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1
Q

describe and give examples of the 3 different types of symptoms of schizophrenia

A

negative (come first):
- absence of normal behaviours
- reduced emotional response, speech poverty, lack of initiative, anhedonia, social withdrawal

cognitive (second): reduced: sustained attention, psychomotor speed (fluent movement of the arms and legs), abstract thinking, problem-solving.
Weinberger 1988: ALL associated with frontal lobe HYPOfunction: decreased performance in Stroop tests (attention), sensory-motor gating tasks - P50 and PPI, oculomotor function

positive (last):
- additional behaviours
- though disorders, delusions, hallucinations
- though disorders: disorganised/irrational thinking, difficulty w though arrangement, jumping from topic to topic, rhyme over meaning

  • delusions: beliefs contrary to fact –>
    Persecution: false beliefs that others are plotting and conspiring against you
    Grandeur: false beliefs about one’s power/ importance - god-like
    Control: related to persecution - he/she is being controlled by others
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2
Q

Describe the structural differences of schizophrenic brains

A

Weinberger and Wyatt (1982)
CT scan of matched aged sample of schizophrenics vs healthy

  • schizophrenic lateral ventricles 2x the size of controls
  • but had reduced grey matter in temporal, frontal lobes and hippocampus

–> faulty cellular arrangement in the context and hippocampus

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3
Q

Discuss the heritability of schizophrenia

A
  • twin and adoption studies lead to - yes there is a genetic component
  • no actual schizophrenic causing genes
  • but instead - multiple that increase susceptibility which can be triggered by environment
  • DISC1 gene = disrupted in schiz
  • involved in regulation of neurogenesis, neuronal migration and postsynaptic density on excitatory neurons + mitochondria function
  • ^ chance by factor of 50
  • as well as BD and ASD
  • children with OLDER father = more likely to develop schizophrenia
  • mutations in cells that produce sperm
  • divide every 16 days so more time = more chance of mutation
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4
Q

statistics of schizophrenia

A

general pop: 1%
DZ: 17%
MZ: 48%
Both parents schizophrenic = 46%

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5
Q

describe the neurodevelopmental theories of schizophrenia with evidence

A

the ‘early’ neurodevelopmental model:
- early life events (prenatal) e.g. infection–> cause deviations from normal neurodevelopment –> these lie dormant until the brain matures + the affected systems are called into operation

Walker et al: Home movies 1994,96
- independent observers examined behaviour of families with schiz child
- subsequent schizophrenics –> ^ negative facial expressions and ^ abnormal movements

Schiffman 2004: Danish lunch tapes
- blind raters –> subsequent schizophrenics = less sociability and deficient psychomotor functioning

SUGGEST DEVIATIONS IN BRAIN DEVELOPMENT

CORRELATIONAL

The ‘late’ neurodevelopmental model: Feinberg ‘82/3
- abnormality/deviations in adolescence when synaptic pruning takes place

The ‘two-hit’ model: Fatemi & Folsom 2009 & Kehavan and Higarty 1999
- COMBINES THE TWO
- atypical development at both early brain development and adolescence
- early development –> dysfunction in specific neural networks = premorbid signs
- adolescence –> excessive synaptic pruning and loss of plasticity = emergence of symptoms

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6
Q

describe the neurochemistry theories of schizophrenia with evidence

DOPAMINE

A

The dopamine (DA) hypothesis):
- schiz is caused by abnormalities is DA functioning in the brain
- ^ overactivity of DA in mesolimbic system = positive symptoms
- v underactivity of DA is the mesocortical system = negative and cognitive symptoms

EVIDENCE:
- DA agonist drugs = schiz like symptoms e.g. amphetamine, cocaine, methylphenidate and L-DOPA –> symptoms can be reduced by antipsychotic drugs - ^ argument that the drugs block DA receptors

  • chlorpromazine (CPZ) is a DA antagonist/inhibitor - first antipsychotic –> dramatic effects on schiz
  • typical antipsychotics followed - D1-type family and D2-type family
  • ^ all block D2 receptors
  • IBZM = radiotracer that binds with the same D2 receptor as DA
  • measured displacement of IBZM after amphetamine in striatum
  • ^ displacement = more DA
  • more DA in striatum correlated with positive symptoms
    BASICALLY DRUGS ARE GOOD EVIDENCE

PROBLEMS:
- explains only positive symptoms
- the drugs that have weaker anti-dopamine mechanisms work better?
- negative symptoms = underactivity is mesocortical so it underactivity rather than over

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7
Q

describe the neurochemistry theories of schizophrenia with evidence

Glutamate

A
  • glutamate = major excitatory neurotransmitter in the central nervous system
  • many brain neurones - ALL from cerebral cortex = use glutamate as neurotransmitter
  • balanced with GABA - the main inhibitory neurotransmitter
  • NMDA receptor (Glutamate receptor) = ionotropic, at rest blocked by magnisum at open = calcium influx
  • activation = learning and memory –> too much = excitotoxic (cell death)
  • critical for neural survival, migration, plasticity
  • HYPOTHESIS: schiz is due to NMDA receptor hypofunction = explains why there are treatment-resistant negative symptoms, onset is early in adulthood, association with structural changes and cognitive deficits
  • explains all 3 symptoms, accounts for lack of effectiveness of DA
  • hypofunction NMDA receptors account of excessive DA release in mesolimbic and reduced in mesocortical
  • when glutamate is low GABA interneuron isn’t activate to decrease release of dopamine - explains pos
  • loss of glutamine = loss of cortical function = negative functions

EVIDENCE:
- PCP drug and Ketamine = pos, neg, cog symptoms of schiz
- BOTH are NMDA receptor antagonists
- glutamate agonists (mimic) = improve pos and neg symptoms
- animal studies and genome studies

  • ket and PCP symptoms = caused by decrease in metabolic activity of frontal lobes
  • PCP to monkeys 2x day 2 weeks
  • task that relies on PFC function = monkeys = severe deficit if PCP
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8
Q

describe the neurochemistry theories of schizophrenia with evidence

neuroinflammatory hypothesis

A
  • brains immune cells = hyperactive in schizophrenia risk people
  • animals studies = link pro-inflammatory agents and schiz symptoms
  • reversed upon treatment with antipsychotics OR antibiotics that reduce microglial activation
  • supports the evidence of prenatal/perinatal infection = increased schizophrenia risk
  • Genome study found dopamine-receptor gene and glutamate receptor subunits = increased risk

BUT

  • most significant association = chromosome 6 which includes region of genes involved in acquired immunity

MIcroglia:
healthy humans: ramifies state & survey brain for pathogens/debris –> identify = activation - change morphology
- involved in lots of homeostatic functions
- this function grows throughout lifespan
- THUS pre or perinatal primes the micrgolia –> may interact w cells in the development nervous system
- could subtly rearrange circuitry –> behavioural impairment in adolescence

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9
Q

describe the neurochemistry theories of schizophrenia with evidence

estrogen

A
  • female sex hormone
  • ovaries, fat, breasts and brain
  • women = second peak onset of schiz at the menopuase
  • estrogen protects/buffers schizophrenia

women have reduced negative symptoms, later onset, better response to antipsychotics , fewer disability/hospitalisations
- support hypothesis that sex hormones play a role

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10
Q

typical antipsychotics stats/symptoms

A
  • 20-30% of patients do not respond to the drugs
  • Long term use leads to symptoms that resemble Parkinson’s disease

-1/3 of the patients developed tardive dyskinesia –> cannot stop moving

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11
Q

atypical antipsychtoics

A
  • Do not have Parkinson’s side effects as they have lower affinity for D2 receptors -
  • Helps positive and negative symptoms rather than just positive

Clozapine - lower D2 affinity and higher other DA receptors
- use it when others fail
- reduces suicide rates too
- BAD side effects - weight gain, sedation, salivation, hypotension, etc

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12
Q

Parental behaviour

A

MOTHERS:

  • a combination of hormones and experiences trigger maternal behaviour
    i.e., hormones and the passage of pups through birth canal

Hormones:
- influence NOT control
- e.g. nest building is facilitated by progesterone - but continues after birth when progesterone is lower

  • The Medial preoptic area (MPA) = which regulates social behaviours and social reward = crucial for maternal behaviour - lesions disrupt maternal behaviour
  • The VTA-NAC pathway is involved in the reward system = also necessary –> it is activated when mothers encounter their pups
  • In lactating females encountering their pups is more rewarding that cocaine (FERRIS 2005)
  • Humans show activation of the reward systems when presented with pictures of their babies (BARTELS & ZEKI 2004)

PATERNAL:

  • in mammals few fathers show care for offspring
  • MONOGOMOUS prairie voles - share offspring care
  • POLYAMOROUS meadow voles - leave the female post mating
  • The size of the MPA is less sexually dimorphic in prairies voles than meadow voles
  • lesions = disrupt paternal behaviour in rat and voles so it is also involved in paternal behaviour
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12
Q
A
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13
Q

Affiliative behaviours

A
  • positive social behaviours within the same or different species
  • neuropeptides: oxytocin and vasopressin are key for complex social behaviours (both produced in the hypothalamus)
  • released as hormones from the pituitary gland
  • or from axons towards specific brain regions as neurotransmitters
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14
Q

Affliliative behaviours

in animals

A

Pair Bonding in Voles
- 3-5% of mammals are monogamous
- biparental species = females and males raise their young
- voles:
- prairies voles = bond for life
- meadow voles = polyamorous - male leaves female post-mating

Exposure to partner when injected with VP vs OXT

  1. males and females paired for 1H
    - one received administration of OXT or VP
  2. partner preference test:
    - 180 mins
    - choose to enter room with stranger, with partner from earlier when they had the drug or alone

Results:
- VP and OXT increased partner preference in both females and males
–> preference is mediated by hormones

Why?
- after mating male prairie voles tended to spend significantly more time with partner than woith a stranger
- prairie vole had more VP receptors in the rewarding areas of the brain
- as well as more OXT receptors in the prefrontal cortex
- PRAIRIES GET PLEASURE OUT OF BONDING

  • if we block the activation of OXT and VP
  • pair preference is stopped in both sexes
  • overexpression of VP receptor in the meadow voles enhanced mate preference compared to controls

how much can we generalise this ?

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15
Q

Affiliative behaviours

in humans

A
  • we cannot manipulate VP and OXT in humans - ethical BUT they seem to have an influence in humans too
  • oxytocin administration nasally = anxiety reduction in humans
  • maternal and romantic love activated brain rich VP and OXY receptors
16
Q

prosocial in humans

A
  • wide range of positive social behaviours
  • e.g. trust care, empathy
  • hard to study in animals
  • we can manipulate OXY and VP with nasal spray
    Trust:
  • investor and trustee given 12 monetary units
  • investor: donate a multiple of 4 (or 0) to trustee
  • whatever was donated = x3
  • trustee could then give back investor 0-48 MU
  • placebo or OXT nasal administration 50 mins before task
  • investors + OXY = all money invested
  • increased trust?

Empathy:
- OXT or placebo = nasally
- 45mins later = multifaceted empathy test
- OXT adminsteration increased empathy on all dimensions

Altruism: improve welfare of others at cost to person

experiment 1:
- saliva samples measure OXT
- 10 1£ coins
- social or environmental donation task
- correlation between OXT levels and social donation
- no effect on ecological frame

Experiment 2:
- OXT intranasal
- 10 1£ coins
- social or environmental task
- OXT administration increased donations in social frame and decreased in ecological frame

Oxytocin and social approach:
- OXT or placebo nasally
- 45 later - stop distance paradigm
- ‘stop as soon as the closeness feels uncomfortable’
- distance decreased in OXT - unfamiliar, friendly, attractive male experimenter

confounding: OXT also has effects on fear and reward processing

17
Q

Reproductive

A

castration and hormone replacement:

  • castrated chick = does not develop normally
  • re-implanted = normal development
  • transplant from other chick = restores normal development
  • not connected to blood supply or neural networks - must be chemicals they release

gave goat testicles to men with weak sexuality –> success

but ethical methodological and safety issues

18
Q

hormonal definitions

A

hormones = signalling molecule that can carry messages to distant targets through the blood stream e.g. testosterone

neurohormone = hormone released by neuron - targets neighbouring or distant cells - oxytocin

target: organs/cells that can detect hormones and is affected by them

females - estrogen - progesterone - ovaries

males - testosterone - testes

non sexual
growth hormone - pituitary glands

thyroxine - thyroid glad

insulin - pancreas

adrenaline - adrenal gland

19
Q

development of sex organs

A

Gonads –> testes or ovaries are the first to develop
- produce sperm or eggs and hormones

20
Q

Why do we sleep?

A
  • ubiquitous - all animals engage in sleep or a comparable rest state

sleep deprivation in rats:
Rechschaffen 1983: sleep-deprived rats
- looked sick , stopped grooming, became week and lost ability to thermoregulate
- lost weight - even though ate more - eventually died

Human studies: restrictions due to ethical reason - but increased body weight

4 reasons why we sleep:
- adaptive
- restorative
- developmental
- cognitive processes

  1. Sleep is adaptive:
    - original function: conserve energy: 1-2.C decrease in body temp in mammals
    - decrease in muscle activity
    - increase in sleep time when here is scarcity of food
    - normally: brain spends 20% of our energy even tho it is 2% of out body weight
  2. Sleep is restorative:
    - helps us feel refreshed and energised the next day
    - activity during wakefulness = accumlation of free radicals (oxidative stress) and toxic waste (amyloid beta)
    - these are removed through restorative mechanisms during sleep
  3. Sleep promotes development:
    - evidence: sleep hasa role in brain development is that infants sleep more than adults
    - REM sleep accounts for 20-25% of adult sleep vs 50% of infant sleep
    - during stage 3 sleep SWS - growth hormone release is at its peak - important for growth
  4. Sleep facilitates cognition:
    - enhances learning and memory:
    - performance on a newly learned task is better next day if the adequate sleep is achieved whereas ability deficits are prevalent following sleep deprivation
  • Wilson et al 1994: during sleep neurons replay previous experience to retain information
  • evidence shows different types of learning may be supported by different types of sleep SWS vs REM and declarative vs non-declarative

problem solving and creativity:
- brain continues to process material and enables solution to problems as evidenced by ‘aha’ phenomenon upon waking

Muller and Pilzecker - consolidation establishes memories in our brains for future use - memory traces that are thought to be unneccesarry are removed (synaptic homeostasis hypothesis) –> synaptic pruning during sleep helps to reinstate the brain so it is able to function and learn more the next day

21
Q

ways of studying sleep

A

subjective measures: surverys, interviews, diaries

  • objective measures:
  • actigraphy: special watches - actiwatches- that record activity during the day and night –> can estimate duration and quality of sleep
  • easy to use
  • polysomnography
  • gold standard - Hans Beger 1929
  • recordings of electircal activity from multiple sources –> reveals sleep architecture

EEG - brain activity underneath skull
EOG - muscles around the eyes
EMG - muscles in the body
combines with heart rate, temperature and breathing

BETA - irregular = awake
ALPHA - regular = asleep/unfocused

22
Q

what are the stages of studying sleep

A

stage 1: .5 - 7.5 Hz
- transition between wakefulness and sleep
- short

stage 2:
- irregular activity and sleep spindles

stage 3:
- high ampitude low frequency of delta activity <3Hz
- synchronised regular waves - reflect synchrony and coordination in activity of neurons in underlying brain areas
- slowing down of brain activity and bodily functions e.g. heart rate and temperature

REM:
- increased brain activity and asynchrony in the brain waves
- muscle atonia - not producing action potentials
- rapid eye movement
- deep sleep in terms of muscle activity but light sleep in terms of brain activity - paradoxical sleep
- facial switches, erections, vaginal secretions, dreams

23
Q

dreams

A

Dement and Kleitman 1957 - woken from REM sleep = vivid dreams
- freud = royal route to unconscious
- jung - glimpse into collective unconscious
- relevant to daily life
- 64% - sadness, anxiety, anger
- 18% happy
- 1% sexual

Activation-synthesis hypothesis - bottom-up view on dreams:
HOBSON 2004

  • brain stem is activated during REM and sends signals to the cortex –> creates images with actions and emotions from memory
  • frontal cortex = less activated during dreaming = no logic in timing / sequence of events –> the person tries to organise info when awake
  • no meaning in dreaming - based on experiences

Coping hypothesis
- Valli 2009-

dreams = biologically adaptive > to enhanced coping strategies
- top-down view on dreams
- dream about events they find threatening
- problems solving occurs during sleep - ‘sleep on it’

24
Q

the neural basis of sleep

A
  • neurochemical and hormones cause sleep-wake cycles
  • melatonin secreted by pineal gland during dark promotes sleepiness

Adenosine: accumulates during the day after prolonged wakeness –> promotes sleep
- caffeine antagonises its effects
observations: patients with encephalitis:
- some = constant sleepiness - base of brain damage
- some = insomnia - anterior hypothalamus damage
- anterior hypothalamus contains inhibitory neurotransmitters such as gaba
- damage in rats = insomnia and death
- electrical stimulation = sleep

Reticular activating system - RAS: nuclei in the brainstem that extend to the forebrain and promote arousal

orexin/hypocretin –> peptide released from lateral hypothalamus
- responsible for maintenance of wakefulness

  • implicated in narcolepsy
25
Q

circadian rhythms

A
  • associated with 24h cycle such as day or night
  • endogenous cycles = generated from within - our brain and body spontaneously generate its own rhythms based on the earth’s rotation
  • endogenous rhythms can be annual - migration or seasonal - breeding
  • humans = diurnal
  • 24hr rhythm controls sleep, wakefulness, eating, drinking, body temp, hormones, urinations, sensitivity to drugs

Aschoff:
- humans placed in underground bunker - no external cues
- allowed to select light-dark cycle by turning lights on and off
- showed daily sleep-activity rhythms that drifted to more than 24hrs
- have an endogenous biological clock which governs sleep-wake behaviour

  • Zeitgebers - cues that serve to set our biological clock
  • most important = light
  • others = meals, activity, temperature
  • zeitgeber resets biorhythm = untrained

Jet-lag - disruption in circadian rhythm due to crossing of time zone
- stemps from mismatch of internal circadian clokc and external time
- sleepines and impaired concentration

west = phase-delays
east = phase-advances

chronotypes = different patterns of wakefulness and alertness –> individual differences

morning people = larks
evening people = owls

genetic basis but also change with age and other external factors - lifestyle, social factors, etc

infancy and child hood + adulthood and old age = larks

adolescense = night owls/’eveningness’

differences between people = social jet lag

morning people = happier

26
Q

neural basis of biological clock

A
  • Richter suspecting biological clock –> electrical lesions in various areas of rat brains
  • lesion in hypothalamus = loss of rhythm

suprachiasmatic nucleus = the clock
- SCN
- lesion disrupted circadian rhythms of wheel running, drinking, hormonal secretion
- ‘master clock’

  • neurones in SCN = ore active during light period than in dark period
  • single cell removed to culture tissue - continue to function in rhythmic patter
  • transplantation of an SCN into a donor organism = recipient follows donors rhythm

How does light reach SCN:
- through the retinohypothalamic tract
- by special ganglion cells PRGCs

  • PRGCs have their own photopigment - melanopsin responds directly to light –> do not rely on rods/cones

what makes the clock tick?
- per genes and per protein
- builds up in cells overnight and is broken down during the day
- tim gene and tim protein
- tim meets per = period gene shut down

transcription-translation-inhibition- feeback loop
- transcription from DNA to mRNA to translation into proteins - form dimers
- dimers enter the nucleus
- dimers inhibit transcription then decay
- daily rhythm

SCN effects on the pituitary and the pineal gland -

  • SCN regulates waking and sleeping by controlling activity levels in other areas through its effects on the pituitary and the pineal gland
  • The SCN drives a number of slave oscillators, each responsible for the timing of a different type of behaviour i.e. drinking, sleeping, body temperature,activity etc

breeding is controlled by the SCN in winder via the pineal gland:

  • winter = increased melatonin = shrinks the gonads
  • spring = less melatonin - enlarged gonads - testosterone - mating
  • time of day effects human cognitive performance
  • drug toxicity 20-80% depending on time of day
  • illness risk depends too - heart attack/stroke us higher in morning
27
Q

discuss the neurobiological factors related to anxiety and treatment

A

definition: anxiety = apprehensive uneasiness or nervousness over an impending or anticipated ill (Merriam-Webster)

  • normal part of life
  • does not have one broad identifiable trigger - similar response to stress e.g. faster heart-rate/breathing
  • anxiety disorder = more intense fear/anxiety inappropriate for the circumstance
  • ^ likely due to cumulative effects of stress –> contributes to depressive and substance abuse disorders
  • women more likely to experience than men

Panic disorder:
- episodic attacks of acute (seconds-hours) anxiety/terror
- symptoms: hyperventilation (low CO2), irregular heartbeat, dizziness, faintness, fear of losing control and dying
- Culturally: Asian, African and Latin American countries have lower rates than the USA

Agoraphobia:
- intense fear/anxiety about leaving home/being in open/public areas, lines/crowds, etc
- cope through avoidance due to disproportionate fear e.g. staying home for years due to fear of a panic attack

GAD:
- excessive, uncontrollable worrying and anxiety from a wide range of situations and difficulties controlling these symptoms
- e.g., sense of impending danger, sweating, trembling, difficulty concentration
- ^women

Social anxiety disorder:
- persistent excessive fear of being exposed to the scrutiny of others e.g., public speaking/group conversations –> sweating/blushing
- equal in men and women

  • culturally for GAD and SAD –> more prevalent in Europeans than Asian, latino, African Descent

brain changes linked to anxiety disorders:
- functional imagine (PET & fMRI) show changes in the prefrontal cortex, anterior cingulate cortex and amygdala

  • Pfleiderer et al 2007: increased amygdala activity during panic attacks
  • Phan et al 2005: increased amygdala activity in response to presentations of faces with anger, disgust and fear in SAD
  • activation correlates with symptoms
  • Monk et all 2008: adolescents with GAD exhibit increased amygdala and decreased ventrolateral prefrontal cortex activation
  • also see lack of suppression of amygdala via the vmPFC - which plays a role in the surpression of fear
  • Treatments:
  • Benzodiazepines (BDZ) reduces anxiety and anxiety-like behaviours in animals: experiment with rats:
  • enclosed arm - less anxiety inducing - less likely to fall (walls either side)
  • open arm (no walls) anxiogenic
  • BDZ rats spend less time on the open arm - they walk across quicker - less anxious
  • it binds to the inhibitory GABA A receptor as an agonist
  • increasing CI- influx which causes hyperpolarisation

Paulus 2005:
- BDZ reduces amygdala activity when looking at emotional faces
- Flumazenil (antagonist) dishibits action at GABA A receptors and produces panic in panic disorder patients –> can treat BDZ overdose
- if the treatment reduces the symptoms and opposite treatment causes - correlational evidence that these areas are responsible

  • abuse is likely because it causes a relaxing effect /withdrawal and patients typically feel less calm when stop taking

withdrawal and sedation –> better compounds with fewer side effects are needed

Treatment by increasing neurosteroid synthesis:
- neurosteroids are neuroactive steroids –> synthesises in periphery and CNS
- increase activity of GABA receptor
- during anxiety attacks - neurosteroid synthesis = suppressed = suppression of GABA A receptor function

Nothdufter et al 2011: XBD173 enhanced neurosteroid synthesis and reduces panic - without the withdrawal and sedation symptoms

compounds that affect the serotonin and glutamate systems can also be used to treat anxiety:
- Asnis 2001: Fluvoxamine, an SSRI, reduces panic attacks

  • Ressler 2004: similar findings with D-cycloserine (DCS) - an indirect agonist of NMDA receptor
  • also facilitates extinction of conditioned fear in animals - walker 2002
  • the reduction of symptoms allows patients to attend behavioural therapy and extinguish fear responses
28
Q

discuss the neurobiological components that contribute to aggression and their components

A
  • aggression is common across many species
    —> survival, mates, protecting offspring
  • behaviours relate to threat (warning), defensive (attack) and submission (defeat)

Brain circuits and aggression:
- Gregg and Siegal 2001:
- Electrically stimulating the periaqueductal gray (PAG) in cats
–> elicits aggressive attack and predation
- excitatory and inhiborty connections between the hypothalamus & amygdala and the PAG can affect
- medial hypothalamus –> Dorsal PAG –> defensive rage
- lateral hypothalamus –> ventral PAG –> predetory attack
- amygdala nuclei control these pathways

Aggression and serotonin:
- animal studies
- Audero 2013: increasing serotonin transmission reduces aggression
- Mosienko 2012: reducing serotonin synthesis increases aggression

  • Vergnes 1988: reducing serotonin transmission via destruction of serotonergic axons increases aggression
  • Howell 2007: low levels of serotonin metabolite (5HIAA) in cerebrospinal fluid in rhesus monkeys ins linked with aggression
  • picking fights with bigger monkeys
  • higher risk taking
  • this suggests serotonin inhibits aggression and controls risky behaviours

Human studies:
- mixed evidence that serotonergic neurons play an inhibitory role in aggression - Duke 2013
- Low serotonin metabolite in cerebral spinal fluid = linked with antisocial behaviour and aggression
- SSRI have shown to reduce aggressive behaviour in some cases

Aggression as a reward:
- a reward: objects, actions, experiences that attain positive motivational property
THEY INCREASE THE PROBABILITY OF THE ACTIONS THAT LEAD TO THEM

street addiction
- former gang member
- sight of yellow police tape - ‘my heart is beating, my hands are sweating, i am not scared - i am excited - i want back in the game’

  • Elbert 2010: some individuals exhibit appetitive aggression, motivated by intrinsic reward
  • Cronbach 2013: this is an adaption to violent environments –> makes individuals more functional in violent settings (e.g. war-afflicted communities) –> elevated social status
  • Animal models allow us to study this behaviour under controlled conditions:
  • conditioned place preference (CPP)
  • instrumental conditioning

Conditioned Place preference (CPP): Golden 2016
- REWARDS: drug, food, social rewards
- mice/rats
- two chambers with a door between the two
BEFORE CONDITIONING:
- all chambers are neutral stimuli
CONDITIONING:
- one chamber is paired with a rewards
- the other is not
AFTER CONDITIONING:
- several reward-chamber pairings –> reward paired side acquires motivational significance - acts as the conditioned stimulus
- if the substance is ‘rewarding’ –> animals spend more time in the chamber it has been paired with –> preference

CPP with aggression:
BG info: male rats are very territorial after sexual experience and will attack an unfamiliar intruder

DURING CONDITIONING:
- resident attacks intruder in the ‘paired side’
- no intruder in the ‘unpaired side;

AFTER CONDITIONING:
- resident mouse spends more time in the paired side in the absence of the intruder
MEANING:
- mouse finds the attacking as rewarding and associates the chamber with it

Operant/instrumental conditioning:
- animals press lever for food reward in operant ‘Skinner’ chamber
- the reward sustains the lever press response (reward self-administration)
- reward-seeking - animals press lever even in absence of reward

EXPERIMENT: Golden 2019
- animals press lever and intruder chamber opens - letting an intruder in (aggression self-administration)
- trained animals will press lever even in absence (aggression seeking)

Does aggression self-administration and seeking activate the reward system in the brain?

  • nucleus accumbens (NAc) - key role in reward and motivated actions
    e.g. food and drug-seeking
  • activated by rewarding experiences e/g/ drugs of abuse, food, water and sex
  • measured by: activity-sensitive protein - ‘Fos’
29
Q

pain

A

what is pain?
- an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
- promotes avoidance of situations that may decrease biological fitness
- promotes resting behaviour that enhances recovery following injury or modifies behaviour so that further injury or death become less likely

30
Q

pain pathways

A

detecting pain:
- activate sensory receptors and nociceptors

nociceptors:
- sensory neurones specific to pain
- free nerve endings
- synapse in spinal cord to ascending neurons to brain

polymodal nociceptor:
- free nerve endings - contain receptors sensitive to noxious stimuli
- respond to multiple stimuli such as intense pressure, heats, acids, capsaicin and ATP release

high threshold mechanoreceptors: intense pressure stretching, striking, pinching

vanilloid receptor, TRP channels (temperature-gated channels): heat, acids, capsaicin (chilli)

purinergic receptors: ATP release –> channels opne neuron depolarizes - fires action potentials

31
Q
A