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Psych 102 Chapter 12 Presentation 7/26/19 Learning and Memory Chapter 12 Learning as the Storage of Memories Brain Changes in Learning Garrett: Brain & Behavior 4e Learning Deficiencies and Disorders 1 Learning as the Storage of Memories Figure 12.1: Temporal Lobe Structures Involved in Amnesia • Henry Molaison (HM) had frequent epileptic seizures • Treatment removed his hippocampal formation & amygdala. • *Anterograde amnesia: unable to form new memories. • *Retrograde amnesia: few memories decade before surgery • Amnesia usually affects declarative memory (dates, events, etc) Learning as the Storage of Memories Figure 12.2: Stages of Consolidation • *Consolidation: brain forms permanent representation of memory • Short-term (working) memory • Long-term memory • *Long-lasting memory – stored in cortical areas other than the hippocampus Learning as the Storage of Memories Figure 12.4: Hippocampal Activity Related to Consolidation Garrett: Brain & Behavior 4e 4 SOURCE: From “Hippocampal, But Not Amygdala Activity at Encoding Correlates With Long-Term Free Recall of Nonemotional Information,” by M. T. Alkire et al., 1998, PNAS, 95, pp. 14506–14510, fig. 1, lower left image, p. 14507. Learning as the Storage of Memories Figure 12.5: Human Hippocampal Activity During Retrieval • *Retrieval: Accessing stored memories. • Glutamate required for consolidation and retrieval. • *Blocking glutamate receptors prevents consolidation and retrieval • Prefrontal area: directs search strategy for retrieval in hippocampus Learning as the Storage of Memories Figure 12.6: Functional MRI Scans of Brains During Perception and Recall Garrett: Brain & Behavior 4e 6 Learning as the Storage of Memories Figure 12.7: Recordings from Place Cells in a Rat in a Circular Runway • Place cells • Increase firing when individual is in a specific location in an environment • Collectively form a “spatial map” • Dependent on environmental cues and landmarks • Also found in humans and primates SOURCE: From “Neural Plasticity in the Ageing Brain,” by S. N. Burke and C. A. Barnes, 2006, Nature Reviews Neuroscience, 7, 30– 40. Learning as the Storage of Memories • HM, despite his impairments, *had intact non- declarative memory • *Improved on mirror drawing task • *Learned to solve the Tower of Hanoi problem Learning as the Storage of Memories Figure 12.9: A Radial Arm Maze • Declarative • Requires hippocampus • Rat with Hp lesion could not remember which arms it had visited • Non-declarative • *Requires striatum • Lesioned rats could not associate light at end of arm with food SOURCE: © Hank Morgan/Photo Researchers. Learning as the Storage of Memories Figure 12.9: A Radial Arm Maze • Amygdala • *Role in both processes • *Nondeclarative • Unexpected emotional response while performing behavior • *Declarative • Memories of emotional events • Activates Hp SOURCE: © Hank Morgan/Photo Researchers. Learning as the Storage of Memories • Working memory 1. Observe shapes • Temporary “register” for information • Delayed match-to-sample tests • *Prefrontal cortex 2. Delay period • Integrates long-term memory with other information • Manages strategies and decision making 3. Pick the new shape • Directs working memory traffic in brain • Coordinates sensory and motor systems Brain Changes in Learning Figure 12.10: LTP and LDP in the Human Brain • Hebb rule: When two neurons fire together, the synapse between them strengthens • *Long term Potentiation (LTP): Synapse becomes stronger over time SOURCE: From “Long-Term Modifications of Synaptic Efficacy in the Human Inferior and Middle Temporal Cortex,” by W. R. Chen et al., Proceedings of the National Academy of Sciences, USA, 93, pp. 8011–8015. Copyright 1996 National Academy of Sciences, USA. Used with permission. Brain Changes in Learning Figure 12.11: Associative LTP • Hebb rule: When two neurons fire together, the synapse between them strengthens • Long term Potentiation (LTP) • Associative LTP: weak synapse strengthened through induction Brain Changes in Learning • LTP versus LTD • Rate of stimulation matters • High frequency stimulation elicits LTP • Low frequency stimulation elicits LTD • Memories • LTP- forming and recalling memories • Associative LTP- Classical Conditioning • LTD- forgetting, deleting incorrect information *(extinction) and making space for new memories • *“Cells that fire together wire together” Brain Changes in Learning Figure 12.12: Participation of Glutamate Receptors in LTP • *Theta waves - 4 to 7 Hz • Seen in *Hippocampus during novel situations • Activity during theta peak induces LTP • *Glutamate receptors necessary for LTP • Small stimulation triggers AMPA receptors (short acting) • Large stimulation triggers NMDA receptors (long lasting, LTP) Brain Changes in Learning Figure 12.13: Increase in Dendritic Spines following LTP. • During LTP • Postsynaptic nitric oxide release *triggers increased presynaptic neurotransmitter (dopamine) release • Structural changes include: • Increased number, enlargement, and growth of *dendritic spines; • *transport of additional AMPA receptors into the spines Brain Changes in Learning • *Ultimately memory involves strengthening connections between individual neurons, LTP induced changes, and strengthening connections within the network of neurons. • LTP-initiated growth of hippocampus • London taxi drivers with extensive spatial memory had larger posterior hippocampal volume than control individuals • Differences increased proportionally to years as a taxi driver Brain Changes in Learning Figure 12.14: Retention in Normal and α CaMKII Deficient Mice Over Time. • Consolidation involves two enzymes • CaMKII (establishment of LTP) • protein kinase M zeta (maintains long-term memory) Brain Changes in Learning Figure 12.14: PET Scans of Brain Activity During Sleep Following Learning • Consolidation takes place during sleep • Neurons in hippocampus and cortical areas repeat firing patterns that occurred during awake learning • *Sleep-activated genes play roles in protein synthesis, synaptic modification, memory consolidation. Brain Changes in Learning Memory Modification • Extinction • Eliminates useless memories through new learning • Requires activation of NMDA receptors • Forgetting • Active, adaptive biological process • Enzyme PP1, Rac protein encourage memory loss • May prevent the saturation of synapses. • *Reconsolidation • During memory retrieval (happens every time) • Opportunity to refine memory, correct errors (PTSD) • Opportunity to create memories that did not occur (“false” memories”) Learning Deficiencies and Disorders Memory and Aging • Aging and Dementia • Researchers long believed dementia in elderly were inevitable, due to substantial loss of neurons. • However, many show little or no memory loss • Deficits usually reflect motivation on memory tests. • Studies on “old” rodents • No loss of hippocampal neurons • Cortical cell loss is minimal. • *Some loss of NMDA receptors, myelin, and cells in prefrontal cortex. Metabolic rates in cortical areas and LTP rates both slow. • Reserve hypothesis • Active lifestyle throughout life promotes neurogenesis • In elderly, this reserve of neurons prevents cognitive declines • Nuns and idea XXX study Learning Deficiencies and Disorders Figure 12.16: Neural Abnormalities in the Brain of a Person with Alzheimer’s • Alzheimer’s disease • Progressive brain deterioration, *declarative memory loss • Language, visuo-spatial functions, reason, and aggressive problems • Affects 10% of people over 65, 50% of individuals over 85. Learning Deficiencies and Disorders Figure 12.16: Neural Abnormalities in the Brain of a Person with Alzheimer’s • Neural abnormalities • Amyloid plaques * from amyloid protein production or deposit issues (a) interfere with neural transmission • Soluble ADDL causes memory and LTP failure in mice • Neurofibrillary tangles (b) associated with neural death Learning Deficiencies and Disorders Figure 12.17: Alzheimer’s Brain (left) and a Normal Brain • Global loss of neurons in brain • Particularly the temporal/frontal lobes. • Enlargement of ventricles • *Hippocampus is isolated from the rest of the brain by plaques & tangles in the temporal lobes. Learning Deficiencies and Disorders Table 12.1: Known Genes for Alzheimer’s Disease • 4 genes confirmed in Alzheimer’s disease (50% cases) • 3 Early-onset (<60 years) • 1 Late-onset (>60 years) • APOE ε4 allele increases risk 3-8x, associated with plaques and tangle formation Gene Chromosome Age of Onset Percentage of Cases APP 21 45-66 <0.1 Garrett: Brain & Behavior 4e Presenilin 1 14 28-62 1-2 Presenilin 2 1 40-85 <0.1 25 APOE ε4 19 >60 >50 Learning Deficiencies and Disorders • Environmental correlates to Alzheimer’s • Lead exposure in childhood • Pesticides (like DDT, still used in some countries) • Chronic stress • Neural causes and Treatments • Treatments slow down decline, but cannot reverse effects • Too little Acetylcholine • *Treatment: inhibit enzyme that degrades Ach • Too much glutamate • kills NMDA receptors through overstimulation • Memantine (Namenda) reduces levels of glutamate • Drugs that remove plaques and tangles have had mixed results, but mostly ineffective Learning Deficiencies and Disorders • Detecting Alzheimer’s Disease • Brain scans (PET, MRI) can reveal • Atrophy in temporal and parietal areas • Biomarkers for plaques is much more promising • 25% of individuals with plaques contract Alzheimer ’s within 3 years • Low levels correlate to 2% risk of Alzheimer’s • Reserve Hypothesis • High Idea density in early life delays onset of symptoms • 80% of low-scoring
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