essay plans

Question 1

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

Answer 1

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

Question 2

Describe the structural differences of schizophrenic brains

Answer 2

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

Question 3

Discuss the heritability of schizophrenia

Answer 3

• 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

Question 4

statistics of schizophrenia

Answer 4

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

Question 5

describe the neurodevelopmental theories of schizophrenia with evidence

Answer 5

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

Question 6

describe the neurochemistry theories of schizophrenia with evidence

DOPAMINE

Answer 6

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

Question 7

describe the neurochemistry theories of schizophrenia with evidence

Glutamate

Answer 7

• 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

Question 8

describe the neurochemistry theories of schizophrenia with evidence

neuroinflammatory hypothesis

Answer 8

• 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

Question 9

describe the neurochemistry theories of schizophrenia with evidence

estrogen

Answer 9

• 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

Question 10

typical antipsychotics stats/symptoms

Answer 10

• 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

Question 11

atypical antipsychtoics

Answer 11

• 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

Question 12

Parental behaviour

Answer 12

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

Question 13

Affiliative behaviours

Answer 13

• 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

Question 14

Affliliative behaviours

in animals

Answer 14

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 ?

Question 15

Affiliative behaviours

in humans

Answer 15

• 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

Question 16

prosocial in humans

Answer 16

• 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

Question 17

Reproductive

Answer 17

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

Question 18

hormonal definitions

Answer 18

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

Question 19

development of sex organs

Answer 19

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

Question 20

Why do we sleep?

Answer 20

• 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

Question 21

ways of studying sleep

Answer 21

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

Question 22

what are the stages of studying sleep

Answer 22

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

Question 23

dreams

Answer 23

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’

Question 24

the neural basis of sleep

Answer 24

• 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

Question 25

circadian rhythms

Answer 25

• 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

Question 26

neural basis of biological clock

Answer 26

• 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

Question 27

discuss the neurobiological factors related to anxiety and treatment

Answer 27

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

Question 28

discuss the neurobiological components that contribute to aggression and their components

Answer 28

• 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’

Question 29

pain

Answer 29

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

Question 30

pain pathways

Answer 30

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