Learning & Memory

1. Learning & Memory

2. How is it that we are capable of remembering information that we are exposed to? • How is it that someone with a brain injury can learn something, but have no memory of the acquisition of this new learning? • Is there an actual representation of the learning in our brain?

3. 1. Lashley’s Search for the Engram (physical representation of memory) led to his Principles of Learning. • Principle of Mass Action - memories are stored diffusely throughout the brain; the more mass the greater the learning capacity. • Principle of Equipotentiality - every part of the brain has equal potential for learning. ** These hold up today, but not completely**

4. Study with Primates (Glees & Cole) • Studied the motor cortex in primates; found that control of motor activities could reorganize itself until all the motor cortex that controlled the task (e.g. control of thumb) was destroyed.

5. Reinterpretation of the Principle of Equipotentiality learning can occur in any brain area if the behavior is linked to that area in some way. 2. Neural correlates of learning and memory -much of what we understand comes from research of Aplysia. Non associative learning: • Sensitization- simple learning leads to an increase in EPSP’s & increase in release of NT, new learning. • Habituation- repeated exposure to a stimulus leads to a decrease in EPSP’s & NT release, learning has occurred (decrease in novelty of stimulus)

6. Long Term Potentiation (LTP) - neural changes that occur following exposure to a stimulus. Hippocampus - studied extensively because its neural connections are in loops; neural signal will potentiate a neural response for 1-2 weeks after the signal has been terminated. Hebb- If learning is going to occur neural changes have to occur presynaptically & postsynaptically. Reverberating circuits – hypothesis that neural circuits continue to change, leads to learning.

9. Neural changes in LTP involve Glutamate release - Glutamate changes post synaptic neuronal activity - Two types of receptors for glutamate 1) Ionotropic (AMPA receptor) – glutamate stimulates this receptor and causes a depolarization…once the membrane is depolarized then the NMDA receptor can be activated 2) Metabotropic (NMDA receptor) a. Mg+ ion blocks channel until cell depolarizes b. Mg+ ion removed from NMDA receptor c. Ca++ enters into the postsynaptic neuron d. Activation of Protein Kinase :

11. Multiple Effects of the Activation of Protein Kinase 1. Receptors on postsynaptic membrane increase 2. Causes the release of retrograde messenger (ex. Nitric Oxide) 3. Signals the presynaptic neuron to continue the release of NT

13. Changes in NT’s release & synaptic contact Animal research indicates that after learning: ** 60% size change of synaptic membrane during learning ** After learning the postsynaptic membrane ultimately increases in size but by 40% of original size. Neural Changes Associated with Learning: - more NT is released - postsynaptic region is more sensitive • Increase in protein synthesis - blocking protein synthesis can impair new learning - why?

15. LTP might serve as the neural basis of Hebb’s “Reverberating Circuits” - neurons within circuitous structures continue to fire two weeks after the termination of the initial stimulus ** This may form the neural basis of transfer from STM to LTM** What if these circuits where LTP is occurring is “short circuited” or stopped? What happens to the formation of new memories? Why?

16. Theory of Consolidation 1) Consolidation Process appears to be necessary for learning to occur. This is a time dependent process. animal model - the longer amount of time learning can consolidate, the more shock it takes to impair learning. Control group – no shock learning Train Test 3 hour time span Experimental group – shock after 1 hour No learning Test Train 3 hour time span

17. ECT for Humans - learn the same thing through studying Electro Convulsive Treatment (ECT) - Memory of previous 2 weeks impaired for a while, memories return from oldest to newest - Memory from immediately before shock will be lost forever - Formation of memories is time dependent ECT Memories lost New memory formation fine Time: Before & After ECT

19. Points about the plasticity of the hippocampus - Advantage: LTP - Disadvantage: Susceptible to brain damage _________________________________________________ • Case of H.M. (1950s) – studied by Brenda Milner from McGill Univ. a) Lost capacity for new learning b) Surgery: tips of temporal lobe removed Entorhinal Cortex Hippocampus Parts of amygdala BUT – he could learn new motor activities, although he did not know how he was able to learn them: Declarative & Nondeclarative Memories involve different brain areas

20. Declarative Memories a) Processed via hippocampus 1. Episodic (events) 2. Semantic (facts) Nondeclarative Memories a) Processed via subcortical areas: Basal Ganglia (motor program) 1. Skill Learning 2. Priming

21. Involves Hippocampus & Cortical Areas Involves Basal Ganglia & other motor areas

22. Brain Areas involved in Learning & Memory a) Entorhinal or Rhinal cortex: formation of new memories. b) Hippocampus: formation of declarative (new) memories; plays a role in spatial memory. c) Amygdala- formation of memories that involve emotions d) Infereotemporal Cortex-visual images (continue on next slide)

23. e. Striatium to Cerebellum- nondeclarative (skill learning) for Sensorimotor and Motor patterns f. Mediodorsal Nucleus (thalamus) - problem in Korsakoff’s Syndrome (Psychosis) - formation of memory? (Role Uncertain) _________________________________________________ Where is LTM stored? * everywhere that is involved in learning* Secondary & Tertiary Areas of Brain or every part of the brain that is involved in the learning process in some way (note: Principle of Mass Action & Principle of Equipotentiality)

24. Tertiary Area Tertiary Area Tertiary Area

25. Now that you are beginning to understand the neural mechanisms involved in learning, from a theoretical perspective how might you apply this to your own learning?Explain your reasoning?