learning and memory Flashcards
memory
group of mechanisms or processes by which experience shapes us, changing our brains and our behaviour
involves direct changes to the makeup of our brain
amnesia
loss of memory (including an inability to form new long-term memories
HM is the most famous case study. He participated in studies over multiple decades. His amnesia followed surgical resection to control his epilepsy. after his surgery, HM could not form new long term memories.
amnesia damage
damage to regions of the medial temporal lobe including:
hippocampus
dentate gyrus
subiculum
amygdala
parahippocampal area
long term potentiation
the hippocampus receives via the entorhinal cortex highly pre processed input about the “items” encountered in the environment
exhibits this phenomenon which is repeated activation of pathways producing a long-lasting increase in signal transmission between neurons (facilitating AP firing)
after LTP, the same amount of presynaptic stimulation results in greater/stronger post synaptic potential (facilitates action potential firing)
synaptic plasticity
larger graded potentials facilitating APs firing can also come from: interneuron modulation, formation of new synapses
synaptic input can also be rearranged based on usage
midline diencephalic region damage
can also cause amnesia
particularly when the dorsomedial nucleus of the thalamus and the mammillary bodies of the hypothalamus are damaged
what is midline diencephalic region damage caused by
korsakoff syndrome
chronic alcohol abuse
via and accident
retrograde amnesia
memory impairment for information acquired prior to the event that caused the amnesia
temporal extent can vary greatly, from minutes to decades
the greater the damage to hippocampal regions, the greater length of retrograde amnesia
impaired episodic memory
characterized by a temporal gradient where there is a greater compromise of more recent memories than more remote memories
gradients of retrograde amnesia suggest that memory may undergo a process of consolidation during the time after learning
anterograde amnesia
there is a deficit in learning new information after the onset of amnesia
typically occurs in association with at least some retrograde amnesia
episodic memory
memories of events of the past including autobiographical information of our experiences
autobiographical memories of specific episodes in our lives - re experiencing events
remembering your last bday
semantic memory
usually stays in tact for the basic perceptual, motor, linguistic, and intellectual competences a person had before the onset of amnesia
they also retain information learned early on in life about language, objects and the world in general
knowing that monkeys have tails
knowledge of facts, concepts and categories - generalizing knowledge
working memory
the ability to hold a limited amount of information on-line over the short term while information is being actively used or processed
unaffected after damage to hippocampus
HM had an intact working memory span, however once working memory was exceeded performance suffered
the ability to retain limited amounts of information for a short time while actively working with that info
- patients can show a selective impairment in working memory while at the same time, having intact long-term memory
- hippocampal damage patients with intact working memory and disrupted long-term memory suggest that the forms of memory rely on different brain areas
hippocampal damage and skill learning
even after hippocampal damage, skill learning is still possible
this is the acquisition (usually gradually and incrementally through repetition) of motor, perceptual or cognitive operations or procedures that aid performance
first demonstrated in HM via a mirror-drawing task
- even though he could not remember doing the task previously, his performance improved with increasing practice
dissociation in amnesia
skill learning occurs even when patients: cannot recollect the training events, cannot recall or recognize the material or have no insight into their improved performance
dissociation in amnesia is probably best illustated by the word-stem completion task
morris water maze
the dissociation between episodic memory and other forms of memory can be demonstrated in both rodents and nonhuman primates
rat swim to constant ledge but can not see because opaque water
put them in a different starting position they start to wander
explicit memory system
lost in amnesia
permits the conscious recollection of prior experiences and fact
implicit memory system
allows prior experience to affect behaviour without the individual consciously retrieving the memory or even being aware of it
declarative memory system
people know information and can use is flexibly outside of the the situation in which it was aquired
fact
possible to retrieve semantic information without hippocampus
some aspects of semantic memory may rely on domain specific neocortical processors
anterior temporal lobe regions may play a role in retaining info that is not linked to a particular modality
procedural memory system
appears to support memory of “how” things should be done, allowing for the acquisition and expression of skill
how to do smt
skill memory
long term memories broken into
declarative (explicit) and non declarative (implicit)
declarative (explicit) memory is broken into
episodic and semantic
non-declarative (implicit) memory is broken into
skill learning, priming and conditioning
skill learning
knowing how to ride a bicycle
procedural
priming
being more likely to use a word you recently read
conditioning
feeling anxiety when you enter a dentists office
reinforcement from previous visits
the basal ganglia: skill learning
patients with basal ganglia damage (parkinson’s or huntington’s diseases) show memory deficits opposites of those seen in patients with hippocampal damage
deficits on skill learning tasks
intact explicit/declarative memory
their difficulty is observed with habit learning tasks such as the rotary pursuit task and the serial reaction time task
error driven learning
occurs when the prediction between an expected outcome and the actual outcome are at odds
this error driven learning mechanism tends to be implicit in nature
individuals can learn from these action-outcome associations without being aware of them (implicit and procedural)
the basal ganglia and error-driven learning
the basal ganglia rely on dopaminergic neuron signalling
dopaminergic cells increase firing to an unpredicted reward and decrease firing when a reward is predicted but does not occur
dopaminergic cells fire in relation to whether or not a reward is expected, which acts as a learning signal
amygdala
major role is associating stimuli with an emotional response
bilateral amygdala damage disrupts the enhancement of memory for emotional information, but doess not affect memory neutral info
responds to highly arousing, emotional situations by influencing the memory circuitry in the brain (including the hippocampus and striatum)
pavlovian fear conditioning
a stimulus (tone) is paired with an aversive event (shock)
leads to contextual fear conditioning
contextual fear conditioning
a fear response is selective to the environment in which conditioning occurs
fear conditioning
fMRI research shows fear conditioning is associated with increased activation of the amygdala
more activation = stronger conditioned fear response
amygdala damage precludes a person from exhibiting a conditioned fear response
however if hippocampus is intact, a person can report the particulars of the conditioning paradigm, such as that a specific tone was paired with a shock
anterior temporal lobe
integrates sensory input from modality - specific regions to create an amodal representation of information
associated with semantic dementia
areas of episodic memory
hippocampus
medial and temporal regions
diencephalon
areas of semantic memory
anterior temporal lobe
areas of procedural memory
basal ganglia
areas of priming
domain-specific sensory and motor regions
areas of working memory
dorsolateral prefrontal cortex
areas of attentional aspects of retrieval
parietal cortex
areas of strategic encoding and retrieval
ventrolateral prefrontal cortex
areas of emotional memory, augmentation of episodic memories and fear conditioning
amygdala
stages of memory
- memories have to be created (encoded into memory)
- memories must be stored (maintained overtime)
- while being stored, memories are often strengthened = consolidation
- for a memory to be useful, it must be retrieved
medial temporal lobe structures involve in encoding
spatial info comes from the retrosplenial cortex and the parahippocampal gyrus
info about objects and their identities comes from perirhinal cortex
this info converges on the entorhinal cortex and is then transmitted to the hippocampus
encoding in hippocampus
ensures that similar and overlapping representations are encoded more distinctly
encoding in ventrolateral prefrontal regions
selects all information most relevant for encoding from among many pieces of a given episode
encoding in dorsolateral prefrontal cortex
important for encoding info that must be rendered or rearranged
memory consolidation
hippocampus plays large role
the process by which memories are strengthened over time to allow for long-term retention
evidence for this comes from the temporal extent of retrograde amnesia changes as the time since injury passes
- often referred to as shrinking retrograde amnesia
consolidation model
argues that the hippocampal system is required not only to lay down memories, but also to consolidate them
suggests that over time, the hippocampus aids in strengthening the bonds between the distinct pieces of a memory trace, each of which relies on a separate neocortical processor
once they are bound in this way, they can be retrieved independently of the hippocampal system
recognition
knowing
ie/ mc questions
larger left frontal negativity to items people think they have see than correct rejections
relies on the perirhinal cortex and connections with dorsal medial nucleus
have memory representations that are not as precise as those of the hippocampus
recall
remembering
ie/ short answer questions
posterior parietal positivity is larger to studied hits that to non-studies items
relies on hippocampus and related midline diencephalic structures
allow for specifically remembering an item or event along the complexity of its larger spatial and temporal context
dual process model
argues that recall an recognition are two seperate and distinct memory retrieval processes
prefrontal cortex and retrieval
neuroimaging evidence indicated that this is active during memory retrieval
- the effects are lateralized: lefts PFC verbal info and right PFC is non verbal info
damage causes retrieval deficites, especially for free recall
posterior PFC more related to retrieval attempt than success
PFC may also play a role in surpressing retrieval of memories
parietal cortex and retrieval
contributes to memory retrieval through its role in attentional and integrative aspects of memory
- damage does not cause severe memory deficits
- patients with damage have less confidence in their memory recall and are less likely to use retrieval cues
- damage may affect the ability to integrate different components of a memory, direct attention to specific details to be retrieved, or to assess familiarity
central executive
performs the mental work of controlling these subsystems and forming strategies for using information
controls attention (goal driven), handles cognitive tasks, and coordinates the phonological loop and the visuspatial sketchpad
phonological loop
handling spoken and written information
visuospatial sketchpad
processing visual and spatial information, used in navigation
episodic buffer
integrate info across these systems with time sequencing (ie/ chronological order) and link working memory to long-term memory
