocin
(bonding hormone)
- Maternal behaviour
Social bonding
116
Sex and dopamine
- Dopamine regulated feeling
- Dopamine motivates us to engage behaviour important for our survival
117
Why is sex good for our survival
Sexual reproduction increases variation -> quicker evolutionary adaptation -> long term advantages build over generations (including dealing w changes to environment)
118
Cost of asexual reproduction
No genetic variation = less adaptable to changes to environment
119
How to Bonobos demonstrate that sex and social behaviours are interlinked
- Engage in sexual behaviour when in a fight or want something
Can resolve social tensions
120
Steps 1, 2 3 and 4 of sex
1 - getting motivated
2 - finding a mate
3 - attracting a mate
4 - sex
121
Hormone levels when getting motivated for sex
- Testosterone primes the hypothalamus and a few other brain regions to release dopamine
- Dopamine release in turn strengthens the motivation aspect of reproductive behaviour
122
Decreasing testosterone levels in men
Decreases sexual activity
123
Dopamine role in sex
- Strengthen motivation for engaging sexual behaviour. Serotonin blocks dopamine release. Thus antidepressants and SSRIs can lower libido
124
Finding a mate
Neural processing - involvement of the amygdala, orbitofrontal cortex to evaluate attractiveness and social relevance
125
Percieved attractiveness and ovulation
High estradiol coincides with ovulations, and this causes subtle changes in blood circulation (lips red & fuller, face becomes more symmetric, males find more attractive).
126
Female sensitivity during ovulation
- Women look at attractive males longer when they are ovulating vs when they are not
More sensitive to sensory & social cues
127
Difference between womens preferences when ovulating versus not.
When not in ovulation period
- Pay more attention to long-term partnership traits (warmth of facial expression etc)
When in ovulation period
- Pay more attention to masculine (high testosterone) traits - deep voice, muscles
This effect is relatively small
128
What areas of the brain become more active during ovulation?
Amygdala (emotion centre) becomes more active during ovulation, as well as the orbitofrontal cortex (evaluating certain signals). This is the female brain being primed to detect signals & emotions in order to find a mate.
129
Attracting a mate
Displaying genetic fitness. Courtship, honest signallling etc. Males genetic success DEPENDS upon attracting as many females as possible
For females, big investment to choosing only one genetically fit male (always so critical)
130
Biological changes during sex
- Sympathetic nervous system activates - heart pumping, blood circulating faster
- Surge of dopamine (stronger surges seen in males)
Oxytocin and vasopressin get released (during time of orgasm) - this is the release of bonding signalling molecules
131
What happens to fear and thinking centres during sex
- Deactivation of brain regions involves in self-awareness (PFC and amygdala)
- Default mode network (sense of self) also goes down - this also occurs during meditation & psychedelic use
Broader and more variable brain activation patterns in women
132
Insula cortex and sex
- Brain area where pain is percieved
- This is downregulated
During sex your capacity to feel pain is reduced
133
Hormonal changes to prime parental behaviour
- Increased activity in amygdala (hypervigillance)
Just looking at the baby activates the reward centre of the brain (increases level of dopamine and oxytocin)
134
Similarities between romantic and maternal love
- Lack of activity at PFC (shows you are actually NOT thinking with PFC when u look at child & loved one- no more evaluating and thinking areas just shut off)
The active areas are rich in oxytocin and vasopressin receptors (primed to be activated when these are released)
135
The mechanisms of maternal behaviour
- Hormonal changes (increase in oxytocin and prolactin)
Changes in hormone receptors in the brain areas important for maternal behaviour
136
Dolen & Malenka
study of maternal attachment and pair bonding.
When low levels of oxytocin, or oxytocin receptors compromised.Animals/rats not interested in picking up pups. Measured latency of mother to pick up pups - found this often correlates with anxiety or depression later in life (shows the role early maternal care plays in psychological wellbeing of offspring)
137
Hypothalamic nucleus and pair bonding
Hypothalamic nucleus directly stimulates nucleus acumbus (important region in reward centre, key area for addiction & reward related behaviour. This is related to altruistic helping behaviour
- Helping people is rewarding
We get dopamine released from this
138
Oxytocin
- Increases levels of trust
- Crucial in maternal behaviour and pair bonding
- May be related to agression towards 'others'
139
Save pieter study
- When not given oxytocin, equal preference of different ethnicities names
When given oxytocin, preferentially chose names that sounded like different ethncities (racial bias more pronounced)
140
Vasopressin
Crucial role in pair bonding & parental behaviour
141
Prairie voles (PV) versus Meadow Voles (MV)
Closely related species, PV forms long term pair bonds, MV doesnt).
142
Why does PV form long-term pair bonds
Have a high vasopressin secretion level
143
Evolutionary advantage of monogomy.
Comes about when there is imperative evolutionary environmental region
Monogamous animals more likely to like in drier and more desolate region
144
Effect of vasopressin on social and parental behaviour
- Overexpression of vasopressin receptors in MV makes them MORE PV like
In humans, men with genes for less active forms of the vasopressin receptors are less likely to marry and more likely to divorce
145
Two types of strategies for men to pass their genes
- From the evolutionary perspective, males are more predisposed to be interested in multiple mates than women are
Alternatively, men can choose to support and help one partner and raise their children together
146
New fathers and testosterone level
the testosterone level of new fathers drops about 30% on average. Thus, Lower testosterone level associated w high levels of paternal behaviour (but this depends environmentally vs culturally - ie., less pronounced in korea)
147
How does Order of births impacts our risk for GAD and depression
- First born more likely to develop GAD and depression
148
How does culture/environment influence mate attractiveness.
- Preference for high testosterone faces is LOWER than in countries still developing
- If females are PRIMED to think about scarcity of resources than they show preference for high testosterone face
- When resources scarce, prefer more masculine traits (associated with helping bla bla)
149
Bonobos vs. chimpanzees
- Bonobos engage in frequent sexual behaviour, mostly as a recreational activity
- The change of habitat and scarcity of resources might have changed the evolutionary path for the two closely related primates
The lack of clear hierachy in bonobos allows all adults to take care of young together
150
4 components of emotion
Physiological response, action, feeling, cognition
151
Anticipation/Negative contrast
- Mismatch between what is being expected and what is actually received
Dopamine level increases VERY sharply when we anticipate something, when this wasn't rewarded, fed back by emotional response
152
Amygdala
- Classically associated with fear, but also processes emotions, ambiguity and salience
153
3 important brain regions amygdala connects with
Deeply interconnected with PFC (specifically ventromedial cortex), hippocampus (emotional learnings/memories), hypothalamus
154
Amygdala Basal-lateral nucleus
At the base and lateral region
Get input from thalamus and sensory cortex
INPUT
155
Amygdala central nucleus
OUTPUT. Output to hypothalamus
156
Different pathways for predator vs social threat for amygdala processing
- Not ALL info goes through basolateral nucleus (predator related stimuli will often bypass for speed
157
If an experimenter deactivates the central nucleus, what would happen in mouses freezing behaviour?
- No output of behaviour
- Learning part will be intact
Would NOT freeze, but if reactivated, would likely avoid fear-inducing stimulus
158
Amygdala low road
fast/crude/threat detection - good for times where SPEED matters most. Shape vs animal doesn't matter, more important to act fast and run away
Information goes straight to amygdala
159
Amygdala high road
slower, refined by cortical processing
Information goes via sensory cortex
160
What is PFC's effect on amygdala
- PFC normally inhibits the amygdala
- It is primarily the ventromedial PFC that inhibits it (dorsolateral will further stimulate). PFC regulates emotional reactivity and fear extinction
161
How does fear extinsion work?
- In beginning you feel scared and fearful, but you went and nothing happened
- Fear memory then becomes extinct, location no longer feared as fear no longer adaptive
- PFC plays important role in extinction training
162
What is PFC-Amygdala loop impaired by, and what are the effects.
Impaired by chronic stress, trauma, and ESPECIALLY early adversity (or during prenatal period)
- - Emotional regulation no longer works
PFC-amygdala loop is CENTRAL to emotion regulation.
163
What happens to behavioural extinction in animals after leisoning PFC
fear conditioning and behaviour is intact but unlearning of these associations can no longer occur.
164
Glucocorticoid receptors in PFC & hippothalamus
These receptors enable activations necessary to deal with the situations. When these receptors are continuously activated through elevated cortisol = neurotoxicity, hippocampus begins to shrink. Less input sent to PFC and amygdala and all these areas become imbalanced (leading to painful memories, inability to learn positive associations)
165
Amygdala and Cortisol relationship
Amygdala triggers HPA axis --> cortisol release
166
Function of cortisol
- Cortisol readies the body to act quickly in emergency situations
Mobilises glucose in body = more resources for energy
167
Effect of Chronically elevated cortisol
KEY POINT TO KNOW: Hippocampus atrophy, learning & memory goes down, fear response goes up (Our brain is NOT primed to deal with long-term chronic stress)
Neuroplastic effect of having the neurons too excitable
.Disrupts brain structure/function ESPECIALLY hippocampus and PFC. Lowers amount of dendritic spines (lose connectivity, die out)
168
What would happen if amygdala was lesioned in startle rat study
- Depends on where it is lesioned
- Basal-lateral or central nucleus
Deactivation of central nucleus = no freezing behaviour
169
What happens to amount of startle if rats exposed to stress prior to stimuli
Showed increased startle response when exposed to stress before the stimuli
170
Example of how amygdala modulates startle response
ow people emotionally distressing pictures than measures startle response with eyelid.
- Based on airpuff in eye
If amygdala in normal/overactive, if you see fear stimuli beforehand your startle response will be higher
171
Patient S.M
Bilateral amygdala damage - had NO fear.
172
social cautionary behaviour in humans
I.e., standing distance. - When amygdala lesioned/non-functional, cautionary behaviour is missing (S.M will stand VERYYY close to people)
Shows amygdala importance in functioning in a social environment/hierachy
172
Characteristics of patient S.M
- No fear of snakes
- Difficult in recognising fear in faces
- Comes off very happy and joyous
Subtle cognitive impairments (no preferential memories for emotional stories)
172
Kluver-Budy syndrome in monkeys
- Amygdala damage -> Tame, fearless, socially impaired
- NO fear of aggressive group members
Often attacked by other monkeys through invading their personal space (provoked aggression and antagonistic behaviour)
173
When would S.M feel fear/agitation
- Lack of oxygen (breath restriction)
- Increasing CO2 levels - stimulates brain stem immediately provokes agitation
- Suggests there is another fear pathway related to breathing that is not mediated by the amygdala
- If asked to repeat, she said yeah sure - amygdala was not there to connect fearful experience to memory.
174
Toxoplasma gondii
- Parasite
- Host is a cat
- 1/3 of people have this parasite - and it lives in our brain
175
Toxoplasma gondii impact on amygdala
impairs amygdala function. - Results in engagement in reckless activities and impairs fear/avoidance behaviour. - Does not DESTROY amygdala - lowers dendritic branching in amygdala
- Can increase inflammation in general in the brain which can have cascading effect
176
Cooperative eye hypothesis
: Human eyes evolved for social communication
177
Amygdala and social attention
Amygdala supports detecting eye whites, social signals. Patient S.M (and autism patients) struggled to look at eyes (key for fear detection)
178
Amygdala and ambiguity
Activates MORE with ambiguity. Our brains cannot deal very well with ambiguity - we have a natural bias to treat things pessimistically. - Threat detection is not just about fear - its about uncertainty due to our negative bias
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Amygdala and ambiguity WHEN exposed to chronic stress
Especially if exposed to chronic stress, PFC not functioning very well and extinction not working very well = increased threat expectancies. Avoidance = avoiding stressful stimuli and avoiding chance to extinguish maladaptive behaviour
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Individual differences in reactivity
- Some people have hyperactive amygdala responses to threat
Linked to anxiety, PTSD, genetic variants (SERT polymorphism)
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SERT olymorphism and reactivity (orchids/dandelions
- Short allele = also MORE sensitive to good (and bad) things. In collectivist culture, more sensitive to social cues, good support and enriched environment - S alleles might benefit even more
- L alleles - like dandelions, are robust and can do all good anywhere
- S alleles - like orchids, might suffer a lot when environment is not right, when environment is nurturing and nice = spectacular phenotypes.
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James-Lange theory:
Physiological changes precede emotional experience
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Evidence for James Lange Theory
Patients with autonomic failure have blunted emotions (do not have sympathetic activation). Patients with botox = blunted. Posture links to interoceptive awarness & confidence
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autonomic failure
cannot make proper adjustment to nervous system. Our body SHOULD change from the input we get from the environment. - Autonomic failure. = Lack of bodily response to movement & exertion. = dizziness/pass. Associated w reduced emotional intensity due to not having physical response to interpet (james lange)
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Feldman-Barret
Whole idea is that emotions are constructed (modulated according to language and culture)
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How does feldman barret differ from Lange
- More nuanced/modern findings
Emphasized effect of culture and languages in appraisal (people can feel greater emotion when talking in their home language)
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How is language linked to emotional regulation
- More vocabulary we have to describe emotional state in more refined terms, the better the emotional regulation
- May explain HIGH suicide rates in Korea (did not learn proper emotional strategy through limited language)
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BAS - behavioural ACTIVATION system)
- Activation (ACTIVE)
- Tendency to approach
Happiness and Aggression
- Increased activities of left hemisphere
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BIS - Behavioural INHIBITION System
- Inhibition
Sadness
- Increased activity of right hemisphere
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Jack Panksepp emotional mapping
- Map different brain regions to emotional state (and neurochemicals involved)
Emotions can be mapped into evolutionary meanings (threat detection, nurturing, separation distress)
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Jack Panksepp Goal of emotion mapping
If we could separate and map exact neural pathways of emotional states = easier to find therapeutics to treat disturbances in emotional regulations
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How are emotions evolutionarily adaptive
- Serves as a signalling system (for survival and reproduction)
Depression - outward symptoms exemplify their honest need for help - TOO costly to fake (honest signalling)
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Evolutionary adaptation of anger
Anger = usually a result of unfairness.
- Anger works as a signal to others "don’t do that again"
- Evolutionary, hunter gatherers had to share food, hunt together - this cooperative behaviour requires fairness
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Evolution & gossiping
- We talk to each other about feeling treating unfairly & immoral behaviours
- Try to indirectly punish individuals who do not stick to group norm
- Groups allowed to gossip perform better than groups not allowed to
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Social inequality effects & air rage
- Phenomenon called "air rage"
- One group went straight to economy class, the other group could go straight to economy
- Acute aware of economic status made people aggressive
Situational aggression triggers (very context dependent)
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How can physical state influence agression
- Can be primed from previous actions/fight
- Even in new context, body still geared for fight and James Lange (interpret physiological state as emotion (shows that even when source of anger is gone, you still feel SO angry.
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Implications of social inequality effects on anger for society
- Perception of inequality so prevalent
More inequality (PERCEPTION of inequality) effects mental and physical health of people in society
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Testosterone and aggression
Testosterone FACILITATES (rather than causes) aggression. Its not reallt about absolute level of testosterone, instead relativity (sharp relative increase = predictable of aggressive behaviour.) - Status seeking - try to argue more, speak louder, dominate discussion (more common than actual physical aggression in our day)
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Children high risk for aggression and interventions
Did aggression behavioural therapy on children identified to be high risk due to testosterone levels. - Children in intervention group had lower testosterone increase
- Shows importance of accessible early interventions
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MAOa gene
- Codes for enzyme that breaks down serotonin & dopamine. People with low activity in MAOa gene links to aggression
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The three-way interaction for aggression
- Testosterone (facilitates aggression)
- Serotonin (inhibits impulsive behaviour)
Cortisol (inhibts aggression, become more withdrawn)
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When does high testosterone confer risk of aggression
High testosterone confers risk of aggression when cortisol and serotonin levels are lower (seen in high status individuals)
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Ventromedial PFC and moral decision making
- Ventromedial PFC integrates emotional information with decision making processes.
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Ventromedial cortex engagement and trolley problem
Ventromedial cortex engaged when you have to make direct choice
- Can predict 1-4 seconds BEFORE you make choices what kind of choice you will make
People feel very distressed and uneasy when making choices to directly push someone
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Observational fear task
- One mouse in chamber gets electric shock, the other mouse observes
- The observer mouse exhibits freezing/jumping behaviour
Same neuronal groups that induce freezing behaviour are activated (mirror neuron mechanisms) - enables us to feel what other people who are in distress feel
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Mirror neurons & experience
greater activation if mouse went through experience in the past
Shows previous history has a role in our ability to feel empathy for others
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Oxytocin role in empathy & procosial behaviour
- oxytocin enhances emotion contagion and facilitates helping behaviour
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Emotional contagion effect in social media
- If they read one negative post = post LESS happy posts
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Notification stress
- Leads to cortisol release
Sympathetic nervous system arousal
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Core symptom of depression
Persistent low mood, anhedonia, fatigue, sleep disruption, cognitive difficulties
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Anhedonia
- lack of feeling joy, no increase in pleasure
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Core symptoms of anxiety disorders
Excessive worry, hypervigilance, autonomic arousal, avoidance behaviours
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Core symptoms of PTSD
Intrusive memories, flashbacks, nightmares, hyperarousal, emotional numbing * Significant overlap
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Olfactory signals & emotional memory
Olfactory signals go straight to limbic system - Emotional memory can so easily be evoked by certain smells
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Why group anxiety, depression, PTSD together?
Co-morbidity (chance you have multiple diagnoses). 50% or higher people w depression have anxiety (rule, not exception)
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Traditional silo-approach
Disorder-specific mechanisms
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How have we moved beyond diagnostic silos
- There is growing evidence of shared biological and social pathways. This matters because important to acknowledge SHARED pathway and address the underlying issue
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First line of treatment for psychological disorders
Often SSRI
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When anxiety is really bad - treatment
GABA agonist (benzodiazepine) = overactive amygdala becomes calmer
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Problem with GABA agonist
Indirectly increases release of dopamine = addictive potential - baseline may change due to impacted neurotransmitter system - body develops tolerance
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Alternative to silo-approach
P-factor approach
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P-factor approach
Stands for psychopathology factor - the idea that one general factor affects all disorders so instead of categorising into seperate boxes we should look at a more dimensional approach
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p-factor implication for treatment and research
Instead of focusing on disorders, focusing on mechanisms ( a lot more tangible due to differential symptoms in things like depression - hypersomnia/insomnia
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Importatnt part of General factor of psychopathology model
It's a gradient, and there are levels (internalising/externalising factor) - things are clustered together based on symptoms
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Implication for viewing mental disorder as spectrum
Aknolwedges ambiguity - traits aren't necessarily pathological
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Inflammation
Common pathway across psychiatric disorders
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Cytokines
Inflammatory marker. Signalling molecules which activate immune system when there is inflammation (elevated cytokines in PTSD, GAD, and MDD)
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Cytokine and stress
Bidirectional relationship with stress (cytokines elevated = more stressed - higher inflammation = more experience of mental stress)
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How does neuroinflammation influence brain
Neuroinflammation impacts neurotransmitter systems (serotonin availability lower, motivation/mood regulation etc all affected)
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WHy do we develop inflammation when in higher level of stress
"Old friends hypothesis - evolutionary mismatch theory"
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Old friends hypothesis
Evolutionary mismatch: Our immune system evolved in microbially rich environments, developing a hypersensitive, "negatively biased" defense system.
Co-evolution: Immune pathways calibrated by constant pathogen exposure ("Old Friends") became balanced through frequent interaction.
Modern sterility: Lack of childhood microbial exposure prevents immune calibration → system stays overly reactive
Stress link: Without microbial checks, stress hormones directly trigger inflammation (sterile inflammation).
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Sterile inflamation
Stress activating immune system
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Inflammation impact on brain (in term of microglia)
Stress = high inflammatory actions which leads to microglial activation = creation of my cytokines = leads to more cell deaths & less neurogenesis
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Blood-brain barrier permeability
- Permeable and exposed to certain level of inflammation that the body experiences
Not a COMPLETE barrier
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Impaired neuroplastivity
Low dopamine and serotonin impairs neuroplasticity - leads to depressive like behaviours and have low cognitive capacity (seen in people with depression)
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Early life stress impact on brain (rat removal from mothers etc)
- LESS dendritic branches in hippocampus
- Less evidence of neurogenesis
Smaller brains, dendritic loss
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3yo brain of normal vs orphaned child
(specifically in hippocampal area which is extremely small and atrophied)
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Neurogenesis
Common theme in therapeutic techniques.
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Correlation between hippocampal function and PTSD
For people with lower hippocampal function = more severe PTSD
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Where does neurogenesis occur a lot
Hippocampus
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What can size of hippocampus predict
Whether soldiers would develop PTSD or not - larger hippocampus = protective effect
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BDNF & growth factor
Neurotropic (friendly) factor. - It does not cause neurogenesis, but promotes the process. Increasing BDNF expression increases neurogenesis
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What happens when you block BDNF expression
Neurogensis is blocked
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High stress, maternal deprivation, and no exercise correlates with...
Aptosis (neuronal death and atrophy). BDNF expression low, low neuogensis sad neuron
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Importance of social interaction
Promotes expression of BDNF
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If you wanted to make fear extinction behaviour in rats faster, what would you give them?
BDNF - fear extinction depends on new learning and forming new connections between fact & context which depends on synaptic plasticity (assisted by BDNF)
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Conventional therapies
SSRI's (does not work for 40% of patients, often takes more than a few weeks)
Psychotherapy
Lifestyle interventions (exercise, meditation)
Anti-inflammatory diets
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Why do SSRIs take long to work
Takes indirect route, people dont experience direct benefit immediately which can pose stress
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Issues with exercise as a treatment
People low in motivation do not want to hear that they should exercise
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CBT pros and cons
Works well, unlike other options will work at all levels of depression & gives people feeling of agency. Has cost and time barrier and is inaccessible to many patients
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Ketamine as treatment
Directly stimlates neuroplasticity via BDNF (does not take indirect route compared to SSRI - at least on short term)
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Psychedallics
Not only the drugs people also need to make sense through the therapies --> Combined with therapy for safer, more effective outcomes
- Dendritic branching increases dramatically in psychedallic condition
- Dramatic increases in structural and functional plasticity
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How do psychedallics cause neuroplasticity
Work on the 5-HT2A receptor activation which causes neurplasticity cascade (similar effect to Ket, created dramatic effect on neuroplasticity)
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How do psychedallics differ to traditional treatments
Single dose has lasting effect (still feel better for multiple years when combined with therapy)
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Social determinants of Affective Disorders
Childhood adversity alters development trajectories. Dopamine signalling (and capacity to react to reward) is different when with toys and stimulation as a child compared to in a deprived environment_
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Key mental health risk factor later in life
Social disconnection & loneliness
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Effective social interventions for psychological disorders
- Community based programs show biological effects (cortisol level lower, inflammatory markers down)
- Often comparable to pharmacological interventions
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Meditation and brain health (3 effects)
1. Increases grey matter volume in key regulatory regions - limbic system, ventromedial cortex (can be communal but often individual approach)
2. Increases connectivity between emotional regulation regions (PFC and amygdala - PFC develops capacity to keep amygdala in check)
3. Significant reduction in inflammatory markers
(Effects can be seen in as little as 8 weeks)
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Implications of genetics on medication for psychological disorders
- SERT polymorphism respond differently to sertonergic medications
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How to personalise medicine for psychological disorders
Biomarkers, HPA markers, inflammatory markers, social factors & life history
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Digital patient twin
Doctors try one type of medication, if it doesnt work, switch to another class. While waiting for symptomatic relief (distressing) - by training models based on patient data = don't need to do guesswork and predict outcome of medications by stimulation.
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Bidirectional relationship relationship between disorders & inflammation
INFLAMMATION CAUSES PSYCHOLOGICAL DISORDERS BUT WHEN YOU HAVE DISORDER ITS ALSO HIGH
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