2103 Flashcards
The two hemispheres
This is the two halves of the brain which are separated/connected with the corpus callosum. The left side processes info from the right side of the body vice versa.
Hemispheric Lateralisation
The theory that the two halves have different functions, as a function is mainly controlled by one side.
The supposition of hemispheric lateralisation
The left side is language (logical and symbolic) including brocas and wernickes. The right side is perception (Visio spatial and artistic).
What sperry wanted to research
The extent to which functions are localised. He investigated this in those who had their corpus collosum cut due to seizures.
How speedy researched
• Tests of the right hemisphere.
• visual stimuli tests.
• tactile stimuli tests.
Tests of right hemisphere
Puzzles/tests.
Visual stimuli tests
A picture was shown for 1/10 of a second both sides and had to say what it was,
Tactile stimuli test
Had to feel and object and say what it is
Sperry’s research findings
- Naming objects by feeling
- Picking up the object they felt
- Composite words
- Faces
- Drawing abilities
Narumoto’s split brain research
P’s said the emotion on the left of individuals faces as this is where perception is in the brain.
Clarke et al’s research split brain
Lady with right hemisphere damage Could only find her way around familiar places if explained with a visual feature.
Hunger/the cephalic stage as initiation
Hunger is the physiological changes which prepare the body for food which disturbs homeostasis.
The cephalic stage:
1. Senses pick up on food which stimulates the amygdala and hypothalamus.
2. This sends signals to the stomach which via the vagus nerve produces acids as a response
Cephalic stage evidence
• when give animals food stimuli but without food made them hypoglycaemic
• when injected food into animals stomachs caused hyperglycaemia as hadn’t gone through processes
Storing nutrients
• short term - in the liver and muscles as energy for muscles, the liver and converts some into glycogen
• long term - in the adipose tissue in the abdomen which is used when short term energy gets low and then can be used for energy when fasting to nourish brain
Storing nutrients evidence
Glucose detectors were found in the liver for the storing of short term energy which allows maintenance of weight set point
Glucose dual centre model
The liver sends info about glucose to two areas; the VMH and LH.
1. The VMH is activated when glucose levels increase to feel full and stop eating
2. The LH is activated when levels are low to increase eating
Glucose dual centre model evidence
Lesion studies in animals support this
Grehlin for increasing feeding
Grehlin is a hormone produced in the stomach and pancreas which travels to the neurons to activate the LH. This then causes feeding, which is in proportion to hunger.
Grehlin evidence
Blood was tested for levels each 5 mins from lunch to tea on 6 p’s as well as a subjective hunger measure.
This found that after lunch levels were low and high before tea supporting that it acts as a hunger signal.
CCK
Modulates emptying the gall bladder and stomach. This is the opposite of grehlin as reduces feeding, as when food is digested this is released.
PYY - inhibiting eating
A hormone in the gut which is released to suppress appetite in proportion to intake.
PYY evidence
8p’s fasted then had either a saline drip or PYY drip.
This showed those with the PYY drip ate 25% less than saline drip.
Inhibiting eating - leptin & alpha-MSH
Let in is released from adipose tissues which binds itself to receptors in VMH to reduce eating.
Alpha-MSH is then released when strong signals in the VMH are sent. AM is sent to hypothalamus which reduces hunger.
Satiety
• the feeling of fullness after eating
• hunger implicates this
• food tastes better when hungry
• Alliesthesia - a good stimulus can feel in pleasent or pleasant based on fullness
Satiety neural substrates
Linked to the hypothalamus
Satiety neural substrates research
Monkeys stop reacting to smell of food when have enough
Satiety OFC
Links to reward and when full it no longer feels like a reward
Satiety OFC evidence
• OFC activates less when sniffing bananas after satiety
• PET scan showed activation when found chocolate pleasant
Satiety - opioids actions
The more palatable a food is the more options are released, so niceness links with wanting it
Sensory specific satiety
Not all foods loose their pleasantness which can encourage over eating, but when they do it encourages varied eating
Mood in eating
Mood effects eating as stress/anxiety can cause under eating but depression can cause over for the energy in carbs
Serotonin hypothesis - eating behaviours and research
This says when carbs are eaten Thai increases insulin which reduces amino acids in the blood except from tryptophan. This goes to the brain and releases serotonin reducing stress.
• research shows when overweight women were either given a high protein or carb drink and they rated carb better for improving mood
Role of stress
When the individual is stressed this links to high cortisol which causes eating to secure food in times of stress
Dopamine hypothesis - eating behaviours and research
This says when eating carbs they feel better due to the dopamine in these.
• shows when watching g a sad and happy film more choc was eaten in happy
• however another piece showed when shown funny/sad clip and offered popcorn, more ate when sad
Cog aspects - obesity and research
Memory and attention
• can affect memory
- r - those with memory problems may eat more
• when distracted can eat more
- r - number of people correlated with meal size
- r - eat more with people present
Obesity
A >30kg/m3 which can cause strokes, cancer, diabetes etc and has been increasing. Doubled since 1980’s.
Leptin - obesity
Leptin is stored in adipose cells and released into blood when full/at satiety to reduce intake. When dieting and not full, less leptin is released so generates hunger.
Explanations of weight gain - obesity
Thrifty gene, genetic drift, protein leverage.
1. When go through famine, they learn to deposit fat and this often doesn’t come, can also be passed onto offspring (dutch famine study).
2. Genetic drift - animals that’s suffer high predation eat lots to maintain weight and have back up
3. Protein leverage - protein heals through energy intake but can cause obesity
Risk factors for obesity and research
Early development, taste (liking and sensitivity), externality, trauma
1. Thrifty gene babies are smaller and then become obsese to make up for it
2. The CD36 gene can affect pleasantness of food so either need a low amount or a high amount to get this causing obesity (research).
3. Some respond to smell/taste more
4. Trauma correlated. 60% of observe were abused (research).
Sleep- what is sleep
A natural reoccurring altered state of consciousness where muscles movement is reduced as well as reduces interacting with environment
Arousal stages
Arousal - physiologically awake and alert
Sleep - altered states of consciousness
Coma - period of unconsciousness due to tbii
Vegetative state - altering between sleep and moderate arousal
Minimally concious- brief stages of purposeful actions
Brain death - no brain activittyy
Sleep stages
- Awake and alert - beta waves - aware.
- Awake and drowsy - Alpha waves - drowsy but muscles work
- Sleep - light, heavy and dreaming
- • NREM 1 - alpha and theta waves - easily awoken and some dreams
• 2 - bursts of brain activity to respond to stimuli
• 3 - Thelma and delta waves -
• 4 - give off low frequency waves - loss of xoncousness - REM - no dreaming, twitching, muscle paralysis, irregular breathing
Each is 90 mins
Functions of sleep
Is the only universal behaviour which has no clear underlying function
However must do because other wise it would be eliminated and not universal (universal behaviour).
However is fatal without and is used for concentration and mental health
Theories of sleep
Hibernation theory and conservation theory
Hibernation theory - sleep and evidence
It is a way to conserve energy, which the sleep pattern links to energy intake such as size and diet.
• carnivores eat more than herbivores
• Smaller animals need more sleep
• those aware of predators all the time get less sleep
• increased periods of sleep in energy shortages
Restoration theory and evidence - sleep
Sleep is for the repair and regrowth of cells, as REM restores brain cells and more rem is used in brain growth
• less sleep as brain stops growing
• when rats were deprived of sleep for 4 weeks they ate more for more energy but there immune systems failed after 3 weeks
• 50% of REM is restored
Ultradian Cycle - BRAC: biological mechanisms of sleep
90 min cycle unaffected by light, eating, sleep cycles etc. however other bio tyhtms are these bio rhythms however are controlled by endogenous pacemakers (internal clock) and exogenous zeitgebers (external changes). And sleep is controlled by these changing
endogenous and sleep cycle
Fibres in the hypothalamus receive light info
The pineal gland releases cortisol for wakefulness
Exogenous and sleep cycle
Lights, clocks etc…
Genetic mechanisms that underly the body clock
2 genes keep body click regulated within a 24 hour frame (period and timeless) through releasing protein.
Gene mechanisms that underly the sleep cycle
Period gene expressed in SCN linked to eye and pineal gland
Influence of biological rhythms (evidence)
If no windo we get out of sync
Disruptions to sleep research
• shift work have higher risk of heart disease and cancers.
• Women working night shifts 3X a week for 6 years are more likely to have disease as night work reduces melatonin which increases tumour growth
• jet lag impairs baseball performance
Obesity more common with irregular sleep as animals as when following 20 hour light dark cycle gain weight
Sleep deprivation and illness
REM is used in recovery for the brain so deprivation can cause physical symptoms
Brain mechanisms for wake and sleep (which parts) and evidence
• reticular formation - message transfer and motor control which maintains arousal and either keeps awake or wakes (research).
• locus Coeruleus - emits impulses for meaningfulness for awakefulness
• hypothalamus - released histamine which causes drowsiness but also can release orexin causing wakefulness. Also supported by mice lacking this fall asleep when should be alert.
• basal forbrain - releases acetylcholine which increases arousal and sharpens attention
• Thalamus - stimulation here results in immediate wakefulness
• neurotransmitters GABA - sleep depends on GABA inhibition. As when a neuron is active GABA increases
• Brain functions in REM - activity in motor cortex decreases, but increases in pons
Dreaming functions (2 theories) and evidence
• restoring mental and emotional health - during REM there is no noradrenaline activity as research shows sleep removes the emotional value of memories.
> Those with PTSD have disturbed REM as they have higher noradrenaline which prevents REM meaning they can’t take the emotion from memories.
• Improved cognitive abilities - REM sleep allows consideration of knowledge
> research showed an answer popped out when awoken from rem sleep
> if you nap after learning something this improves memory
> sleep deprivation shows worse memory tasks
Dreaming hypothesis (2) and evidence
• Activation hypothesis - dreaming makes sense of info which starts with bursts of energy in the pons
> this activates the cortex which tries to make sense of sensory information
• Clinico-Anatomical Hypothesis - dreams begin with arousing stimuli and memories. We forget dreams when we awake because the prefrontal cortex is suppressed.
Sleep disorders, causes, treatments and what it is
• sleep apnoea - inspired breathing in sleep, sleepless, heart issue.
> hormones, obesity, genes
> airway pressure mask, not drinking, loose weight, surgery to remove tissue from trachea
• narcolepsy - sudden or gradual periods of sleepiness in the day
> lack of orexin or cells that produce orexin which maintains awakefulness
> medication that increases dopamine which keeps awake
• night terrors - fear and are distressed when awoken
• sleep paralysis - feeling of being choked, paralysed and the presence of a demo
> paralysis - due to activation of amylgdala and choking due to paralysis of throat muscles
> wriggling finger and focusing on this
• sleep walking - walking around for seconds to minutes in stage 3 sleep, and don’t remember this
> genes, stress
> antidepressants, reduce alcohol
• REM behaviour disorder - moves around in REM, can injure your self, mainly in older men
> no relaxion of muscles
> anti-anxiety medication
• restless leg syndrome - tingling, unpleasant feeling in legs, more common in women and in the calf
> spinal and brain injuries, kidney damage, iron deficiency
> medications to increase dopamine, massage, exercises
Addiction
Is the chronic relapsing brain disorder made up of 3 aspects
- compulsion/craving - to take the drug
- withdrawal - negative state when access is restricted
- loss of control when reducing intake
Such as gambling, gaming and substances
DSM5 - building a tolerance
Affecting relationships
Wanting to cut down but can’t
Brain structures implicated in addiction and research
• doroslateral PFC - affects judgement - less active - addicts have lots of synaptic connections which reduces reasoned judgments
• Ventral striatum - motivation to act - more active - increased striatum activity shown in many different situations such as tasting sugar, imagining spent being pleasant, gambling
Causes of addiction - nature vs nurture and conclusion with research
Nature/disease model - the NIDA says it’s a brain deserve caused by a genetic vulnerability
• structural changes associated with judgment
Nurture/developmental model of learning - Marc Lewis said it’s a learned skill as deep learning leads to structural brain changes
• hippocampal changes after learning in taxi drivers
Interaction - LEARNING changes synaptic structured such as less synapse growth
Conclusion - because the same brain mechanisms are affected in behavioural and chemical substance abuse doesn’t cause addiction
Psychological explanations for addiction
Developmental learning model of addiction - is a cycle initiated with operant con. First there’s a trigger Wuxi activated the VTA which produces dopamine which accentuates the cravings. These cravings mean the striatum then communicated with the dorsolateral planning how to satisfy cravings. This results in visual activating such as imagining and motor cortex acts out the behaviour. This then causes a decrease in dop so need more, strengthening the pathway.
Delayed discounting model and brain processes
The closer we are to a reward the higher value we believe, so craving makes a short term reward better than a delayed benefit. Therefore effecting judgment.
Cognitive fatigue
When people suppress cravings it effects cognition and cues so abstinence is exhausting and they relapse
Effects of drugs on the brain (addiction)
Drugs interfere with synaptic transmission as they either facilitate/agonists (mimicing the effects of drugs) or inhibit/antagonists (block the neurotransmitters) at synapses.
Drugs have an affinity (how strong it acts as a key and a look) and an efficacy (how well it activates the receptors).
Stimulant drugs
For example xoxiane which does this through stimulating dop in the synapse by preventing reuptake of dopamine.
Low doses of stimulants enhance attention whereas high impairs as blocks dop reuptake
Nature vs nurture in addiction
Nature - twin studies show a 50-60% relation in nicotine dependence
Nurture - however if you never smoke the gene is redundant and the learning theory shows that a close paring of thing and reward causes a stronger association
Harm reduction - packaging
Knowledge on operant conditioning means marketing stopped and replaced with bad pictures or blank
Example of drugs and their effects
• research on cocaine shows it stimulates more dendrites and some stimulate fewer.
• Resecarh shows nicotine stimulates nicotine receptors increasing dop release . Research also shows animals with more receptors respond more to rewards.
• research shows opiates bind to endorphin receptors in the brain increasing firing of dop
• Marijuana causes 2 chemicals to bind to cannabinids which causes more dop release.
• hallucinogenics increases dop and serotnin.
• alcohol increases responses at GABA receptors, but research shows this increases dop and risks but research also showed decreasing brain activity.
• caffeine - enhances mood and causes physical symptoms. Research showed it increased co-ordination symptoms
Concepts of addiction and research
Tolerance
• more needed to reach desired effect - rays constantly having opioids could cope with more without affects as built a tolerance
Withdrawal
• the body prepares for a drug and when not there causes symptoms. Produces opposite effect of drug. - rat study.
Cravings
• associated with cues - a lit cigarette caused cravings. Supported by cue reactivity paradigm - when given peppermint and a cocaine the peppermint smell caused cravings
Aggression
Anger causing the hostile behaviour
Genetic factors affecting aggression
Chromosomal abnormalities
MAOA gene
TS
Selective breeding
Chromosomal abnormalities and research
1/1000 males have extra Y chromosome
9/314 in high security hospital were aggressive
However only characteristic associated with height
Twin studies and research
To explain using concordance rates
- 50 and 19 physical
28 and 7 verbal
MAOA gene
A dysfunction affects how this gene codes for enzymes to break down neurotransmitters such as serotnin
Selective breeding and research
Breeding for a purpose
- nice without MAOA more aggressive
- an extremely aggressive ditch family showed all males had this
However a study for 25 years showed only backed aggressive if suffered child abide
Free will for ag re Asian
Law
Animal research for aggression
Have different more complex brains and social enviro however can study ethically
Neural and hormonal mechanism in agression
• lingic systen
• neurotransmitters - serotonin
• hormones - testosterone
Limbic system and research
The limbic system is made up of the hypothalamus and amygdala which are involved in motivation, emotion and agression.
The amygdala responds to threats.
• A link shown between amygdala and criminal aggressive behaviour
• When damaged amygdalas in animals shows predator like attacks such as rats
• FMRI’s show this activation in brains when offered an unfair offer of money
• However Gage was prefrontal cortex
Serotonin and research
A link between lower serotonin levels and showing aggression
• this link shown in rats
• when individuals given a drug to lower this showed more aggression
Dopamine is also associated with reward behaviours such as agression
Testosterone
In cells in the testes which is associated with aggression at birth
• when castrated mice this showed less aggression, and increased when given testosterone
• when held a g this showed increased agression?
Practical applications of agression
Could cause screening to allow for interventions to reduce it
Perception
Recognition of info about the word from sensory input to quickly make sense of world unconsciously.
Theories are either bottom up (due to sensory data) or top down (prior expectations to interpret data).
Is face perception innate/research
- newborns prefer tho look at stimuli resembling humans faces
- babies as young as 4 days old prefer a schematic than jumbled up face
- researchers flash photos at p’s measuring brain activity. EEG showed that temporal lobe areas associated with higher level visual processing for faces and objects in adults but only faces in infants similarly.
Nature nurture debate of face perception
Babies visual perception is yet to fully mature as change with age.
Do these occur a month later due to experience or a maturing visual system
Abilities in new borns could show nature however could be learning the womb which is nature.
Is face perception special
Suggestions that it depends on different mechanisms than object
It also includes identification, gaze and emotional expression all mediated by differ brain systems suggesting uniqueness
What is involved in face perception and research
Cohen identified 3 processes
1. Face recognition
2. Face identification
3. Face recall
- when a teacher was asked to identify a student out of 4 individuals this deteriorated over time supporting identification.
The brain areas involved are fusiform face area
- identified an area specifically involved.
Support for speciality
- FFA is active in faces not objects
Evolution to recognise own child
However
- shown birds and cards while in fMRI and asked to identify them. Found FFA was active in any highly recognisable thing. Therefore may just be a form of expert object recognising.
Bottom up/feature analysis theory of face perception and research
Stimulus driven which receptors transfer to occipital lobes which groups cues into features into a facial image. Which may either match one in memory or create new.
- modelled Ona. Computer and showed it can be taught following the process
- focus on external features to internal as less likely to change
However
- combined wrong combinations of top and bottom faces which showed 2 halves formed a new holistic face, suggesting whole layout is important
- people find it hard to recall face with scrambled features
- p’s recalled features to construct a photo and judges only correctly guessed 12.5%
Top down/ holistic Bruce and Young’s Theory of Face Recognition and research
This most influential theory suggests it is mainly holistic but involves 8 components/sub processes working together in a sequence. Made up of 2 pathways familiar faces and recognising expressions and therefore assumes faces are special.
Stages LEARN
- 22 p’s kept a record of mistakes when recognising people over 8 weeks and this showed most errors involved remembering info about people, but not their name. This is because PIN comes before NRV.
- P’s we’re faster at identifying whether a particular face of a policing than Id wifi ting their names.
However
- found p’s could retrieve name despite identifying PNI
Applications of face perception
Conditions - prosopagnosia and capgras syndrome
Real world applications - legal system and counter heroism
Capgras syndrome - what it is, research, epidemiology and need for treatment
Delusion of doubled when left is not working on Bruce diagram as conciliatory recognition but not emotional.
In non psychiatric brain damage and psychiatric illness
• women reported doubles replaced her husband - reported by capgras
• linked with rh visual processing and frontal lobe brain lesions
• later thought to damage pathways between recognition and emotion areas
Epiodmilogh
Under 1 percent in psychiatric
1/10 in hospitalised with slxuhosis
Need for treatment as leaf’s to 6% Joni ide
Hard to understand meaning treatments are hard
Anti psychotic med and therapy is best
Prospagnosia what is it, research, explanation
Face blindness where unable to recognise faces unless given non facial description where right is working? of Bruce’s diagram.
Up to 2% of population
• Oliver sacks bumped into a man in the mirror to later realise it was himself
Many brain regions
Appear to have unconscious recognition of faces despite not identifying
• showed them unfamiliar and familiar faces and couldn’t identify despite a psotive galvanic skin response which supports the separate nodes in the skin response
(Look at mindmap)
Eye witness testimony - face perception
A description of suspect:
Construct likeness issuing composite graphical representation and can eliminate individuals.
• using bruces’ theory made faces that most resembled suspect using component analysis by repeating until likeness.
• however found efit was no better as only good when had picture with them
35% when done by p vs 25 by operator
Identifying a lineup: tells police whether they recognise
• naturally assume they must be there
Evaluating face recognition in identity parades research
• investigated how successful line up procedures are by conducting meta-analysis of 30 studies to analyse how many false positives. Found more identifications in stimuktaenosis but also more false supporting relative judgment theory.
• sig number of suspects identified by this later found not guilty by DNA
• 40% right however 20 wrong
Serious crimes and terrorise - face perception and research
Techniques extract key features from Dave image then used to search for matching.
• 75% of false convictions caused by eyewitness innacuracy so AI face recognition could replace this
• super recognisers are employed by police as during London riots 20 police identified 600 rioters vs 1 from a computer suggesting it is trainable
Ageing and cog ability
Leads to decline in it and name teyiriveal but not vocab
Plasticity causes early improvements
• research shows loss in retrieved of names
Memory decline research
• gave p’s one min to say names to faces and showed on top of tongue. When given opportunity showed 95 got it right suggesting that we’re still in memory
Aging frontal lobe causes them to struggle recalling where or when event happened called saucer memory
• an item is borrowed by experimenter at beginning and p’s have to remember to ask for it back to test prospective memory (performing a behaviour in the future)
• however research said these are not realistic
Mechanisms of age related decline in memory search across adult life span
3 hypothesis
- Global slowing process - aging slows cog processes
- Cluster switching hypothesis - retrievel is a dynamic process involving search for categories then recall of words within. Aging slows switch between categories
- Cue maintenance - associated with working memory as use cues to assess info as can focus on one cue whereas aging causes focus on distracting cues.
Dementia
Gradual decline in cog functioning in both s/ltm can lead to confusion, thinking issues and judgment
Alzheimer’s may first affect stm and behaviour, speech, concentration, mood changes and progressively worsens.
Biological basis of dementia
- Abnormal brain functions - amyloid plaques and granuovacultoliar degeneration of the cells cytoplasm
- Significant neuron loss - in frontal and temporal gyri shrink 20%
- Affected cortical areas - olfactory and orbiotofrontal cortex
- Genetics - beta amyloid gene carried 21 or 19 may result in abnormalities in plaque form
Amnesia and research/case studies
Anterograde amnesia is the loss of ability to form new memories after the event
- HM had an operation to remove 2/3 hippocampus, parts of amygdala and temporal lobes. This caused STM to be normal but not LTM.
- Wearing had a brain infection which destroyed his hippocampus and was stuck in snapshots of time
Explanation for this - issues with transfer from STM to LTM, retrieval of info from LTM and disruption of consolidation of memories.
Causes - carbon monoxide, alcoholism and head injuries.
Consolidation and the three processes
A process which stabilises memory after acquisition. 3 process have been suggested.
- Synaptic consolidation - within a few hours of learning
- Systems consolidation - hippocampus memories become independent away from hippocampus
- Reconsolidation - where previous memories can be made liable again
Neurology of consolidation
• long term potentiation - type of plasticity underlying consolidation
• synaptic consolidation - across all species and ltm tasks
• systems consolidation - memories from hippocampus where first encoded then moved to neo-cortex for more permanent storage
Timeline of consolidation
Synaptic is much quicker than system which can’t take up to 2 decades
There is evidence to suggest synaptic can take place within minutes of hours of memory learning
Distributed learning
Can enhance memory consolidation
- experimental results suggest distributing lesrning over 24 hours decreases forgetting
Neural representation
Cognitive and neural systems create representations of the world through single cell recordings, EEG and ERP
Single cell recordings
Invasive procedure where an electrode is implanted into the neuron to collect data is stinuktanelusly recorded from 100 neurons using multi cell recordings and how much a cell responds to a stimulus is recorded to make inferences of cog processes.
This can be coded through rate coding - an increase in the rate of firing of a neuron in response to a stimulus or temporal coding - do neurons respond to the same stimulus
- 2 areas in visual cortex were stimulated fired but with 2 bars of light
- grandmother cell of just 1 thing
Eeg
Non invasive, activated whole population do neurons to create large electric fields
Uses wave structures as these rhymitic oscillations arise as large groups of neurons synchronise firing action potential
For example to look at different sleep stages
ERP
Non invasive, activated whole population do neurons to create large electric fields
Most common EEG when a excitatory neurotransmitter is released this causes positive ion flow into dendtiyes of the post synaptic neuron.
M
For example could investigate face processing
+ good for cognition timings
- not good for spacial resolution
The imaged brain
Structural imaging as different tissues have different properties
CT and MRI
Whereas functional imaging measures moment to moment characteristics in the brain associated with processing
Computerised Tomography
CT scan is where narrow beams of X-rays sent by a computer moving around the head to produce a slice of the brain to calculate how much radiation is going through and produces a slice of the brain pic
Advantage - located brain damage
However invasive
Magnetic resonance imaging
MRI works by applying a magnetic field on the brain aligning the water molecules
Advantages - no ionising radiation
Better spatial resolution than CT
Can detect blood oxygen changes
Position emission tomography
Invasive measure of blood flow by injecting radioactive substance and accumulates to one area and represented as coloured maps
Functional mangentic resonance imaging
Used mri equipment but looks at oxygen whcih distorts magnetic field
Memory where types are consolidated
Episodic and semantic memories are consolidated by the hippocampus and stored in the cortex.
Procldcursl memlries are consolidated by basal ganglia
Contemporary research in memory
Mainly considering how we recall/retrieve information that had already been consolidated
This is most easy to study using episodic memory such as through free recall, serial recall, yes no recognition etc
Original research in memory
For ages it was believed recognition memory involved a single process - familiarity
But
Others thought two processes were involved - recollection (remembering information about a memory) and familiarity (a sense of knowing without knowing context).
Yonelinas’ fual process signal detection model
Familiarity is faster and both processes are independent.
Familiarity can be described via signal detection theory.
Recollection is a threshold proceeds. Info is either retrieved or not,
- changed to context of recognition memory only affects recollection.
- doffenrce levels of processing also only in this, suggesting functionally independent.
Neural correlates of recognition memory
Reservations investigated the temporal lobes role in recognition memory and identified 3 structures in temporal lobe for recognition
1. perirhinal cortex - item based info for familiarity
2. Parahippocampal cortex - where info
3. Hippocampus - binds what and where info
More recently unitisstion hypothesis has been suggested saying the structures in temporal lobes have different roles in recognition but may integrate
Evaluation of neural correlates of recognition memory
Fmri is correlational as it shows it is more active in certain conditions but not nessercarily showing that they are nessercary or what they do
Some areas are feel such as medial temporal love and therefore tricky to investigate in neuroimaging
Biological bases of memory and contemporary research
Remember - know: procedure - a remember response indicates you consciously recollect the word. Where as know indicates you have no recollection of it but you know it was presented before. We’re asked to give confidence ratings on their answers.
Originally developed to differentiate between types of conciseness.
Advantages
Inclusive measure of recognition as it tests both recollection and memory.
Has consistent findings.
Disadvantages
Needs very clear instructions so they understand.
Investigator bias as p’s asked to justify each judgement to the experimenter.
Feedback cycle in addiction
- See a trigger which activates the VTA producing dop.
- Dop activates striatum/nacc which leads to cravings
- Midbrain also releases dopamine which accentuates craving in the nacc meaning it communicates with dpfc to act on craving
- This planning increases visual cortex activation as they imagine doing the behaviour
- Recruits motor cortex to act out the behaviour causing pleasure which reinforces it
- The behaviour causes loss of dopamine and encourages them to seek out the cycle again
- More it is done, more it is strengthened
