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110 Cards in this Set

  • Front
  • Back
What is learning?
>Acquisition of new information or knowledge
What is memory?
>The retention of learned information
What is retrieval necessary for?
>The recall of stored memory
What is the difference between declarative and procedural memory?
Larry Squire's definitions
1. Declarative memory
- memories for facts and events that can be accessed for conscious recollection
(e.g. my first bike was a present on my sixth birthday) this can be subdivided into
- episodic memory (recollecting specific events in time)
- semantic memory (remembering familiar objects or facts)
- working memory (a short-term hold)
2. Procedural memory
- memories that do not require conscious recollection including habits (e.g. knowing how to ride a bike)
What is the difference between short term and long term memory?
>Short term memory
- lasts for a few minutes, usually involves mental rehearsal and is easily disturbed (e.g. the initial stages of learning a telephone number)
>Long term memory
 - more permanent, does not require continued rehearsal, has greater capacity and is quite resistant to disturbance (e.g. memory for familiar telephone numbers)
What proposed processes are there for the development of short term and long term memories?
a. Serial processes
Sensory information -> Short term memory -> (Consolidation) ->Long term memory
b. Parallel processes (shown through drug interference with short term memory without affecting long term memory)
- Sensory information leading to either memory type (consolidated in long term memory)
What is amnesia?
>Memory loss due to brain insult
- typically caused by concussion, chronic alcoholism, tumours, stroke can cause amnesia
- may be retrograde or anterograde
What is the difference between retrograde and anterograde amnesia?
Often occur in parallel
>Retrograde amnesia - loss of memory for events prior to the trauma
- tends to be a defined period of time rather than loss of all memories
>Anterograde amnesia - inability to make or retrieve new memories after the trauma
THERE ARE NO RETROGRADE OR ANTEROGRADE MEMORIES - JUST AMNESIAS
Where are memories stored?
>The engram is the physical storage of memory
>Brain lesions have been used to study which circuitry is essential for memory
>Lashley, in the 1920s studied maze learning in rats with cerebral cortical lesions
>Maze learning impairment was related to the size of the lesion, so Lashley concluded that memories are distributed
>Locations of lesions seemed to be unrelated to the learning deficit so Lashley concluded INCORRECTLY that cortical areas are equipotential for learning
What is the relationship between temporal lobes and memory?
>Kluver and Bucy (1939) - monkeys with large bilateral lesions of the temporal lobes showed 'psychic blindness' - repeatedly put the same inedible objects into their mouths
>Patient H.M. - the most famous clinical case in the human memory literature
- to treat severe epilepsy, at age 27 years, he received bilateral, medial temporal lobe resection (temporal lobes were the source of his epileptic discharges)
- after surgery, the epilepsy was greatly imporved but H.M. shows a nearly profound amnesia that persisted until his death in Dec 2008
- memory deficits were declarative, not procedural
- temporal lobe contains entorhinal cortex, parahippocampal cortex, perirhinal cortex, hippocampus
What are the characteristics of temporal lobe amnesia displayed by H.M.?
>Partial retrograde amnesia
- early childhood
>Profound anterograde amnesia
- no new declarative memories
- in spite of lack of declarative memory
>Retrieval mechanisms undamaged
>Short term memory relatively normal
>Procedural memory normal
Which area of the brain is implicated in recognition memory?
>Temporal lobe
- lesions here, and especially perirhinal cortex
What are the critical structures involved in medial temporal lobe amnesia?
>Originally the hippocampus and amygdala were thought to be critical for declarative memory loss
>More recently it has been shown that the critical areas are the rhinal and perirhinal cortex
>Reciprocal connections allow for additional output pathways from the associative circuitry
- very few connections are one way connections
Which structures in the diencephalon are involved in memory?
>Anterior or dorsomedial nuclei of the thalamus, or the mamillary bodies of the hypothalamus also disrupt memory
>Hippocampus -> Fornix -> Mammillary bodies ->Anterior nucleus of thalamus -> Cingulate cortex
>Temporal lobe cortex, amygdala -> Dorsomedial nucleus of thalamus -> prefrontal cortex
>Midline thalamic lesions in monkeys produce deficits in DNMS (delayed non match to sample)
What occurred to N.A. when he received damage to his diencephalon in the midline?
>Stabbed with a fencing foil through his right nostril
- traveled leftwards through the midline thalamus - particularly left dorsomedial thalamus
>Severe anterograde amnesia and retrograde amnesia for the two years before the accident
- difficulty watching TV programs
- strong similarities with H.M.
What occurs in Korsakoff's syndrome?
>Chronic alcoholism depletes thiamine (vitamin B1) reserves and can lead to an amnesic state with anterograde amnesia and limited retrograde amnesia (Korsakoff's amnesic state)
Amnesia relates to degeneration of the mammillary bodies and dorsomedial nucleus of the thalamus
>Other neurological signs can include ataxia, especially of gait, due to degeneration of the cerebellar anterior lobe vermis, so gait is affected by distal limb control is not. There may also be a confusional state
>Treatment with B1 can lead to remarkable and rapid recovery of the motor and confusional problems but the amnesias usually persist
What other neuropathologies cause memory loss?
>Alzheimer's disease
- age dependent
- neurofibrillary tangles (phosphorylated tau) and neuritic plaques (amyloid), disease severity correlates with tangles, not plaques
- Structures affected first = hippocampus and posterior parieto-temporal cortex
>Also degeneration of basal nucleus of the forebraine (nucleus of Meynert) cholinergic neurons, noradrenergic neurons in locus coerulus, and serotonergic raphe neurons
>Retrograde amnesia spreads back in time as disease progresses
>Episodic memory affected the most, working and semantic memory less so
- procedural memory not impaired until the final stages
What is the nucleus which degenerates in Alzheimer's disease?
>Basal nucleus of the forebrain (nucleus of Meynert) cholinergic neurons
What therapy is being evaluated for Alzheimer's to maximise residual cholinergic function?
>Cholinesterase inhibitors
- results are marginal but progress of the disease may be slowed
What is working memory?
>Sometimes, information of several types needs to be held in a short term store at the same time (e.g. a book title, colour of the cover, location on the shelf)
>This information may be new sensory information, or information retrieved from long term storage ready to access
>This ready to use form is working memory
What memory straddles the episodic / semantic divide?
Working memory
What is the structure of the circuit from the medial temporal lobes to the cingulate and prefrontal cortex?
TO CINGULATE CORTEX
Medial temporal lobe structures -> Hypothalamus -> Anterior nucleus of the thalamus -> Cingulate cortex
TO PREFRONTAL CORTEX - working memory functions:
Medial temporal lobe structures -> Dorsomedial nucleus of the thalamus -> Prefrontal cortex
What are the key points to remember about memory?
>No single place in the brain for memory formation and storage
- different forms of memory may be mediated by different brain areas
- even within a brain area, memories seem to be distributed
>Short term memories are fragile, long term memories are robust
- therefore long term memories probably depend on some form of structural change
>Declarative memories are critically dependent upon medial temporal lobe and nuclei in the diencephalon
>There is good evidence that procedural memory with a strong motor component e.g. riding a bike is dependent upon the cerebellum
What are examples of animal models for the study of learning?
PAVLOV
- classical conditioning
- autonomic reflexes or skeletal muscle reflexes were conditioned to previously neutral stimuli
THORNDIKE
- puzzle boxes, testing cats abilities to learn complex escape procedures
- Skinner introduced a box for use in studying rats
What is non associative learning?
1. Habituation - the gradual waning of a response with repeated presentations of a stimulus
2. Sensitisation - the enhancement of responses to a stimulus after exposure to a highly arousing event
What are memories made of?
Donald Hebb 1949 suggested:
""when an axon of cell A is near enough to excite cell B or repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such athat A's efficiency, as one of the cells firing B, is increased""
>it is now widely agreed that alterations in synaptic strength are the most likely mechanism underlying learning and memory formation

THOSE CELLS THAT FIRE TOGETHER, WIRE TOGETHER
What is LTP?
>The long-lasting enhancement in signal transmission between two neurons that results from stimulating them synchronously
>Induced by strong (tetanic) activation of an afferent input sufficient to activate NMDA receptors
>Alternatively, a weak input can also undergo LTP if it coincides iwth post synaptic depolarisation caused by another strong input
What is altering at a cellular level post LTP induction?
>The number of glutamate receptors present on the postsynaptic neuronal membrane
What are the key characteristics of LTP? "1. A brief high frequency tetanus leads to a long lasting potentiation
2. It is input specific
3. LTP can be associative
- a weak input can also undergo LTP if it coincides with postsynaptic depolarisation caused by another, strong input
- or two weaker inputs can summate to depolarise the neuron and can each undergo LTP
What is meant by associative learning through LTP?
>A neurone receives inputs relating to the sight of a rose (A), the smell of a rose (B) and the smell of an onion (C)
- individually none sufficient to depolarise the neurone
>A and B often occur together so LTP occurs at both inputs
- A or B can now activate the cell but C cannot
>The neuron can now 'recognise' a rose by sight or smell and the modalities are associated
- this sort of learning is more likely a property of networks of neurons rather than individual ones
INCREDIBLY SIMPLIFIED, WOULD BE OCCURRING IN NETWORKS OF NEURONES ETC.
What is the mechanism for LTP?
LTP depends upon post-synaptic Ca++ levels
>Ca++ enters through the NMDA receptor to activate protein kinases
>These can change the effectiveness of existing AMPA receptors or contribute to inserting new AMPA receptors
>Postsynaptic Ca++ levels are critical and depend upon the exact level of NMDA receptor activation
>If Ca++ levels are not so high LTD can occur
What is LTD and what causes it?
>Removal of postsynaptic receptors, associated by intermediate to low levels of Ca++
>If an input is stimulated with a low frequency tetanus, an input specific LTD can be measured
>If LTP were the only synaptic mechanism available for learning, then neural networks might saturate through a lifetime
>Information storage in learning and memory formation is likely to depend upon LTP and LTD processes
What occurs in cerebellar long term depression?
>Conjunctive activation of climbing fibre inputs and parallel fibre inputs leads to a long-term depression of parallel fibre synapses upon Purkinje cells
What are the mechanisms for cerebellar long term depression?
>Molecular mechanisms are the same as for cerebral LTD
- differences in receptor type (Na+ voltage gated channels in lieu of NMDA receptors)
>Parallel fibres activate AMPA receptors, climbing fibres Na+ voltage gated channels
- in purkinje cells it is LTD rather than LTP
What is the difference in memory formation between frontal cortex vs. cerebellar?
>LTP driving force in frontal cortical areas whereas these changes are drawn back by LTD
>In cerebellum, LTD drives memory formation and reversed by LTP
What does eyeblink conditioning depend upon in the brain?
>The cerebellum
- large cerebellar lesions abolish NM CRs ipsilaterally
- simple implementation for eyeblink/NMR conditioning"
What cell is essential for normal eyeblink conditioning?
>Purkinje cells
- suggests pf-LTD could be an important mechanism in cerebellum-dependent procedural learning
What are likely candidates for memory formation?
>LTP and LTD
- cellular and molecular mechanisms of learning and memory are still to be confirmed
What are typically shrunken in Korsakoff's syndrome?
>The mammillary bodies
What are the conventional tools used for brain imaging?
>CT-MR-Angio
>Conventional MR
>DWI
>fMRI
Historically what has been used for the brain?
X-Ray
- radiography
- myelography / cisternography
- angiography
- computerised tomography
What is CT used for?
>To review skull and brain parenchyma
- very powerful for eye diagnosis
How do hypo and hyperdense structures appear on a CT?
>Hypo = dark e.g. stroke, infarct
>Hyper = white e.g. tumour, calcification
What is the chance of causing a neurological deficit in contrast angiography?
>0.5%
What is DW MRI
>Diffusion weighted MRI
- very clear view of extent of damage
What is fMRI used for?
>Detecting function
>Regional blood flow is closely related to neural activity
- neural activity results in increased local blood flow and oxy-Hb
- bulk effect is a regional decrease in deoxyhaemoglobin
- from an imaging perspective deoxy Hb is useful as a contrast medium
What is interventional MR?
>Patient is scanned during surgery to visualise progress of surgery
- effective procedure
How do viruses invade the CNS?
1. Via nerves
- HSV - latency in trigeminal or sacral ganglion
- VZV - latency in dorsal root ganglia
- rabies virus (can take a while to travel through nerves, e.g. bite on foot can take up to a year to reach brain)
- prions - e.g. Creutzfeld Jakob Disease (NOT A VIRUS)
2. From blood vessels by:
a. passive transfer of free virus
b. in leucocytes e.g. HIV
c. infection of endothelial cells
- aided by inflammation
3. Getting in via the CSF
What are the characteristics of the blood brain barrier?
>Capillary endothelium - tight junctions
- vessels surrounded by pericytes (glial cells)
What are the characteristics of the blood CSF barrier?
>Capillary endothelium - fenestrated in choroid plexus
What types of CNS disease can viruses cause?
1. Meningitis
- infection and inflammation of meninges (enteroviruses)
2. Encephalitis - genetic predisposition to disease
- Inflammation of brain, infectious (HSV, enteroviruses, rabies, JC - opportunistic), post infectious
3. Paralysis
Flaccid - lower motor neuron
- infectious: poliovirus
- post infectious: Guillain Barré syndrome
Spastic - upper motor neuron
- after severe encephalitis
What sort of paralysis does polio cause?
>flaccid - lower motor neuron
What sort of virus is poliovirus?
>Picornavirus
>Genus enterovirus
>RNA positive sense
>Capsid but no envelope (persistant in environment)
>Type 1, 2 and 3
What occurs in polio infection?
>Disease = tip of the iceberg
>Poliomyelitis
- meningitis and flaccid paralysis
- rarely encephalitis
Etymology of poliomyelitis?
Polio = grey
Myelon = marrow i.e. spinal cord
It is = inflammation
How does poliovirus get to the central nervous system?
>Ingested, enters gut, infection and disease is distant from portal of entry
- into lymphatics, via thoracic duct, bloodstream, primary viraemia, multiplies, secondary viraemia, enters CNS - could be volume dependent entry, then invades the CNS, high level of antibody in serum, paralysis, virus shed in faeces
What cells can be found in the CSF upon poliovirus infection.
>Bacterial infection - neutrophils
>Viral - t-lymphocytes
Where can virus be detected in polio?
>Blood
>Throat
>Faeces
>CNS
What can polio vaccine convey?
>Immunity to wild type infection
- life long
- type specific
>Vaccine available for types 1, 2 and 3
- killed (IPV) or live (OPV)
What is the difference between killed or live vaccine?
>Killed or Salk (IPV):
- virulent wild virus infectivity
- inactivated physically / chemically
>Live or Sabin (OPV)
- attenuated avirulent mutants
- may reactivate"
How were avirulent mutants made? ">Poliovirus grown in tissue culture
>Repeated subpassage mutations accumulate
>Test for paralytic activity in monkeys
>Use non virulent strains for clinical trials in humans
cDNA used for sequencing
What is the risk of developing polio from OPV?
<1/1,000,000 recipients
<1/1,000,000 contacts
agammaglobulinaemics risk >x10,000
Can polio be eradicated?
>Effective injectable vaccine
>No animal reservoir
>Lifelong immunity
>Not like smallpox which is visible, not easy to see polio - can remain
What is the major barrier to complete eradication of poliovirus?
>Faecal shedding of virus
>Risk of reversion to neurovirulence
- can be shed neurovirulently for many years
Which countries have endemic polio?
Nigeria, Afghanistan, Pakistan
Why doesn't the brain become typically affected by antigens?
>Normally the brain is shielded from the immune system to limit inflammation
>The blood brain barrier restricts the movement of immunologically important cells and molecules into the brain parenchyma
- all or nothing situation
- there is regulation of entry of these cells
What is the structure of the blood brain barrier?
>Endothelium with tight junctions, surrounded by pericytes and astrocytes
What is meant by the term 'immune privileged site'?
>Areas that would be particularly damaged by an inflammatory response
- e.g. brain, eye, testes
>Lacks classical lymphatic drainage
- lymphoid cells are normally excluded from the brain, spinal cord and peripheral nerves
HOWEVER
- multiple anatomic and physiological connections exist between the CNS and the immune system
- Macrophages are physiologically present
- It is now known that other cells of the immune system are able to enter the CNS
- But classical inflammatory reactions are avoided in order to avoid intrathecal swelling
What are the four main types of marrow derived CNS macrophages?
>Microglia - Parenchyma
>Perivascular macrophages - Basal lamina of small blood vessels
>Meningeal macrophages - Meninges
>Choroid plexus macrophages - Interface between blood and CSF
Which CNS macrophages have the fastest rate of replenishment from blood monocytes?
>Meningeal macrophages
followed by:
- perivascular
- choroid plexus
- microglia
What are the characteristics of microglia?
>Resident macrophages of the CNS parenchyma
>Largely replaced by proliferation of the microglia within the CNS
>First line of immune defense in CNS parenchyma
>Phagocytic
>Can present processed antigen to T-cells
>Can secrete proinflammatory cytokines including IL-6, IL-1 or TNF-α
When do microglia become activated?
>Only when they encounter damaged tissue
- e.g. local damage to nerve cells, encourages slight activity
>Serious damage induces reactivity
How do immune cells enter the CNS?
>Across the BBB
>Across blood spinal cord barrier
>Across choroid plexus (blood CSF barrier) into ventricular system
What is meant by multiple sclerosis?
>Skleros = hard (plaques)
>Multiple - many areas of the immune system have affected myelin
What are the characteristics of MS?
>Can occur at any age - but in most cases symptoms are first seen between the ages of 20-40
- F:M 2:1
>Polygenic, including HLA-DR15/DR5 in caucasians, environmental factors are also required
>Most common neurological condition among young adults in UK, affecting ~85,000 people
>CNS becomes demyelinated (plaques)
>Characterised by episodes separated in time and space
>Around 50% of patients unable to walk unaided within 15 years of diagnosis
What is the mechanism for MS?
ANTIGEN IS DRIVING THE IMMUNE RESPONSE
1. For some reason, perhaps viral infection or tissue damage, the antigens recognised (autoantigens) are released from the CNS, which end up in secondary lymphoid tissues
2. Lymphocytes activated, Th, CTLs and B cells, leave tissue and home back to CNS
3. Damage caused!
What are possible myelin sheath antigens in MS?
1. MAG: Myelin associated glycoprotein
2. MBP: Myelin basic protein
3. MOG: Myelin oligodendrocyte glycoprotein
4. PLP: Proteolipid protein
What are the culprits for causing serious damage in the CNS?
a. CD8+ T Cells
- induces apoptosis via FAS
- cell lysis
b. Glutamate, neurotoxins
c. Antibody - Antigen binding
- complement activation
- MAC
d. Cytokines and chemokines
- may be beneficial and harmful
What is the role of Th17 cells in MS?
>Th17 lymphocytes appear to be essential in the pathogenesis of numerous inflammatory diseases
>Expression of IL-17 and IL-22 receptors on BBB endothelial cells in multiple sclerosis lesions
>IL-17 and IL-22 disrupt BBB tight junctions
>Th17 lymphocytes transmigrate efficiently across BBB-ECs, highly express granzyme B, kill human neurons and promote CNS inflammation through CD4+ lymphocyte recruitment
What is myasthenia gravis?
>Disorder of neuromuscular transmission characterised by abnormal fatigability of skeletal muscle ranging from transient double vision to life-threatening respiratory paralysis
>Prevalence is 1 in 10,000
>All ages can be affected
>Often presents with weakness in muscles controlling eye and eyelid movement
>Transient neonatal myasthenia in ~10% of babies born to myasthenic mothers due to transfer of maternal IgG autoantibodies
What does the autoantibody in MG cause to happen?
>Prevent Ach binding to receptors and causing response
>Cause a loss of receptor from the surface
What is Guillain-Barré syndrome?
>An inflammatory peripheral neuropathy
>Often preceded by a viral like illness - cause unknown but myelin and nerve axons destroyed
>First symptoms are numbness, paresthesia (burning or prickling sensation), weakness, pain in the limbs
>Progressive bilateral and relatively symmetrical weakness of the limbs
>Respiratory insufficiency in 25% of patients
>Significant mortality risk
What events trigger GBS?
>URTI or diarrhoea precedes onset in two thirds of cases
>Immunisation
>Pregnancy
>Surgical procedure
>Lymphoma
What infections are linked to GBS?
>Campylobacter
>CMV
>EBV
>VZV
>Mycoplasma pneumoniae
What are the immunological features of GBS?
>Mononuclear cell infiltration of affected peripheral nerves
>Antibodies to myelin components
>Peripheral T cell activation
What is the pathophysiology of GBS?
>Potential cross reactivity between GM-1 ganglioside in nerve cell membranes and campylobacter jejuni lipo-oligosaccharide
>Ab response made against pathogenic Campylobacter, but binds to our own body components with a similar structure
>Leads to Ab binding, complement activation, nerve damage, macrophage activation etc.
What is the treatment for GBS?
>Intravenous Ig or plasma exchange
What is the prognosis for GBS?
~5% patients die from respiratory failure, pulmonary emboli or infection
~20% of patients have residual disability, with weakness or persistent sensory disturbance
What are early behavioural warning signs for children at risk for psychopathy?
>Lack of remorse and guilt
>Callous lack of empathy
>Shallow affect
>Manipulation of others for own gain
>Thinks is more important than others
NB.
- children with these traits differ from other children with antisocial behavious and from children with Autism Spectrum Disorder
- these traits are predictive of persistent and violent behavioural disorders in adolescence and adulthood
- often these children have lower levels of anxiety and do not worry about hurting others
What is CU?
>Callous Unemotional
How do CU and antisocial behaviour children have issues with affective processing?
>Have problems processing other people's distress - fear and sadness
>Report feeling less fear themselves
>Low startle response
- blink in response to threatening images
>Poor ability to learn from punishment
- poorer set of tools to teach children
What are the varying risk factors between CU and non CU antisocial individuals?
>CU - genetics predominate
>Non CU - environmental and genetic factors are involved
With what sort of parenting and treatment is antisocial behaviour with CU associated?
>Not associated with harsh and incompetent parenting
- may get better with warm parenting
>Does not respond to all existing treatments
With what sort of parenting and treatment is antisocial behaviour without CU associated?
>Associated with harsh and incompetent parenting
>Responds to existing treatments
What are the ethical implications of studying psychopathy in children?
>Negative connotations associated with the term callous unemotional
- studies suggest that labelling effects are not more negative than the label conduct disordered
>Worries about the connotations of a stable and untreatable dispositional tendency
- appropriateness of this assumption is questionable even in adults
- especially in children for whom there is clear evidence that these features can change across development
>Previously attempts ro reduce the potentially stigmatizing effect of the label - the term undersocialised was used in diagnostic classifications
- lack of clarity led to poor research in the area
>Terms that only focus on part of the definition e.g. unempathic could lead to other dimentions e.g. lack of guilt and remorse that research has indicated as being important being ignored in clinical assessments
- important that the term used is very clear and descriptive of the construct that is being assessed in the diagnostic criteria
>Danger if less severe terms (e.g. uncaring) used for labelling
- can widen population diagnosed unnecessarily
- treatment development for the severe subgroup of children is more urgently required
Which aspects of cognition and behavior involve memory?
Almost every aspect of cognition and behaviour requires memory
- remembering significant events
- talking
- reading
- deciding
- navigating
- recognising friend's faces
- riding a bike
- imagining your future
What is memory?
>Capacity for storing and retrieving information that is acquired through our senses
>The record of past experiences acquired through learning, ability to recal or recognise previous experiences
>The mental capacity or ability to store, retain, revive and use facts, events impressions
>An alliance of systems allowing use to learn from the past and predict the future
What three things must a memory system be capable of?
>Registering information (encoding)
>Storing information over time (storage)
>Retrieving information when required (retrieval)
In what functional ways might memory systems vary?
>Storage duration
- fraction of a second to a lifetime
>Storage capacity
- tiny buffer stores to an unknown large capacity for long term
Who was patient HM?
>Henry Molaison
- September 1 1953, 27 year old man underwent surgery to stop epileptic seizures
- Dr. Scoville bilaterally removed HM's medial temporal lobes
Which structures were removed from HM's brain?
>Medial temporal lobes containing
1. Anterior hippocampus
2. Amygdala (fear, emotions)
3. Perirhinal/Entorhinal cortex
What is the function of the hippocampus?
>Present in medial temporal lobe, important for long term memory formation
Where is the amygdala found?
>Area of the brain close to the hippocampus involved in emotional processing
What memory was affected in patient HM?
>Anterograde amnesia
- HM could remember everything that happened prior to the operation (i.e. elementary school), but couldn’t hold on to new information for more than a few minutes
- normal short term memory, impaired long term memory for new events
:. hippocampus must be required for transforming short term memories into long term memories
What type of memories was HM able to acquire?
>Skill memories (e.g. mirror drawing)
- not long term declarative memories
- can't remember doing the task, but the motor skill improves
What is the difference between declarative and non declarative memory?
DECLARATIVE:
- episodic (specific, personal events)
- semantic (facts)
>Consciously accessible or explicit
- you know that you know
>Easy to verbalise or declare your knowledge
>Open to intentional retrieval
NON DECLARATIVE:
- skill memory
- priming
- conditioning
>Not always consciously accessible or easy to verbalise
>Retrieval of information from LTM through performance rather than explicit conscious recall or recognition
>Skill/Procedural (mirror writing, riding a bicycle)
>Priming (influenced in a non conscious was to what has happened to you recently)
>Conditioning
What is anterograde amnesia?
>Inability to form new declarative memories
What is retrograde amnesia?
>Loss of episodic memory prior to the trauma
How is declarative memory tested? Who would have failed these?
1. Free recall = asked to generate info from memory
2. Cued recall = hint or prompt used to jog memory
3. Recognition = correctly deciding whether they have encountered a stimulous previously in a particular context
>Someone without BTLs e.g. HM
How is non declarative memory tested?
>Skills - mirror drawing
>Priming - previous exposure will tend to elicit replicative responses
What does no fear conditioning response indicate?
>No amygdala
What does no declarative memory for association indicate?
No hippocampus