Higher Cortical Function: Memory Flashcards
Define learning
Define memory
Learning = acquisition of knowledge Memory = retention of knowledge
How can memory be classified?
- nature of memory e.g. declarative vs non-declarative
- duration e.g. short vs long term
For how long are the following stored?
- sensory memory
- short term memory
- long term memory
- sensory memory = <1 second
- short term memory = >1 min
- long term memory = lifetime
Define the following
- explicit vs implicit memory
- declarative vs procedural memory
- episodic vs semantic memory
1. explicit = conscious implicit = unconscious 2. declarative = facts and events procedural = skills, tasks 3. episodic = events and experiences semantic = facts and concepts
Draw the memory tree
see lecture notes
Describe the nature of declarative memory
What are the two types of declarative memory?
- explicit
- consciously aware
- able to describe in words
- fades with type
Two types - episodic = events, experiences
- semantic = facts, concepts
Describe the nature of non-declarative memory
Give two examples of conditioned responses
- implicit
- skills, habits, behaviours
- procedural memory e.g motor tasks, acquiring experience
Conditioned responses: - associative reflexes e.g Pavlov’s dog
- emotional response –> strengthens declarative memory
What is the functions of sensory memory?
How long is it stored?
- sensory processing
- lasts for fractions of a second
What is meant by working memory? What is its function?
Working memory is a cognitive system with a limited capacity that is responsible for temporarily holding information available for processing. Working memory is important for reasoning and the guidance of decision making and behavior.
What are some causes of amnesia?
TBI
neurodegeneration
resection
stroke
What are the two types of amnesia and how are they different?
Retrograde amnesia = can’t remember anything before the insult
Anterograde amnesia = can’t form new memories after the insult
What is Ribot’s law?
- Retrograde amnesia is not usually complete
- Ribot’s Law = recent memories are more likely to be lost than remote ones
What is the anatomical location for declarative memory?
What disease provides evidence for this?
- medial temporal lobes
- evidence for this is lesions
- the pathology of alzheimers disease –> lose episodic, then semantic memory
What is the declarative memory pathway?
sensory info –> rhinal cortices and hippocampus –> neocortex
hippocampus –> hypothalamus (MB’s) –> thalamus –> neocortex
What memory is lost in Korsakoff’s?
episodic memory
- mamillary bodies in hypothalamus key step in memory formation
What is the anatomical location procedural memory?
What disease provides evidence for this?
- supplementary motor area, basal ganglia and cerebellum
- ## parkinsons disease, difficult to acquire new procedural skills
What is the anatomical location of working memory?
What is the evidence for this?
- prefrontal cortex
- evidence in ADHD and schizophrenia
Describe the HM case study?
- bilateral temporal lobectomy –> severe anterograde amnesia for declarative memory
- childhood memory intact
- temporal lobe required for new declarative memories but not old
- no effect on procedural memory
How do neurones store memories?
- change in neurotransmission
- change in synaptic structure
- neuronal plasticity = dynamic synapse formation/retraction
- long term potentiation
Where was long term potentiation first shown?
- hippocampus in vitro
What is long term potentiation?
- neurones in the hippocampus have a baseline level of activity
- if you stimulate the hippocampus with lots of afferent input, then remove the input
- the baseline activity of the neurones has increases
- the nature of these neurones has been changed
What kind of memory is LTP shown in?
declarative memory
What is happening at the synapse during LTP?
Glutamate transmission critical in LTP
- glutamate normally binds to AMPA receptor
- if stimulated, you unblock NMDA receptors and so get AMPA and NMDA activity
- NMDA allows calcium entry
- leads to changed gene expression and altered kinase activity especially CAMKII
- CAMKII affects cellular processes = biological equivalent of memory
LTP also triggers physical transformation of neurones
- spine formation
What are key theories for the biological basis of memory formation?
Long term potentiation
- changes in baseline activity
- changes in receptor activity on postsynaptic knob
- calcium entry –> changes to cellular processes
- enzyme CAMKII activity
- physical changes e.g. spine formation in response to glutamate
How can be manipulate memory?
Pharmacological
- enhancement by nootropics, NMDA agonists enhance memory formation in animals, other mechanisms target ACh transmission e.g. ACh loss in Alzeheimer’s
- suppression by NMDA antagonists e.g. ketamine
Non-pharmacological
- CBT - changes in network activity
