week 6 - memory Flashcards
Outlin
learning and memory types of memory brain regions involved in memory false memories memory loss
Learning and Memory
Learning: process of acquiring new information
Memory: created when something is learnt
sensory memory
time course: milliseconds to seconds
capacity: high
conscious awareness: no
mechanism of loss (primarily decay)
short-term / working memory
time course: seconds to minutes
capacity: limited (7+-2 items)
Conscious aware: yes
mechanism of loss: primarily decay
Long-term nondeclarative
timecourse: Days to years
capacity: high
conscious awareness: no
mechanism of loss: primarily interference
Long-term declarative
time:course -days to years
Capacity- high
conscious awareness: yes
mechanism of loss: primarily interfence
3 Major processing stages
Learning & memory 3 major processing stages 1. Encoding --Acquisition --Consolidation 2. Storage 3. Retrieval
Impairments in memory function: Amnesia
Memory loss due to lesion/s in brain
Memory deficits dependent on lesion location
—Can impact STM, WM, and LTM abilities
Anterograde amnesia
- -Inability to learn new info
- -No memory for after time of lesion
Retrograde amnesia
- -Loss of memories from before lesion
- -Loss ranges widely (few hours before lesion >majority of lifespan)
hypothesised structure of human memory
see slide 7:
LTM vs sensory/short term and working
LTm consists of declarative (explicit) and nondeclarative (implicit)
declarative memory consists of
events (episodic) and facts (semantic) memory
episodic memory = specific personal experiences from a particular place and time
semantic memory = world knowledge, object knowledge, language knowledge, conceptual priming
Nondeclaritive (implicit memory) = procedural (skilss (motor/cog)), perceptual reprresentation system (perceptual priming), classical conditioning, nonassociative learning (habituation, sensitization)
What is Sensory Memory / whats it do
Transient retention of sensory information in sensory structures
Echoic
- -Auditory
- -Lasts around 10s
Iconic
Visual
300-500ms
High capacity but only for a short time
What is Short-term Memory / what is its function?
short duration (~30s) limited capacity (7+/-2 items) Modal model --decay: info degrades over time --Interference: new info displaces old info
short term memory - Atkinson and shiffrin modal model of memory
Sensory information enters the information-processing system and is first stored in a sensory register. Items that are selected via attentional processes are then moved into short-term storage. With rehearsal, the item can move from short-term to long-term storage.
Working Memory model proposed by baddeley and hitch
see slide 10
This three-part working memory system has a central executive that controls two subordinate systems: the phonological loop, which encodes information phonologically (acoustically) in working memory; and the visuospatial sketch pad, which encodes information visually in working memory.
working memory (capacity/mental ops) anatomical correlates
slide 10
Limited capacity store for retaining info over short term (maintenance) and performing mental operations (manipulation)
Seconds to minutes
Baddeley & Hitch (1974)
- Phonological loop: BA44 and BA40 (supramarginal gyrus)
- -Visuospatial: parieto-occipital region
Lateral view of the left hemisphere, indicating that there is an information loop involved in phonological working memory fl owing between BA44 and the supramarginal gyrus (BA40).
What is episodic memory/hows it work?
Memories of personal experiences about own lives
What, where, when, and with whom
Autobiographical memories
Differs from personal knowledge
what is semantic memory
Objective knowledge that is factual in nature but does not include learning context
–Fact can be learnt after single episode or after many exposures
Examples
- -Capital of France = Paris
- -Red Light = Stop
Procedural
Requires extensive and repeated experience
Learning motor or cognitive skills
Test: serial reaction time task
–Healthy participants respond faster to repeated sequences over time even if unaware of them
—Anterograde amnesiacs respond faster to repeated sequences over time but don’t remember doing the task
–Procedural learning can proceed without episodic memory
Brain region: Basal ganglia (impaired in Parkinson’s and Huntington’s)
Priming
A change in the response to a stimulus, or in ability to identify a stimulus, following prior exposure to that stimulus
Perceptual
- Acts within perceptual representation system (PRS)
- E.g. word-fragment completion task
- Depends on perceptual system (visual cortex)
Conceptual
- Not as long as perceptual
- Related to conceptual features
- E.g. Landmark in Paris
- Impacted by lesions in lateral temporal and prefrontal regions
Semantic
- Prime and target words different but related semantically
- Lasts only a few seconds
Classical conditioning
CS + US = CR
Delay conditioning
-US begins while CS is still present
-Not impaired with hippocampal damage
Trace conditioning
- Time gap, memory trace is necessary for association to be made between the CS and US
- Impaired with Hippocampal damage
Conditioned stimulus (CS) paired with unconditioned stimulus (US) and becomes associated with it. CS will evoke a conditioned response (CR) similar to that typically evoked by the unconditioned stimulus (UR).
Nonassociative learning
Habituation
- Response to an unchanging stimulus decreases over time
- E.g. ticking clock
Sensitization
- Response increases with repeated presentations of the stimulus
- E.g. rubbing your arm
https: //www.youtube.com/watch?v=aOLxQGLJouI
Nonassociative learning primarily involves sensory and sensory motor (reflex) pathways
While not exactly sensitisation, think of it like this the more the stimulus, the greater the response:
Important Brain regions for memory
Medial Temporal Lobe
- Hippocampus
- Entorhinal, peririhinal, and parahippocampal cortices
- Mammillary bodies
- Anterior thalamic nuclei
- Bilateral resection results in severe amnesia
Important Brain regions for memory
Hippocampus: involved in encoding, consolidation and retrieval of LTM’s
Primate studies: hippocampus lesion or damage in/output connections with neocortex = cannot form new LTM’s
Circuitry to MTL/hippocampus
-Tumours, stroke, trauma, Korsakoff’s syndrome etc.
Encoding and the Hippocampus
Ranganath et al (2003) used fMRI
- Subsequent-memory paradigm
- Hippocampus and posterior parahippocampal cortex active during encoding
see slide 22 (watch this)
Retrieval and the Hippocampus
Eldridge et al (2000) used event-related fMRI
- -Encoding phase: remember list of words
- -Retrieval phase: 20 mins later with imaging
- –Recollected versus familiar
- -Hippocampus active only for correctly recollected items
- –Not familiar words
- —(familiarity = perirhinal cortex)
False Memories
Roediger & McDermott (1995)
- Memory test examining false memories
- Present words (i.e. pin, sewing, eye etc.) highly associated with word not presented (i.e. needle)
- Strong tendency to falsely remember associated word not presented
Cabeza et al (2001)
- -Reject new items but strong tendency to falsely recog closely related false items
- -Hippocampus (bilateral) = more activation for false and true items than new
- -Retrieval of semantic info
- -Left parahippocampal gurys = more activation true items than false and new
- -Retrieval of sensory info
Real-world applications (EWT)
https://www.youtube.com/watch?v=qQ-96BLaKYQ
Case Study: H.M.
VIDEO: https://www.youtube.com/watch?v=SQASyR0w8Qo
Bilateral resection of medial temporal lobes to successfully treat severe epilepsy
—Removed temporal lobes including amygdalae, entorhinal cortex and hippocampi (half of posterior region intact but atrophied)
–Anterograde amnesia: no new LTM’s
Retrograde amnesia: 2 yrs pre-op
STM, sensory, working and procedural memory stayed intact (and no other cognitive deficits)
-Could learn new skills but not remember learning/practicing them
Conclusion: medial temporal lobes involved in forming new LTM’s
Hippocampus
Case study R.B.
Case study R.B.
Lost memory after ischaemic episode during heart surgery
-Anterograde amnesia: no new LTM’s
-Mild retrograde amnesia (1-2yrs pre-op)
- Autopsy: bilateral lesions to CA1 pyramidal cells in hippocampus
- Conclusion: hippocampus crucial in formation of new LTM’s
Transient Global Amnesia (TGA)
- Similar evidence found in TGA
- –When lesions occur in CA1 in hippocampus
- –Causes transient anterograde amnesia and retrograde amnesia (spanning weeks – years) that lasts approx. 24-48 hours
Alzheimer’s’ Disease
https://www.youtube.com/watch?v=9Wv9jrk-gXc
Amyloid plaques and neurofibrillary tangles
congregate in MTL area
More atrophy in MTL = more episodic memory loss
Hippocampus deteriorates more rapidly in people with AD than healthy adults
Large loss of acetylcholine cells that connect hippocampus and prefrontal cortex > loss of ability to form new episodic memories
Comparison of cortex in Alzheimer’s patients and normal participants.
see slide 27
These diagrams depict a normal section of cortex with cortical neurons (a) and a section of cortex in an Alzheimer’s patient containing amyloid plaques between neurons and neurofibrillary tangles within neurons (b).
https://www.youtube.com/watch?v=9Wv9jrk-gXc
Case Study: Clive Wearing
https://www.youtube.com/watch?v=fhrmsK6jtjc
Musicologist, conductor, and musician
- Contracted herpes virus encephalitis that attacked CNS
- -Damaging hippocampus
Both retrograde and anterograde amnesia
- -Remembers that he has children (not names) and that he loves his wife
- -Memory lasts between 7-30 seconds
- -Constantly ‘waking up’
- Can still conduct and play piano (procedural memory still intact)
- Memory important for the human experience
