Memory & Amnesia Flashcards
What processes are required for information to be learned/remembered?
- input
- hold
- output
Define input
Acquisition - perception and encoding
Define hold
Storage - consolidation and maintenance
Define output
Retrieval - performance, recall, recognition
What causes forgetting?
Temporal decay/interference from other learning
- most input immediately forgotten
What are the main 2 types of memory systems?
- Long term
- Short term
What are the 2 types of long term memory?
Declarative
Non-declarative
What are the 2 types of declarative memory?
- episodic (remember experiences, dependent on hippocampus)
- semantic (remember facts, depends on prefrontal cortex)
When would semantic memory be defective?
Schizophrenia
What are the types of non-declarative memory?
Procedural
Priming and Perceptual Learning
Simple Classical Conditioning
Non-associative learning
What is procedural memory?
- remember skills (easier to show others than to talk about it - opposite to declarative)
Which parts of the brain take part in procedural memory?
Striatum, cerebellum and motor cortex
Basal Ganglia
Which part of the brain is involved in priming and perceptual learning?
Neocortex
Which part of the brain is involved in simple classical conditioning?
Amygdala and cerebellum
What is the involvement of the hippocampus in spatial memory?
Allows you to be aware of your surroundings
Remember how to get home from a certain place
What are the temporal aspects of memory?
Immediate to LT memory - do not need working memory in between
All of this can be forgotten
What are the 3 types of amnesia?
Anterograde - new events not transferred to LT memory
Retrograde - unable to recall events which occurred before onset
Dissociative - Blocking out of critical info. (usually traumatic/stressful nature)
What are the causes of amnesia?
Physical trauma, infections, drug and alcohol abuse
What is LT Potentiation?
Form of synaptic plasticity
- memories formed when neurons form new connections/strengthen existing synapses
- persistent increase in synaptic strength = long lasting increase in signal transmission between 2 neurons
- repeated stimulation = more dendritic receptors appear
What is LT depression?
Memory no longer needed/rarely recalled = synapses weaken
- reduction in efficacy of neuronal synapses lasting hours/longer following long patterned stimulus
How is LT depression involved in NMDA and AMPA receptors?
- weakened pre-synaptic signal = only AMPA activated
- NMDA channels remain closed as spore blocked by magnesium ions
How is LT potentiation involved in NMDA and AMPA receptors?
- large glutamate release binding to AMPA post-synaptically
- AMPA stays open longer = greater depol
- magnesium expelled from NMDA channel
- allows calcium into cell so LTP induction
- gene transcription creates new proteins for memory formation
