What is the Information processing model
Theory that memory consists of multiple components and processes.
What are the components and processes of the Information Processing Model?
Sensory input -> Sensory Memory -> Short Term Memory -> Long Term Memory
What is sensory memory?
- Immediate, initial recording of sensory info.
- Large capacity
- very short duration (~1-2 seconds)
- reflects residual activity of sensory neurons.
What is short term memory?
- active “workspace” for conscious thought and reasoning
- requires encoding from sensory memory and/or retrieval from LTM
- Small capacity (~ 7items)
- short duration (~30 sec)- longer with rehearsal
- prefrontal cortex
Long term memory
- potential infinite capacity & duration
- accessed via working memory (retrieval)
- requires consolidation by limbic system (enhances REM sleep)
- strengthened by frequent rehearsal (although details may change)
- different subtypes distributed throughout the brain.
What are some key questions concerning memory?
- how is sensory information encoded into STM? (Attention)
- Where and how does consolidation (STM to LTM) take place?
- Where an how is LTM stored?
- WHere and how is LTM stored?
- Are there different types of LTM?
What is retrograde amnesia?
- Loss of memory for past events (i.e. prior to injury), typically limited to a short time period.
- a temporary interruption of consolidation from STM to LTM (or ITM)
- Caused by concussion, loss of consciousness, alcohol
Anterograde Amnesia
- loss of ability to retain new information (a permanent impairment of consolidation from STM to LTM)
- Dues to bilateral damage to the limbic system, especially the hippocampus (medial temporal lobes). e.g. strokes, korsakoff’s syndrome
- famous cases: H.M., Clive Wearing
What have studies shown on anterograde amnesia?
- amnesic show improvement on implicit skills- (mirror tracking, fragmented pictures)
What is declarative (explicit) memory?
- info acquired through learning
- memory we are aware of accessing
- requires intact limbic system
Procedural (implicit) memory
- memory shown through performance rather than conscious recollection
- memory we are not aware of accessing
Declarative Memory (semantic memory)
- generalized memory of information
Declarative Memory (episodic memory)
- autobiographical memory
2. memory for events in time and place
How does damage effect Declarative Memory
- Frontal-parietal damage can selective impair episodic memory (source amnesia)
- Semantic memory appears to be more widely distributed. (focal cortical lesions impair ability to name objects from specific categories)
Procedural (non-Declarative memory
- Stored in sam areas responsible for carrying out the behavior
- sensorimotor skills = basal ganglia, cerebellum, motor cortex
- classical conditioning = cerebellum
- emotional memory = amygdala
Animal Lesions
general consistent with finding from humans
- hippocampal lesions impair performance , especially spatial memory
- cannot easily discriminate and explicit memory in animals
What is Hebbs view on synaptic plasticity?
- learning is dues to increases in synaptic strength
- existing connections between simultaneously active neurons are strengthened (“Hebbian synapses”)- Neurons that fire together wire together
What are the 4 mechanisms of synaptic plasticity
- Changes in existing synapses (amount of NT or # of receptors)
- changes in interneuron modulation (axo-axonal connections)
- more or fewer synaptic contacts between neurons
- rearrangement of synapses.
What are the effects of behavioral intervention on synaptic plasticity (environmental condition)
Enriched environments produce:
- better learning & problem solving
- faster recovery from injury or malnutrition
- less age-related declines in memory
What are the effects of behavioral intervention on synaptic plasticity (neurological changes)
- increased amounts of AChE (more neural activity)
- larger cortical volume & thickness
- larger cell size
- more dendritic branching
- larger synaptic contacts
What are the effects of behavrioal intervention on synaptic plasticity ( Habituation in aplysia)
- a decrease in response to repeated presentation of a stimulus.
- short term habituation- decreased release of NT at sensorimotor synapse.
- Long term habituation- retraction of some synaptic terminals at sensorimotor junction.
How was Long Term Potentiation discovered?
- repeated high intensity stimulation of neurons in the perforant pathway of the rat hippocampus results in a prolonged pattern of elevated EPSPs in the mossy fibers (receiving neurons)
What is the role of NMDA receptors on long term potentiation
- at least 2 types of glutamate receptors:
- AMPA: ionotropic Na+ channels
- NMDA: ionotropic Ca++ channel blocked by Mg+
What are some more roles of NMDA receptors on long term potentiation
- repeated stimulation of AMPA receptors (Na+ channels) by Glu produces depolarization of post-syaptic cell
- knocks Mg+ block out NMDA receptors, allowing Ca++ inside (when Glu is present)
- Ca++ triggers activity of protein kinases.
