1. Memory Systems Chapter 23 Friday, December 5, 2003

2. What is Memory? • Memory is a change in the synapses of the neurons comprising a network. • Memories are not static “records” but products of a change in the connections among nerve cells. • Memories extract and store the meanings of events, not their exact details. • Sensory aspects are reexperienced not recalled. • Recall is reconstructed, not just retrieved.

3. The Search for the Engram • Engram – the physical memory trace. • Lashley couldn’t find one: “This series of experiments…has discovered nothing directly of the real nature of the engram. I sometimes feel in reviewing the evidence on the localization of the memory trace, that the necessary conclusion is that learning just is not possible.” pg 276 of text

4. Where is Memory? • Both cortical and subcortical structures are involved in creating memories. • Although memories appear to be stored in the cortex, they are: • Distributed – spread out in a network • Redundant – represented in multiple ways • Hebbian cell assemblies (loops) permit access at various points in a network.

5. Stages of Memory • Sensory buffers – one for each sense: • Iconic – for visual information • Echoic – for auditory information • Working memory/short term memory: • Limited capacity – 7 plus or minus 2 • Capacity can be expanded by chunking • Executive functions • Long term memory – permanent.

6. Amnesia • Retrograde amnesia – inability to recall previously stored memories of one’s life. • Anterograde amnesia – inability to form new memories of events in one’s life. • H.M. -- surgery removed parts of the temporal lobe, including hippocampus. • With amnesia, some kinds of memory are spared, others impaired, suggesting there are different kinds of memory.

7. Working Memory • Unimpaired in amnesics. • In humans, localized to frontal lobes. • Delayed development of frontal lobes in humans and monkeys: • “A not B” task • Can’t tolerate delays (8-10 sec) until 1-1/2 yrs old

8. Infantile Amnesia • Inability to remember events of one’s childhood before ages 3-4. • 10 year olds couldn’t remember preschool classmates • Attributed to immaturity of memory systems in children.

9. Long Term Memory • Localized to temporal lobes: • Hippocampus – memory formation and consolidation • Entorhinal cortex (adjacent to hippocampus) • During memory storage the temporal region forms a connection between the relevant networked areas of the brain.

10. Procedural vs Declarative • Procedural memory – memory for how to do things, skills. • Declarative memory – memory for abstract knowledge, facts and events of one’s life. • Only memory for events of one’s life is affected by amnesia – not procedural memory or memory for facts.

11. Explicit vs Implicit • Implicit memory – does not involve conscious awareness – unimpaired in amnesics. • Procedural memory • Priming, recognition tasks • Classical conditioning, habituation • Semantic memory • Explicit memory – involves conscious attention – impaired in amnesics. • Episodic and autobiographical memory, recall

12. Conditioning • A form of learning: • Classical (Pavlovian) conditioning – present at birth, unimpaired in amnesics. • Operant (instrumental) conditioning. • How are learned associations maintained? • Amygdala (and emotional arousal) mediates activity of the hippocampus to form neural connections.

13. Types of Amnesia • Damage to Temporal Lobe – H.M. • Damage to Thalamic Structures – N.A. • Most impaired with verbal material. • Korsakoff’s Syndrome • Chronic alcoholics with thiamine deficiency • Retrograde and anterograde amnesia. • Electroconvulsive Shock Therapy (ECT)

14. Amnesia and Forgetting • Forget at normal rate – thalamic (diencephalon): • N.A. • Korsakoff’s patients • Monkeys with medial thalamic lesions • Forget rapidly – hippocampus: • H.M. • Bilateral ECT • Monkeys with amygdala/hippocampus lesions

15. Semantic Memory • Unimpaired by anterograde amnesia. • Children with amnesia develop normal semantic memory. • Intact entorhinal cortex may be used to store semantic memories despite hippocampal damage. • Context-rich, episodic memory impaired.

16. Cellular Mechanisms • Habituation involved suppression of action potentials through decreased release of neurotransmitter – change is at the synapse. • Sensitization – increased neurotransmitter release • Explicit memory involves long-term potentiation, LTP (a physical change to neurons) in hippocampus and neocortex. • See Chapter 24 for details