Exam 1 Flashcards

(173 cards)

1
Q

What are emotional responses

A

automatic response programs, generated by the limbic system, based on sensory or other input, causing bodily
sensations

Rapid physiological change in response to altered conditions to promote survival

They are genetically based and evolutionarily based

Intuitive response

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2
Q

Learned emotional responses

A

Learn from experience about dangerous stimuli for which evolution could not prepare us

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3
Q

Limbic system role in emotion

A

Limbic system:
- Generates emotion
- Evolved very early in mammalian history
- does not require consciousness (not aware of why you are feeling the way you feel)
- closely connected with more recently evolved cortical areas

Cortex allows emotions to be consciously felt + thoughts to affect emotions (rational about why we may feel these emotions)

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4
Q

Four components of emotions in humans

A
  • Feelings
    – Actions
    – Physiological arousal
    – Motivation (desire to perform or not perform an action)
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5
Q

Emotional component: Feelings

A
  • Subjective experience generated by cortex
  • Wide range of states (not just positive or negative)
  • Most mammals do not experience subjective feelings during an emotional response
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6
Q

Emotional component: Action

A

Emotions may involve actions:
* Defending or attacking in response to threat
* Laughing out at a good joke

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6
Q

Emotional component: physiological arousal

A
  • Bodily responses
  • Generated by autonomic nervous system
    Sympathetic system: fight or flight
    Parasympathetic system: rest and digest

ANS activity: changes in heart rate, blood pressure, distribution of blood flow, perspiration, release of hormones, gastrointestinal motility
- Some emotional states (sadness vs. happiness) > differentiated by their associated physiological changes
- Positive emotions elicit different array of autonomic responses than negative emotions
- But within those categories, different emotions elicit approximately the same autonomic profile

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7
Q

Emotional component: Motivation

A
  • Emotions are motivational programs that coordinate responses to solve specific adaptive problems
  • We are motivated to seek pleasure and avoid pain
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8
Q

Lie detector tests and physiological responses

A

Test is based on assumption that lying produces an emotional and physiological response

Because all negative emotions involve same physiological
responses

Polygraph (lie detector) is poor at distinguishing liars from anxious innocent people

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9
Q

Ekman: Outward expression of emotion and culture

A

Ekman says there are distinctive expressions for anger, sadness, happiness, fear, disgust, surprise, contempt and embarrassment.
These different emotions can be detected in facial expressions that are similar across cultures.

There is cross-cultural similarity in expression production, but there are
culture-specific differences in display. (e.g more of a ‘poker face’ in certain cultures)

A role of facial expression is
paralinguistic–an accessory to
communication, providing extra info

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10
Q

Model for Emotional Facial Expressions across Cultures

A

1) Elicitors (We have learned to associate certain stimuli with emotions e.g recollections or situations that make us feel a certain way) >
2) Facial affect program (associated facial responses with the emotional is pan-cultural are pan-cultural) >
3) Mediation by culture-specific display rules (make one exaggerate, minimize, counteract, or camouflage facial expression) >
4) end result = facial expression

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11
Q

Basic emotions summary

A
  • Most universally recognized
  • Paul Ekman et al. showed photo’s > societies all over world
  • Hunting-and-gathering tribes, western societies: facial expressions remain similar
  • Humans of all cultures, regardless of experience, recognize facial expressions of basic emotions to certain degree
  • Facial expressions in blind people = similar/identical
  • Must be genetically based
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12
Q

Link between facial expression and emotion

A
  • Facial expression = signal of state of mind / intention
  • Facial expression of other person: amygdala reacts by mirroring the emotion via mirror neurons
  • Emotion mirroring = basis of empathy
  • Smile triggers signals that begin process of smiling back
  • Fearful expression triggers fear in observer
  • Autism: less mirror-neuron activity > old hypothesis, not considered good explanation anymore
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13
Q

Facial expression and emotion experiment

A

Volunteers inhaling disgusting smell
* Later watched video of someone else smelling and expressing disgust
* Both produced same kind of activity in brain area associated with disgust
(insula)

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13
Q

Voluntary vs. emotional expressions

A

Humans can recognize difference between forced/voluntary and emotional smile

Voluntary smile via motor cortex and cranial nerves

Emotional smile via limbic system (medial forebrain) (motor areas in anterior cingulate cortex)

2 anatomically and functionally distinct sets of descending
projections to facial muscles

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14
Q

Experiment: voluntary vs facial expressions

A

Duchenne
Transcutaneous electrical stimulation to specifically activate facial muscles

Duchenne connected electrodes to face to elicit facial expressions
> muscle around the eye were not contracting as much as they would with intuitive + spontaneous laughter

Muscles around eyes (obicularis oculi) not easily controlled by force
of will > but is emotion driven via projections from medial forebrain
and hypothalamus

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15
Q

Limbic lobe + emotional response

A

Limbic system
> cingulate gyrus
> fornix
> hippocampus
> temporal lobe
> amygdala
> corpus callosum
> etc etc

Hippocampus and fornix not very important for emotion

Important for emotion:
Amygdala, (orbital and medial) prefrontal cortex, ventral basal
ganglia (= ventral striatum), hypothalamus, (mediodorsal) thalamus
> important in experiencing + expressing emotions
(+ cingulate gyrus)

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16
Q

Role of the amygdala + its connections

A

role in experience of fear and expression of fearful behavior

Amygdala connections with prefrontal cortex, other parts of cortex,
hypothalamus, thalamus, basal ganglia

Amygdala = nodal point in network that LINKS cortical and subcortical brain regions involved in emotional processing WITH subjective
emotional feelings in humans

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17
Q

Amygdala: Conciousness

A

We have evolved a conscious emotional system, but we retain the primitive, automatic responses

Both conscious and unconscious route

Frightening sight / sound = registered by amygdala before we become consciously aware of it

It allows body to react very quickly to threat or reward

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18
Q

Circuity of fear

A

Visual input (frightening sight/sound) > relayed in the thalamus > passes on to the sensory cortex ( to be made concious) and the amygdala (activating an intuitive emotional response very quickly)

Slow and accurate route (high road)
Thalamus > sensory cortex > hippocampus > emotional stimuli are processed (they produce conscious awareness and more thoughtful response)

Quick and dirty route, low road
Thalamus > amygdala > hypothalamus > eliciting a physiological response

Hippocampus feeds back stored information, confirming or modifying the initial response

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18
Q

Amygdala activity level variation

A

Depression: exaggerated left amygdala activity when interpreting emotions for all faces, and especially for fearful faces.

Hyperactivity was normalized when patients went on antidepressants or behavioural therapy

Individuals with psychopathic tendencies show
– significant bilateral volume reductions in the amygdala
– decreased amygdala and orbitofrontal cortex responses to emotionally provocative stimuli

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19
Q

Lateralization of emotional functions

A

Left and right hemispheres different role in emotion

Right hemisphere: emotional aspects of language (prosodia: tone, emotional coloring of speech): damage > aprosodia (monotone speech)

Auditory experiments: right-hemisphere superiority in detecting emotional nuances in speech

Facial expressions in left visual field (projects to right hemisphere): emotions in face more accurate identified

Left facial musculature: more fully expressed emotions

However, BOTH hemispheres participate in processing emotion!

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20
Q

how the resting membrane potential arises

A

In resting cell main ion channels are K+ leak channels > cell membrane in rest much more permeable to K+ than to other ions

K+ channel: ions flow down conc gradient, moving out the cell = uneven distribution of charge, negative charge intracellularly, positive charge extracellularly = accumulation of charges across the cell membrane (+ve lined up on extracellular, -ve lined up on intra)
> So +ve ions that try cross the channel are pushed back into intracellular side (repelling) and pulled back in by attraction of -ve ions lined up
> equilibrium potential is reached (Veq): no net flux of ions (chemical driving force is equal and opposite to electrical driving force, for every K+ moving out, there is one moving in
> dynamic equilibrium (-70 mV)

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21
Q

Distribution of ions inside and outside of a neuron

A

Na+: many outside, few inside (+60mV)
K+: few outside, many inside (-90mV)
Cl-: many outside, few inside
Ca2+: many outside, few inside
Proteins (negatively charged): few outside, many inside

Maintained by Na+-K+-ATPase

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21
Zone of a neuron
Input zone (dendrites and cell body, receives signal) Integration zone (axon hillock, when threshold is reached = decision to make a new AP) Conducting zone (axon, AP rises and travels) Output zone (axon terminals, presynapse)
22
Which factors influence the movement of ions?
Driving forces: > Concentration gradient > Electrical/voltage gradient Combine to give: Chemical electrical gradient
23
How does an AP arise
Change in membrane permeability by opening / closing voltage gated channels = flux of ions AP triggered by sudden local depolarization in ‘input zone’ = membrane potential less negative (closer to zero) Local depolarization and synaptic integration at axon hillock until threshold voltage of -50 mV is reached > opening of voltage gated Na+ channels > Na+ influx > positive charges in cell = further depolarization > Self-amplifying process = positive feedback loop
24
Phases/course of an AP
1) Starts at resting potential (-70mV) (both channels closed) 2) Signal received = local depolarization = opening of voltage gated Na+ channels = influx of Na+ = threshold reached (-50mV) (Na+ channel is open, K+ still closed) 3) Rising phase, AP peaks at +40mV (overshoot) 4) Falling phase: Na+ channel is inactivating and K+ channel is opening. K+ goes out (wants to flow toward -90mV) = membrane potential drops = reaches undershoot phase and starts to repolarize (this is afterpotential) (where Na+ channel is inactivated) (-80mV) 5) resting potential is reached again: Na+ is closed, K+ is closed. neuron is ready for another AP
25
Refractory periods
Absolutely refractory: impossible to generate AP (Na+ channels go from active > inactive, and K+ channels start to activate) (rising and falling phase) Relatively refractory: new AP can be induced if stimulus is higher (during afterpotential, undershoot phase) (stimulus needs to be higher bc membrane potential further away from threshold of -50mV)
25
"all or none" phenomenon of AP
For AP to occur, threshold needs to be reached Constant amplitude, independent from stimulus strength > Increasing influx of positive ions does not affect amplitude of AP (all or nothing) > Increasing influx of positive ions (intensity of stimulus) does increase frequency of AP (firing rate) (e.g low stimulus can not reach threshold during relatively refractory period, while stronger stimulus can)
26
Propagation of AP
Occurs in a non-decremental manner AP at a certain area will locally depolarize neighboring areas, creating circumstances in which the regions on the axon will open voltage gated Na+ channels, recreating the AP in the other spot This continues down the length of the axon Does NOT travel backwards as the areas behind the AP are still in the refractory period Larger axon = lower internal resistance = larger distance for AP propagation = AP propagation is too slow > SOLUTION: layers of insulation (myelin) where current cannot leak away (as there are no channels in these myelinated sections)
27
AP saltatory conduction
AP jumps from node to node: Saltatory conduction Node of ranvier: location of many channels + pumps = local depolarization
28
Explain the process of synaptic transmission
The AP depolarises a region of Ca2+ voltage-gated channels = Ca2+ influx into cell Ca2+ activates proteins that aid fusion + docking of vesicles filled w/ NT NT is released from vesicles + enters synaptic cleft (chemical signal) NT bind to postsynaptic receptors = opens or closes the receptors = allows for flux of ions + changes membrane potential = either excitatory or inhibitory postsynaptic potential
29
Neurotransmitter criteria + deactivation mechanisms
Synthesized or present in the neuron (endogenous) When released it produces a response in the target cells Agonist will have same receptor action There must be a mechanism for removal after NT has given signal to postsynaptic side > Enzymes that breakdown NT > Neuronal transporters that bring back NT into the axonic end + vesicles for reuse > Transporters located on glial cells
30
Ionotropic receptor vs metabotropic receptor
Ionotropic receptor: ligand gated channels, fast direct effect on synaptic transmission - Assembled by 4/5 subunits that assemble in the cell - NT binds directly to channel protein = channel opens = ions flow across mem Metabotropic receptor: G-protein coupled receptor, no channel, slow, indirect effects - NT binds to G protein-coupled receptor = G-protein is activated = alpha subunit activates an enzyme = messenger cascade = effect - Often w/ second messengers - 1 subunit
31
How does an excitatory post synaptic potential arise? (fast synaptic transmission)
NT binds to ionotropic receptor Depolarization of postsynaptic membrane = open of channel = influx of positively charged ions = excitatory postsynaptic potential = increase chance of AP
32
How does an inhibitory post synaptic potential arise? (fast synaptic transmission)
NT binds to ionotropic receptor Hyperpolarization of postsynaptic membrane = open of channel for negatively charged ions = influx of Cl- = inhibitory postsynaptic potential = decrease chance of AP
33
Summation of synaptic integration
* One synapse causes 1 EPSP = depolarization of only 0.5 mV in postsynaptic membrane = 1 EPSP will never result in AP = at least 40 EPSPs to create AP Neurons have 1000 synapses on their dendrites and cell body = incoming PSPs from several synapses will add together = summation of synaptic integration = you can reach threshold at axon hillock to create an AP Spatial vs temporal summation Spatial: On one dendrite you have several localized synapses sending an AP Temporal: many different AP firings on one synapse
34
What is the mechanism of action of drugs
Drugs interfere with neuronal mechanism - They can bind to receptors by mimicking the structure of NT - Agonist: mimics NT effect - Antagonist: blocks receptor from being activated by NT Most drugs are exogenous (from outside the body) but some are endogenous (brain-produced)
35
NT and their receptor subtypes
the same NT may bind to a variety of subtypes, which trigger different responses NT action is determined by subtype receptor it binds to! NT have ionotropic and metabotropic receptors > The effect can be excitatory or inhibitory Exceptions: - dopamine, noradrenaline, and adrenaline ONLY have metabotropic receptors (w/ inhibitory or excitatory effects) (NO IONOTROPIC RECEPTORS) - GABA NT only has inhibitory receptors/effects (from both metabotropic and ionotropic receptors)
36
Acetylcholine system
Versatile NT Present in the CNS and Autonomic NS Neuromuscular junction (nerve synapses on muscle) Major NT of the parasympathetic system (rest and digest) Receptor to know: nAChR: ionotropic, non-specific cation channel (K+ and Na+) (pore that opens and closes to alter flux), present in CNS and NMJ mAChR: metabotropic, present in CNS and peripheral organs ACh opposite effects on heart (M2, inhibitory) and gut (M1, M3, excitatory) via different subtypes mAChR (some mAChR are inhibitory, some are excitatory)
37
Adrenergic system (+ medications acting on the receptors)
5 types of receptors for (nor)adrenaline, all metabotropic: * Excitatory & inhibitory * α- and β-adrenergic receptors – In CNS but also on glands and smooth muscle organs: airways, gut, bladder, heart... - NT of the sympathetic nervous system - Often noradrenaline and acetylcholine have opposite effects on the same organ Medications acting on these receptors: - Inhaler works via adrenergic receptors on the airways > Ventolin (beta receptor agonist) mimics the effects of sympathetic nervous system of noradrenaline on the airways (local effect) - Sinex (alpha-receptor agonist) only binds to receptors in the nose (local effect) - Propranolol (Beta-receptor antagonist), blocks the effect of the sympathetic nervous system in a body-wide way. Block adrenaline effect = high blood pressure, irregular heartbeat STABILIZE = removes feelings of nervousness to address stage fright
38
GABA and Glutamate system (+ medications acting on them)
GABA = most important inhibitory NT in CNS Glutamate = most important excitatory NT in CNS Alcohol and benzodiazepines (valium) act on GABA system via GABAA-R – GABAA-R: ionotropic, Cl- channels (always inhibitory) – GABAB-R: metabotropic, (always inhibitory) - Binding of benzodiazepine allows the receptor to stay open longer and allow much more influx of Cl- ions and a stronger effect of the negative charges on the inside = stronger and longer hyperpolarization of the postsynaptic site = decreases the likelihood of a next AP in that cell
39
Dopamine synthesis
Made in the body from tyrosine (the precursor) and the aid of enzymes per step Noradrenaline is made from dopamine which is made from tyrosine Tyrosine > dopamine > noradrenaline
40
Dopamine system
5 subtypes dopamine receptors: D1 > D5 * All dopamine receptors are metabotropic! * Excitatory as well as inhibitory Inactivation mechanism: Dopamine transporter > pumps dopamine back into the cells and puts it back into vesicles for reuse > localized presynaptically or they are inhibited postsynaptically via enzymes (COMT and MAO) > People have different variants of genes that encode these enzymes Excitatory receptor D1, Inhibitory receptor D2 Either causes more or less cAMP D2 auto-receptor: - On the presynaptic site - Causes a negative feedback loop: when dopamine is realized it will not only bind to postsynaptic receptors but also to the presynaptic autoreceptor - It is a metabotropic receptor which shuts down the further synthesis and release of dopamine Dopamine cell bodies are in the brain stem and then there are axonal projections throughout the brain
41
Cocaine MoA
Dopamine reuptake inhibitor: Fits into the dopamine transporter, blocking it > prevents dopamine from being taken up and brought back into the axon Result: increase in conc of naturally occurring dopamine in the synapse, binding to the postsynaptic receptors several times = very strong dopaminergic effect = increase in energy + self-esteem Lasts 45 mins Also acts as local anesthetic: Blocks the voltage gated Na+ sodium channels = prevents influx of Na+ ions = AP can no longer flow = signal no longer transferred
42
Amphetamine MoA
Dopamine reuptake inhibitor Molecule is much smaller than cocaine molecule = it can be taken up by the dopamine transporter + moves into the axonic end = changes the conformation of the transporter Change in conformation of the transporter makes it work in the opposite direction, pumping out dopamine from inside the axon and into the synapse Result: dopamine release by reversal of the dopamine transporter and thus amphetamine has a stronger effect on the conc of dopamine in the synapse Amphetamine also blocks the transporter preventing dopamine uptake = not only is there the naturally occurring conc of dopamine but also active pumping of dopamine into the synapse Lasts 4-6 hrs
43
Serotonin System
Serotonin role in mood, aggression, anxiety, appetite, sleep-wake cycle, body temperature At least 15 (!) 5-HT-receptor subtypes * Most = metabotropic * Except 5-HT3 = ionotropic * Excitatory as well as inhibitory Synthesis Tryptophan is the precursor and enzymes aid the reactions Effects Large variety due to the great amount of different types of serotonin receptors there are Characteristics Serotonin stored in vesicles Inactivation mechanisms: serotonin transporter (SERT), 5-HT autoreceptor, MAO enzyme (breaks down serotonin), SSRIs (block reuptake via 5-HT transporter) Serotonergic neuron cell bodies are localized in brainstem and project into different areas of the brain
44
LSD MoA
Has a serotonin molecule in part of its structure > Act as serotonin 2A receptor agonists
45
XTC MoA
Double mechanism of action = increased serotonin concentration in synapse * Serotonin reuptake inhibition by blocking SERT * Serotonin release (MDMA enters axon via SERT = MDMA stimulates release 5HT from vesicle in cytoplasm and there is reverse transport of 5HT by SERT into synapse) Massive serotonin release > XTC effects: * XTC in axon-terminal > possible brain damage (memory impairment) * XTC depletes serotonin > disturbed serotonin balance after use + downregulation serotonin receptors > low mood after use (‘Tuesday dip’)
46
Downregulation of receptors via drug use
during the high there is such a high conc of serotonin (or other NT) your body feels that this is a natural high and tries to compensate for it by downregulating the amount of serotonin postsynaptic receptors
47
Serotonergic drugs
SSRIs (selective serotonin reuptake inhibitors): major depressive disorder, anxiety, Obsessive-compulsive disorder (OCD) Atypical antipsychotics (risperdal) blocks Dopamine D2-R but also is a 5-HT2A antagonist
48
Cannabis MoA
THC (tetrahydrocannabinol) binds to cannabinoid receptor 1 (CB1-R) * CB1-R = metabotropic – Inhibition cAMP synthesis – Inhibition voltage gated Ca2+-channels: influence on NT release – Opening K+-channels
49
Why is there a cannabinoid receptor present in the brain?
We have an endogenous ligand (endocannabinoids) that does bind to this receptor Endocannabinoids are NT-like molecules (not classical NTs) CB1-R is localized predominantly presynaptically Endocannabinoids synthesized on demand post-synaptic by enzymatic degradation of phospholipids cell membrane * Endocannabinoids flow from post- to pre-synapse and bind to presynaptic inhibitory metabotropic CB1-R (retrograde transmission) * CB1-R activated = G-protein closes voltage-gated Ca2+-channels > inhibition neurotransmitter release * Cannabinoid system is a regulatory system
50
Opiates MoA
3 opiate-receptor subtypes * μ-, δ-, κ-opiate receptor, all inhibitory metabotropic * Morphine, heroin, codeine and other opiates are μ-opiate receptor agonists Heroin binds to mu-opiate receptor = G protein activation = outward current of K+ hyperpolarizing the area of a neuron = less likely it will transmit another AP (decreasing firing rate) * Endogenous ligands: Endorphins, enkephalines and dynorfines = neuropeptides (relatively large transmitters)
51
De-sensitization of receptors due to drug use
Repeated use of opiates: tolerance and physical dependence by adaptation of receptors De-sensitisation of mu opiate receptor: Mu-opiate receptor senses too much activity = it desensitizes itself to protect the organism from an overactivation of that receptor (homeostatic reaction) Desensitization = quitting opiates leaves you with a receptor that does not have the normal inhibitory power = leaves your neuronal circuit hyperexcitable = more activation in your system = withdrawal symptoms Acute actions and withdrawal signs are opposites of each other
52
Alcohol Tolerance & Physical dependence
Adaptation of receptors: * Down-regulation and de-sensitisation GABAA receptor > Alcohol acts on GABAa-R = influx Cl- = too much effect on GABA-R > Down-regulation (less present) + de-sensitization of GABAa-R Results: hyperexcitable neuronal circuit, electrical signals can arise a lot more quickly Especially convulsions during withdrawal can be very lethal Alcohol withdrawal: tremor, anxiety, sweating, high blood pressure, sometimes convulsions and hallucinations (delirium tremens) > Potential life threatening: detoxification under medical supervision (whereas opiate withdrawl is not lethal)
53
Which factors can contribute to traits / (mental) characteristics and brain disorders
Genes and environmental factors (e.g stess, diet, family situation etc)
54
Hard reductionism in the nature-nurture discussion
‘all psychiatric illness is best explained solely in terms of molecular neuroscience’ This is not a good approach > Etiological models for psychiatric disease need to be pluralistic or multilevel > view brain as in constant interaction with environment, society and culture via plasticity
55
How can environmental factors exert their influence (general mechanisms)
Altered gene expression via – Stress system – Epigenetics
56
heritability of disorders
Twin studies v insightful (concordance rates indicate heritability) Heritability = proportion of variance in symptoms that is explained by the variance in genetic factors Heritability does not explain risk * Major depression 40-50% * ADHD: 75% * Autism, bipolar disorder, schizophrenia around 80%
57
Model of single / few risk genes
Single abnormal gene > abnormal gene product > neuronal malfunction > ‘mental illness’ - Single abnormal gene is not sufficient to cause mental conditions - overly simplistic paradigm
58
New models and hypothesis for linking genotype to phenotype (endophenotype approach)
1. ‘Complex Genetics’ or ‘Diathesis-Stress Model’ 2. ‘Differential Susceptibly to Environment Hypothesis’ 3. ‘Balancing Selection Hypothesis’
59
Stress – diathesis model
Predisposition (genetic) + environmental stress > disease Hypothesis: mental conditions are caused by multiple small contributions from several genes, all interacting with environmental stressors ('complex genetics) Complex set of risk factors that bias person toward condition/illness but do not cause it (inherits risk not disease) Reaching tipping point: high probability developing condition/disorder Concept also applies to obesity etc
59
Endophenotype approach
Idea that there are important intermediaries between gene (genotype) and disease/behavior (phenotype) Endophenotypes: - Measurable, inheritable and closely linked to disease/condition - More precisely measurable than disease/condition Two types: – Biological endophenotypes (measurable bio phenomena) e.g Electrophysiological response to startle, Neuroimaging response to information processing, Activation of certain brain circuit – Symptom/system endophenotypes (single symptoms associated with mental disease/condition) e.g insomnia, executive dysfunction, hallucinations, poor fear conditioning etc
60
New paradigm on psychopathology and brain circuits
New paradigm: psychiatric symptoms are increasingly linked to malfunctioning specific brain circuits * Genes + environmental risk factors conspire to produce inefficient information processing in neuronal circuitry * Brain imaging helps us focus on brain circuit
60
Pathway linking genes and psychiatry
Gene > molecules > circuits > information processing (biological phenotype) > single symptom (system endophenotype) > full syndrome of mental condition/disorder Closer to gene on pathway > more readily linked to gene: Link gene to endophenotype easier than to condition/disease Genes only loosely linked to psychiatric conditions/disorders, therefore hard to identify
61
Why are subtle molecular abnormalities not more ‘penetrant’ at behavioral level?
Multiple genes complementary / redundant effects ‘healthy compensatory backup system’ Risk genes are not necessary / sufficient to cause mental conditions / disorders > requires combination with environmental risk factors (stress, life events, biological stressors such as viruses, toxins...)
62
Social-ecological framework
Dynamic interplay of multiple risk and protective factors * Risk and protective factors: occurring along ‘social ecology continuum’ – individual – relationship – cultural/environmental factors ^ different spheres/levels
63
Environmental factors from social-ecological framework Pre/peri natal risk factors
Pre/peri natal risk factors *Maternal stress during pregnancy * Maternal nutritional deficiency * Maternal use of tobacco / alcohol / drugs / medication * Birth complications * Perinatal nutritional deficiency * Maternal seperation * Abuse: sexual, physical or emotional * Neglect * Poor parental care * Attachment * Infections * Toxins * Brain trauma * Drug use * Stressful life events More social factors *Low SES * Poverty * Community violence * (Mental) health care & health care policy – Access to care – Stigmatization of mental health problems * Minority group position * Cultural factors * Religious factors
64
Stress system
HPA axis: hypothalamus, pituitary, adrenal Fast-acting pathway Hypothalamus sends neural message through the spinal cord > sympathetic division of the ANS is activated to stimulate the medulla of the adrenal gland > adrenal gland releases epinephrine > epinephrine activates bodys cells Slow-acting pathway hypothalamus releases CRF (corticotrophin) releasing factor) into pituitary gland > releases ACTH onto the cortex of the adrenal gland > adrenal gland releases cortisol > activates body cells Hypothalamus activates pituitary gland which activates adrenal cortex > inhibitory feedback loop of glucocorticoids (CRF) back towards the pituitary and hypothalamus and hippocampus Ability of body to tune down the stress response depends on expression of receptors (GRs)
65
HPA axis overview
* Stress > hormone cortisol * Cortisol important in defence response: protective + promote adaptation * Cortisol binds to glucocorticoid receptor (GR) in body * GR acts as transcription factor and can alter gene expression * GR also in several brain areas * GR in hypothalamus, pituitary gland and hippocampus: negative feedback loop > shut down CRF release Sustained high levels of cortisol > harmful > hypertension, immunosuppression, cardiovascular disease, structural effects hippocampus + amygdala, increased chance psychopathology ... Early life stress can lead to life long overactive HPA-axis (eg. Less GR = less negative feedback to shut system down)
66
What part of genetics is epigenetics affecting
* Life experiences change person’s mind * Chemically coating the DNA is altered which affects accessibility of genetic code > Ease or block access to genes on DNA > Coating alters gene expression, but NOT genetic code Results in epigenetic changes
67
How is DNA modified in epigenetics
methylation: addition of a methyl group to the cytosine, causes a molecular stick which physically prevents transcription factor from binding to that section/gene or acetylation
67
Rat epigenetics paper hypothesis
Good maternal care (licking + grooming), results in rats with a normal functioning stress system (there is normal binding of the transcription factor to the promoter of a gene for the brain cortisol receptor = high expression of this receptor = sufficient amount of these receptors in the stress system). Whereas: Low quality maternal care = methylation of the promoter = preventing transcription factor binding to the promoter = inhibiting transcription of the gene = lower amounts of brain cortisol receptor protein = negative feedback loop cannot occur as efficiently = hyperactive stress system w/ high levels of cortisol + anxiety in the pups Are differences in methylation on the promoter area due to to maternal behavior
68
Healthy brain stress system
Healthy brain system is a brain with lots of brain cortisol receptors so it can shut itself down when necessary (otherwise a hyperactive stress system which = disorders) The system can shut itself down e.g when we have prolonged cortisol release - Uses a negative feedback loop: cortisol shuts down its own production by binding to cortisol receptors in the brain Glucocorticoids (cortisol) binds to brain cortisol receptors (present in pituitary gland, hypothalamus, and hippocampus) Binding = shut down of production of precursors e.g CRH, ACTH
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Emotional development depends on:
* Cognitive development * Nature & nurture * Emotion: understanding & regulation (coping styles) * Social referencing * Theory of mind * Attachment & stranger situation
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Piaget: characteristics of stages of development
Stages of development are invariant and universal, i.e there are universal specific stages of development Learning is a spontaneous and child-oriented process i.e the child needs to be ready to learn otherwise it will not work
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Piaget’s stages of cognitive development
Sensorimotor: Birth – 2 years (touch, smell) Preoperational: 2–7 years (motor skills) Concrete Operational: 7–11 years (logic) Formal Operational: >11 years (abstract reasoning)
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Sensorimotor stage
Schema’s are built by sensory & motor exploration and experience 8-12 months: Object permanence > Understanding the object is there even if it is visually blocked by something > At first 'A not B' mistake is made but then not anymore: child looks for the object where they last found it not where they last saw it being hidden > depending of type of test this might be mastered earlier 1-2 years includes: Delayed imitation > Delayed imitation: someone does something and child repeats it = ‘pretend play’ > ‘Rational imitation’: not only things they see but also actions that are done specifically by the adult e.g lip smacking (not only facial expression) > imitates meant but unfinished gestures Categorization (simple) > starts in sensorimotor but is incomplete, ready in preoperational > Perceptual categorization (sensorimotor): Based on similarity in total appearance or very prominent part thereof e.g 2 year old: Stack rings on a peg from largest to smallest; name objects in picture book
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Categorization abilities in the preoperational stage
Conceptual categorization > Based on common function or behavior > Later: categories of events added to this
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Preoperational stage
Language Drawings > from scribbling to first forms that look like something Pretend play: increase in complexity > Less based on concrete (real-life) situations > Less self-oriented > More complex: Sociodrama > Functions: - Exercise for schema’s (representation) = increase in cognition - Understanding and integration of emotions - Social & language skills: how to formulate an emotion - Attention, memory, logic reasoning - Imagination, creativity Dual representation > symbolic items can be viewed as symbol and as item (e.g. a picture of a tomato cannot be eaten, of a shoe cannot be put on) > Experiment of Judy DeLoache: hide a miniature toy in a room just like the real room you are in. Ask children to retrieve the real toy from the real room (3 years = ok, 2.5 years not) > Maturation of cortex > Difference between 3D vs 2D version of task (younger, 2D is easier) No complete logic
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limitations of pre-operational thinking according to PIaget
Unable to process thought mentally (reasoning, deduction) Egocentrism & animistic thinking Unable to perform conservation task Hierarchical classification is lacking
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Egocentrism
Egocentrism: Unable to discriminate between your own and someone else’s POV - Piaget: children are born to focus attention on themselves - e.g moutain between child and doll, can doll see what child can see - only reason from their own perspective
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Animistic thinking
lifeless / inanimate objects possess life and are capable of doing all types of things they can do > They grow out of it earlier than Pidaget thought
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Age-dependent limitations at conservation tasks
e.g pouring water from one glass to another > Younger child focuses on one task: because liquid is taller (ignores that liquid came from other glass) or that coins are farther away (ignores that coins were simply moved apart) > Older child focuses on several tasks: deductive reasoning (where the liquid came from) and change in shape of glass Perception-bound > Drawn by changes in the appearance Centered thinking > Focus on one aspect, neglecting others No transformation > Focused on the ‘now’ state and not on the transformation Irreversible > Unable to reverse-transform; i.e. returning the material to its original state. >> Reversibility is a crucial aspect of the logical (operational) thought of later stages Preoperational children are capable of simplified conservation tasks in a gradual manner * Order: numbers, length, width, content, surface) * Ask them to re-count, and answer again Reason according to analogy; not always able to give the complete reasoning
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Evaluation of Piaget preoperational stage
Right in: Toddler start logic thinking already Not entirely right in: Logic thinking develops more smooth that Piaget thought
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What skills are present in preoperational thinking stage
Able to adjust their language and their perspective to that of others in easy situations Capable of simplified conservation tasks in a gradual manner Everyday knowledge is categorized Able to solve tasks (real vs not real) without words
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Concrete operational stage skills
Conservation > Decentered thinking > Transform & Reverse Classification (& inclusion problem) Seriation (order) > Transitive inference Spatial visualization ability / spatial reasoning (jig-saw) > Direction > Map (Deductive) Reasoning Less egocentric
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Classification and inclusion problem
They can count (e.g dogs or cats, gentians or daffodils) but to see that these are all part of animals/flowers is the challenge
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Seriation and transitive inference
Transitive inference: e.g height: emma > dounia > anna therefore emma > anna
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Deductive reasoning
Logical problem: if you throw a feather into a glass, the glass will break. What happens when John throws a feather into the glass? According to reasoning you would say yes despite it not fitting real life A younger child cannot comprehend this, if it does not happen in real life it cannot be true, they cannot go with abstract reasoning proposed by the problem Children BEFORE the concrete operational stage focus on realife issues, not the abstract thinking
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Formal operational stage
Hypothetico-deductive reasoning (abstraction) > To deduce a hypothesis from a general theory, bring it to the test, and adjust it based on outcome Propositional thinking > Solve a logic problem mentally; solve a problem you have no real life experiences with (math) Relativistic thinking > Critically reflecting on multiple perspectives and determine the most suitable answer in a particular situation (cultural dependent) Formal operations are not correctly performed by all adolescents (and neither by all adults!) > Exercise helps, just as being in the right context (parents/peers can stimulate this) > Tendency to fall back to non-formal-operational when it is too difficult
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Piaget & current principles of didactics
Learning while discovering - Sensitivity in willingness of children to learn > Individual (Nature) > Age (nature) > Exercise to stimulate this (nurture) - Acknowledge individual differences
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Evaluation of piagets sensorimotor stage
Right concerning: timing of searching objects, A not B, and pretend play Not very correct in: timing of object permanence, categorization, problem solving via analogy (all begin earlier than piaget thought)
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What are emotions?
Physiological reactions - Change in rate of breathing, heart, blood pressure Feelings & cognitive processes - Subjective experience Behavioral reaction - Laughing, grinning, crying
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functions of emotions
Effect on Cognition: helps with learning (essential for survival, decision making) Social behavior: Influences behavior of others and regulation of your own emotions Health: influence wellbeing and growth and pressure of mood e.g stress related to disease
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Basal emotions in babies
Joy > Develops from a social smile into a specific smile (e.g for parents but not strangers) Anger Sadness Fear > e.g height
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Emotional competence
Capacity of an individual to recognize/monitor their own emotions and those of others, to discriminate between different emotions and label them appropriately, and to use emotional information to guide thinking and behaviour Requires: * Self-consciousness * Feel what someone else feels or use social referencing * Manage emotions (angry?, count to 10) * Social skills / Theory of mind * Emotion regulation
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Social referencing in emotion
The individual’s ability to decide how to respond to ambiguous situations, through the observation and recognition of the reaction and facial expression of others > Parents teach their children how to react > Child’s recognition of parent’s emotional intention begins ~12-14months on
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Self-reflective emotions
18-24 months * Shame * Proudness 2-3 year * Shyness * Guilt * Jealousy > Start at mid 2nd year > Parents start engaging their children to think and understand how they feel when they feel
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Cognitive development & emotional competence
While growing up, children become better at judging emotions, and their source, because... > Balance between external (environment) and internal (brain development) factors > Recognize that thinking and feeling are connected > Conflicting cues are taken into account (i.e pretending) > Understand mixed emotions (more than 1 emotion at the same time; happy & sad)
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Social experience & understanding (the roles people play in understanding emotions)
Care takers: * Teach children about emotions * Support emotional thoughts Friends: * Negotiation * Use emotions in play (pretend play)
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Theory of mind: what is it + how to test it
Possibility to ‘feel’ or ‘think’ someone else’s feelings/thoughts, or to recognize them and think & act upon this Recognize that others might have feelings or thoughts that are deviating from yours How to test this: Sally-anne test (links to egocentrism, if they cannot complete test successfully) > sally leaves marble, you move it, when sally comes back where will she look for it > can be tested in animals via empathy regarding pain sensation and mimicking of behavior
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Factors contributing to theory of mind
Language is needed to reason Cog ability Attachment Mind-focused parents who can explain these kinds of emotions Pretend play to test your cog and social skills Social exposure: not only being home and seeing only a specific set of individuals
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Emotional competence & regulation
Emotional competence * Self-consciousness (awareness) * Emotions of others * Emotion process Emotional regulation: The extrinsic and intrinsic processes responsible for monitoring, evaluating, and modifying emotional reactions, especially their intensive and temporal features, to accomplish one’s goals. > Dependent on social rules (what is and what is not allowed at a certain age) > Cultural dependent (boy/girl) > Cognitive strategies (coping mechanisms – e.g. counting to 10) > Individual differences
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Development of emotion regulation: ages
Baby 0-2: develops from 1st year, parents play important role in guiding Toddler 2-4: coping strategies are learned, personality influences capacity to do so, fears (shame and guilt) are normal School period + adolescence (4-14): fast increase in emotion regulation, env is important, individual coping skills lead to self regulation
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Emotional Coping strategies
Problem-focused coping: when you are able to see the situation is changeable > requires PFC to evaluate this and take a decision to plan the strategy type and solution Emotion-focused coping: situation is percieved as unchangeable > problem-focused coping does not work > elicits emotional response > more common in younger person as PFC is not fully developed so necessary cog processes to percieve situation as changeable are not fully developed
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Theory of development of attachment
Relation between 2 persons Balance in being close by (responsiveness to child) vs. exploration > Secure base (from which to explore) > Safe haven (to return to): otherwise child is less likely to explore or be guarded off Mental representation of relationship caretaker/parent > Relative stability over time, is adapted by experience > Different stages of attachment Trust and confidence (others and self) Dependent on culture and person/temperament
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Ethological theory of attachment
1. Pre-attachment (0-2 months) 2. Attachment-in-the-making (2-8 months) * Family vs. non-family * Preference for parent/care-taker 3. Clear-cut attachment (9-18 months) * Making contact * Separation fear (from 8 months) 4. Mutual relationship (from 2 year; goal-corrected partnership) * More and more dependent on child (language to show affection) > Dependent on culture and person/temperament
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How to evaluate ones attachment style
Measuring reaction of child on disappearance of parent and exposure to stranger Style is predictive for skills of child, but also for problems of the parents, e.g. maternal depression
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Attachment types
Safe attachment (60% > child cries when parent leaves and is fine when parent returns > correlates with +ve outcome during school age Unsafe attachment (type of contact after return of parent): 3 subtypes 1) Avoiding (no contact with parent) (15-20%) > Not associated with situations like given below 2) Resistant/Ambivalent (lots of stress, +/- contact) (~10%) > Not associated with situations like given below 3) Disorganized / disorientated / fearful-avoidant (repetitive behavior, immobility) (10-15%) > Often found in child abuse or maternal depression > ~80% abused children vs. ~20% non-abused children
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Factors influencing attachment
Possibility to attach > Note: working ≠ no attachment! Quality of care > Sensitive care = Responsive to children’s need Family situation > Attachment is relatively stable > Multiple attachment; all care takers Individual differences
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Attachment and anxiety
Golden Lion Tamarins In frightening situation children go to those who : * Food transfers * Carried child * Oftentimes not the mother but care taker
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Sex chromosomes and aberrant sex
XX - normal female X - female phenotype –50% fertile (Turner’s), also mosaic XXX - female phenotype – mild growth retardation / reduced intelligence ; can oftentimes go unnoticed XY - normal male XXY - Klinefelter’s – male phenotype, bit taller, youthfull appearance, gynecomastia ; reduced fertility (1 in 500 boys) XXXXY- severe Klinefelter’s syndrome, infertile XYY - bit taller, bit more tomboyish (1 in 1000 boys) Y - monosomy Y - embryonic lethal
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Genetics and sexual differentiation: the 2 stages
1) Genotypic sex: determined during fertilization (father determines sex of child) 2) “Environmental” sex: determined by gonads (Gamete producing cells, testis or ovaries), or phenotypically (internal genitalia (ducts) and external genitalia) E.g temperature affects sex of turtle
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Sex and gender: definitions
Sex * Genetic sex: chromosomes * Gonadal sex: gonads * Genitals: internal and external Gender * social meaning attached to being male or female * Sexual/gender identity - one’s identity as male or female * Develops in utero throughout childhood
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Intersex
mixed biological sex characteristics in humans Incongruent sex characteristics that include: * Chromosomes * Gonads * Ducts * Genitals * Sex hormones * Brain
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Intersex phenotypes
Medical model: conform as soon as possible with that is the sexual gender (most physicians recommend they be reared as women) > but many do not end up feeling comfortable this way > indicating hormones are involved in determining gender identity by changing the brain Social model: leave child to determine
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Gonadal sex determination
System starts bisexual: gonads are undifferentiated > then develop into either testis or ovaries > depends on whether wolfian (male) or mullerian (female) duct survives
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Male fetal development
1. Genetic factors initiate process that directs the indifferent gonads toward testis development 2. Activation of Sertoli cells (sustentacular cells) to produce Mullerian inhibiting hormone (MIH), causing Mullerian duct degeneration 3. Stimulation of Leydig cells (interstitial cells) to secrete testosterone, which then directs development of the Wolffian ducts towards epidydimes, vas deferens and seminal vesicles -Testosterone conversion to dihydrotestosterone (DHT) - Directs development of the urethra, prostate gland and penis
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Spermatogenesis
Seminiferous tubules role: spermatozoa production, via rete testis to ependymis Contain spermatogonia > Stem cells involved in spermatogenesis > Production of spermatozoa Contain sustentacular cells > Sustain and promote development of sperm
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Sex chromosomes determining gonadal sex: Male
Y-chromosome: * Shortest chromosome * Internal repeats to allow self-recombination * Produces Testis Determination Factor (TDF) * SRY (TDF) is a transcription factor that via a molecular cascade activates Sertoli and Leydig cells * Acts together with an autosomal gene SOX9 Sox9 binds to promotor of MIH (or AMH, anti-mullerian hormone) and regulates its expression SRY/SOX9 induce FGF9: chemotactic factor for primordial germ cells to penetrate gonadal ridge (without this no testis can be formed) Induction of steroidogenesis factor 1 (SF1): stimulates differentiation of Sertoli & Leydig cells SF1 stimulates Leydig cells to make enzymes for testosterone production Default may seem the develop as a female. Male hormones are indeed needed to promote differentiation into a male, no SRY = female appearance on the outside
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Virilization
I.e making the structures male Testosterone > internal male structures DHT > external male structures
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XX chromosome into gonadal differentiation
Y chromosome ( SRY region; Testis Differentiation Factor gene) is not present - no TDF to tell it to form testis Gonadal tissue under influence of X-chromosome factors develops towards ovary formation - In the absence of testosterone – Wolffian duct system degenerates - In absence of MIH – Mullerian ducts continue to develop towards fallopian tubes, uterus, and upper vagina - External genitals become feminine
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Normal Prenatal Development: Genitalia
Testosterone (via DHT) causes unisex genitalia to develop into penis and scrotum Absence of testosterone (together with female- specific factors) causes unisex genitalia to further develop into clitoris, labia, vaginal opening
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X-chromosome inactivation in females
Out of the 2, in every cell 1 X-chromosome is inactivated > Reason for decreased likeliness of X-chr related diseases in females Inactivated X: yet complete penetrance of disease-phenotype > Complete: Male of 14 years old, who had hypospadias at birth, currently breast development (gynecomastia) * Test blood cells on SRY translocation and found positive: X/XSRY (unusual, SRY normally on Y) * But 50% would have X-chromosome inactivation, so why not incomplete penetrance * This translocation is on parts that escape X chromosome inactivation (namely, Pseudo Autosomal telomeric Region 1 (PAR1)) If the SRY translocation occurs in PAR1, it remains active in all cells, bypassing X-inactivation and leading to a fully expressed phenotype. This explains complete penetrance (full disease presentation), rather than an incomplete or mosaic effect.
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Swyer syndrome
SRY mutation/lack in XY 'female' No TDF = no testis No ovaries: undifferentiated gonads (oogenesis needs other autosomal and X-chromosome factors) Wolfian duct fails to develop (no testosterone) Internal and external genitals appear female; infertile, but able to carry a child to term by embryo transfer Defect arose during spermatogenesis Hormones (estrogens) are necessary to induce breast formation and menstruation (no eggs!!!)
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Persistent Mullerian Duct Syndrome (PMDS)
deficiency of Anti-Mullerian hormone Gonads are male (SRY is present) Testosterone present = Wolfian duct remains; yet Wolfian duct and hence vas deferens might be hampered in normal development (then: infertility) Mullerian ducts persists, and rudimentary uterus may be present; cryptorchidism (so MIH may play a role in descendance of testis!)
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5-alpha-reductase gene mutation (abnormal sexual phenotype)
decreased DHT converting enzyme External structures lack due to lack of 5alpha-reductase; development (initially) as female-like, internal structures are male! > brain is masculinized > at puberty, genetically driven male phenotype emerges from an apparent female phenotype (testis descending) > fertile (mostly)
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Effects of testosterone and DHT on phenotype
Testosterone in blood is converted to DHT in target organ Testosterone effects organs e.g hair, muscle, brain, testes, prostate DHT affects behavior and reproduction e.g aggression, libido, spermatogenesis etc In utero, DHT is responsible for normal differentiation of the male external genitals
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Androgen insensitivity
Genetic males (XY) with a female phenotype Gonadal sex = correct –> gonads differentiate to testis Produce MIH – females duct system has degenerated Produce testosterone and DHT, but .... > No receptor to ‘see’ these hormone > Cannot respond to the androgen surge at puberty (unlike 5-a reductase deficiency) because testosterone and DHT use the very same receptor > Puberty: breast development, but no menstruation normal external female appearance * feminized external genitalia, short, blind-ending vagina * absence of internal female genitalia - no fallopian tubes, uterus, or cervix (because there is MIH due to presence Sertoli cells in testes) * absence of male internal genitals: Wolfian duct has degenerated * Gonads: male, but un-descended testes (may require surgery) * at puberty, normal female development (e.g., breasts) * female gender identity, heterosexual orientation * Despite high levels of estradiol, this did not masculinize the brain (subjects feel female, in contrast to many other forms of hermaphroditism)
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Partial to complete Androgen Insensitivity (AIS)
partial androgen insensitivity there is partial virilization of the genitals * Dependent on the type of mutation (=severity) in dysfunction of the androgen receptor * PAIS might characterize itself by elevated testosterone levels
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Prenatal hormonal contribution to being intersex
e.g high testosterone exposure during pregnancy Sheep + cow study Twins with 1 genetic male and 1 genetic female lamb leads to latter being a freemartin * ‘Genetic’ female carries XX/XY blood cells * Anti-Müllerian hormone expressed (infertile) Prenatal hormones are important for gender identification + sexual preference
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Congenital Adrenal Hyperplasia (CAH)
Genetic defect leading to excessive production of androgens (too little glucocorticoids) Mutations in enzymes for glucocorticoid production, such as (CYP21A2) High concentrations of 17-hydroxypro-gesterone (~100x higher than normal) Higher levels ACTH (adrenal-pituitary feedback) Individuals are 46XX (genetically female) > excessive androgen production causes virilization of external genitals (in fetus of female gonadal sex) Environmental cause: girls exposed to excessive androgens prenatally (prenatal exposure to synthetic steroids can produce similar condition to CAH) Dependent on severity, phenotypic males could continue living like a male (-> sterile), or in lighter cases could revert to the female genitals (-> fertile) CAH females have a larger non-exclusive heterosexual orientation than average * Not the case for CAH males Masculinization of the brain > more tomboyish, aggressive etc
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Gender, sexual preference & brain
While androgens seem to play an important role in male gender development (brain), females seem relatively protected to high androgen levels in terms of gender identity, but not in sexual orientation * CAH females: more non-heterosexual orientation, yet little trans-gender identification * CAIS XY: brain activity similar to XX females (e.g. during spatial rotation task), gender & sexual preference similar to general population (XX females) * PAIS XY: mostly content with initial gender assignment (more assigned males revert to female identity), sexual preference less studied * Male sexual orientation depends on fraternal birth order
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Fraternal birth order and sexual orientation
Increase in % homosexual son with multiple older brothers > Independent of being raised by biological parents, # older sisters or younger brothers, culture > Associated with right-handedness & extends to asexuality 2018: Mothers develop antibodies against Y-linked proteins involved in brain development with every consecutive male pregnancy > NLGN4Y: post-synaptic adhesion receptor > Antibodies would block interaction
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Heritability of sexual orientation
Predominant non-heterosexual orientation in males: ~2-3% (females more fluid) Monozygotic twins have higher incidence of concordance in non-heterosexual orientation (65%) than dizygotic twins (30%) Sex-specific regulation in sexual orientation: For male- / female-bodied people: * Genes: 40% vs. 20% * Unique uterine environment: 60% vs. 65% * Familial / social factors: 0% vs 15%
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What is antisocial behavior and what disorders stem from it
Antisocial behavior = behavior that lacks consideration for others and that may cause damage to society * Antisocial Personality Disorder (ASPD) * Psychopathy = subset of ASPD * Conduct Disorder (CD) (childhood antisocial disorder)
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ASPD characteristics
* Apparent lack of remorse * Persistent lying or stealing * Cruelty to animals * Recurring difficulties with the law * Promiscuity / Poor or abusive relationships * Aggressive, often violent behavior; prone to getting involved in fights * Inability to tolerate boredom * Lack access to own feelings and emotions * Not good at detecting emotions (especially fear) in others * Reduced empathy * Severe disruption in moral behavior
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Psychopathy characteristics vs ASPD
Psychopathy: Callousness, manipulativeness, glibness and superficial charm Often (highly) intelligent Grandiose sense of self-worth Psychopaths fake normal emotions: appearance of normalcy ‘mask of sanity’ + seemingly charming Often: seems to function normally in society ASPD only: * More pronounced poor behavioral controls = inadequate control of anger and temper * Often: more rude, aggressive, abusive and angry behavior
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Brain structures and activity in ASPD
Volume of brain matter in PFC is substantially lower is ASPD group ANS: heart rate when doing stress test is lower in those with ASPD
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Neural foundations of moral reasoning in ASPD
impaired only in antisocial groups (anterior cingulate, hippocampus, temporal lobe) activated only in moral decision-making (posterior cingulate) and regions common to both antisocial behavior and moral decision- making (PFC, AMYGDALA, angular gyrus). ASPD: disruption in neural circuitry underlying moral thinking and feeling
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Which brain structures are related to rule-breaking behavior
Impairments in some of structures (PFC, amygdala and angular gyrus) for moral cognition and emotion
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Amygdala and ASPD
sig reductions in amygdala vol and activity (leading to rule-breaking behavior and failure of moral reasoning) Subjects with higher psychopathy scores showed reduced acitvity in amydgala during moral decision making Amygdala disfunctioning = core deficit in ASPD / psychopathy Amygdala plays a role in fear + recognising fear in others > reduced amygdala response to fearful photos
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Fearlessness in ASPD
* Not good at detecting emotions, especially fear, in others’ voices * Trouble identifying fearful facial expressions * Poor fear conditioning * Unusually high disgust thresholds, tolerating repellent smells and images (due to reduced insula functioning) * Reduced empathy
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difference between ability and propensity for emphaty
Propensity: do people show a natural inclination to show a certain behavior Psychopathic offenders were scanned while viewing video’s of people experiencing pain They were first told to watch the movies carefully (‘just watch the movies’) Next, to deliberately feel what the individuals in the movies felt (‘try to feel with the victim’) Results: Psychopaths showed reduced empathy under instructions simply to observe, but these differences largely disappeared under instructions to empathize! (suggesting ability not propensity) Any person with an ability but reduced propensity for empathy could choose to use his ability for seduction but not for rape because empathy would facilitate the former but hinder the latter But also ‘normal’ people can turn the dial of empathy up and down!
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TWO lines of evidence for neurodevelopmental basis of antisocial behavior
1. Fear conditioning research 2. Cavum septum pellucidum (CSP) marker of limbic maldevelopment but no biological determinism! > crime is caused by complex interactions between multiple bio + env factors
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What is fear conditioning and what role does it play
basic form of learning mediated by amygdala > fear is associated with previously neutral stimulus Fear conditioning is mechanism by which we link antisocial acts with negative consequences (punishment, social exclusion) Failure fear conditioning = failure social learning > predispose to antisocial behavior If poor fear conditioning causal role in crime > detectable early in life before antisocial behavior becomes manifest
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Testing fear conditioning in young children
unconditioned stimulus (loud noise), preceded by conditioned stimulus (neutral noise) If trained: electrodermal response should show a peak when conditioned stimulus is presented Compare to these participants showing criminal record later on in life > Healthy participants showing successful fear learning: no criminal record > Criminal offenders: significantly reduced electrodermal fear conditioning at age 3 compared to matched comparison subjects Poor fear conditioning at age 3 predisposes to crime at age 23 Poor fear conditioning early in life implicates amygdala dysfunction and a lack of fear of socializing punishments in children who grow up to become criminals Findings consistent with neurodevelopmental basis
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What is the Cavum septum pellucidum (CSP)
Septum pellucidum = thin membrane separating lateral ventricles; fusion by two leaflets Cavum septum pellucidum = fluid filled cavum inside two leaflets of septum pellucidum > marker for fetal limbic maldevelopment > causes: many e.g prenatal alcohol use
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CSP and ASPD
CSP brain defect = higher probability of ASPD CSP > higher ASPD score > higher psychopathy score > greater number of charges and convictions compared to those without CSP (controls) Conclusion: Early brain maldeveloment of limbic structures predisposes to antisocial behaviors
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Factors affecting brain development during prenatal and early postnatal periods: ASPD
* Stress during pregnancy * Birth complications * Prenatal alcohol or nicotine use * Prenatal malnutrition * Early postnatal malnutrition * Failure to bond to caregivers * Childhood maltreatment * Traumatic head injury * Parental neglect / Inconsistent parenting * Parental criminality * Poverty * Malnutrition
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Heritability of ASPD
Twin studies estimate heritability antisocial behavior: 40-50% > i.e 40-50% of the variance in ASPD-symptoms can be explained by variance in genes Life circumstances are just as important as biological inheritance Male sex is risk factor (testosterone levels) Risk variant genes: low activity MAO-A
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Childhood maltreatment and ASPD
Childhood maltreatment is a universal risk factor for antisocial behavior > But: Large differences between children in their response to maltreatment > Maybe MAO-A gene variant can explain differential response
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MAO-A and maltreatment
MAO-A (enzyme that breaks down serotonin, dopamine and noradrenaline): two Variable Number Tandem Repeat (VNTR) polymorphisms, low and high activity gene-variants Relation between these 2 variants of MAO-A, maltreatment and anti-social behavior > Severe maltreatment condition + low MAOA: high anti-social behavior Gene-env interaction ONLY when childhood maltreatment is present: * Low MAOA activity-gene variant (creating low-activity MAOA-enzyme) risk gene-variant * High activity MAOA-gene variant (creating high-activity MAOA- enzyme) is protective gene variant In ABSENCE of childhood maltreatment (almost?) NO difference between gene-variants
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Neurodevelopmental hypothesis of antisocial behavior
Risk genes, prenatal risk factors, risk factors / protective factors = anti-social behavior
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Evolution and psychopathic tendencies
Every sub-characteristic exists in continum/spectrum: * Remorseless * Charming * Concentration * Callousness (emotionally hardened) * Daring (onbevreesd) * Risk taking * Influencial / Manipulative behavior * Propensity for empathy Little amounts of these can prove advantageous e.g soldiers, lawyers Sample of 203 corporate professions participating in management development programs * Prevalence of psychopathic traits was higher than that found in community samples * Psychopathy was positively associated with in-house ratings of charisma/presentation style (creativity, good strategic thinking and communication skills) * but negatively associated with ratings of responsibility/performance (being a team player, management skills, and overall accomplishments)
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Central Nervous system
brain, spinal cord
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Somatic nervous system
Cranial nerves, spinal nerves > nerves to and from: sensory organs, muscles, joints, skin > produces movement > transmits incoming sensory info to CNS
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Autonomic nervous system
sympathetic division and parasympathetic division > balances bodys internal organs > parasympathetic: rest and digest, acetylcholine > sympathetic: fight or flight, noradrenaline
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Origin and development of the CNS
Brain originates from a tube > three-part structure: encephalon Forebrain = prosencephalon > becomes telencephalon and diencephalon Midbrain = mesencephalon Hindbrain = rhombencephalon > becomes metencephalon and myelencephalon
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Thalamus, hypothalamus and cerebellum levels of function
Thalamus: relay center, preprocessing sensory information Hypothalamus: feeding, sexual behavior, temperature Cerebellum: fine motor control, balance
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Telencephalon
Two cerebral hemispheres * Two lateral ventricles * Cerebral Cortex: thin layer of wrinkled tissue with clefts and ridges > function: create and respond to perceptions of the world * Basal Ganglia: collection of nuclei that play role in control + coordination of movement * Limbic system: play role in emotion, memory, motivation and reward
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Cerebral cortex divisions
- Frontal lobe – Parietal lobe – Occipital lobe – Temporal lobe – [Insula] – [Cingulate cortex]
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Localization of function
different regions have different functions - the cortex is a projection map of this - frontal lobe: motor function > primary motor cortex (precentral gyrus) PFC: planning, reasoning, and impulse control - parietal lobe: body senses > primary somatosensory cortex (postcentral gyrus) - temporal lobes: auditory functions > primary auditory cortex - occipital lobes: visual functions > primary visual cortex - insula: interoception (awareness of internal bodily sensations), emotions - cingulate cortex: emotions and social behaviours
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Basal ganglia
Collection of nuclei below cortex – Caudate nucleus (curved tail part) – Putamen (disc laying on top i.e outer layer) – Globus pallidus (egg area that you can see through, inner layer) Role in control and coordination of movement patterns
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Limbic system
Amygdala (almond); role in emotion and fear Hippocampus (sea horse): role in memory Cingulate cortex (limbic cortex) emotion regulation * Fornix (connection hippocampus) * Parts of thalamus and hypothalamus * Mammilary bodies (memorypart of hypothalamus)
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Diencephalon
Thalamus: relay center (all info recieved by the cortex is first relayed through the thalamus), acts as a 'sensory filter' to prevent sensory overload (projection map also on thalamus) Hypothalamus: role in appetite, eating, drinking, sexual behavior, body temp, sleeping, integrates NS and endocrine system via control of pituitary gland - Every person has 2 thalami and 2 hypothalami (but 1 pituitary gland) - Surrounds third ventricle
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Distinguishing basal ganglia and diencephalon in a brain slice
You need to know where the vertical section is made more anterior: only touching the basal ganglia and lateral ventricles > no sign of third ventricle not of diencephalon more posterior: will be touching the basal ganglia, lateral ventricles, third ventricle, diencephalon, limbic structures > diencephalon surrounds the 3rd ventrical > thalamus is more dorsal (up) > hypothalamus is more ventral (down) > near end of hypothalamus there are the mammilary bodies
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Brain stem
Begind where spinal cord enters skull Consists of Midbrain: tectum (superior colliculi (visual) + inferior colliculi (auditory) and cerebral aquaduct) and tegmentum (substantia nigra) Pons Medulla
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Hindbrain
Cerebellum: - Coordinating and learning skilled movements (bicycling, playing musical) – Not initiate movement – Balance – Maintaining movement accuracy – ‘little brain Pons (bridge) * connection to cerebellum Medulla * Basic life support (breathing, heartbeat) * Centers for vomiting, sneezing, swallowing and coughing * Vegetative centers which sustain live, even if person is unconscious
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