essay plans Flashcards
describe and give examples of the 3 different types of symptoms of schizophrenia
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
Describe the structural differences of schizophrenic brains
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
Discuss the heritability of schizophrenia
- 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
statistics of schizophrenia
general pop: 1%
DZ: 17%
MZ: 48%
Both parents schizophrenic = 46%
describe the neurodevelopmental theories of schizophrenia with evidence
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
describe the neurochemistry theories of schizophrenia with evidence
DOPAMINE
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
describe the neurochemistry theories of schizophrenia with evidence
Glutamate
- 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
describe the neurochemistry theories of schizophrenia with evidence
neuroinflammatory hypothesis
- 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
describe the neurochemistry theories of schizophrenia with evidence
estrogen
- 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
typical antipsychotics stats/symptoms
- 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
atypical antipsychtoics
- 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
Parental behaviour
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
Affiliative behaviours
- 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
Affliliative behaviours
in animals
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
- males and females paired for 1H
- one received administration of OXT or VP - 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 ?
Affiliative behaviours
in humans
- 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
prosocial in humans
- 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
Reproductive
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
hormonal definitions
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
development of sex organs
Gonads –> testes or ovaries are the first to develop
- produce sperm or eggs and hormones
Why do we sleep?
- 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
- 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 - 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 - 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 - 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
ways of studying sleep
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
what are the stages of studying sleep
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
dreams
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’
the neural basis of sleep
- 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
circadian rhythms
- 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
neural basis of biological clock
- 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
discuss the neurobiological factors related to anxiety and treatment
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
discuss the neurobiological components that contribute to aggression and their components
- 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’
pain
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
pain pathways
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
