1 / 28

The physical basis of memory formation

Connect those neurons. The physical basis of memory formation. The Role of the neuron in memory formation. We know that there is a neuronal basis to memory formation, what we do not know is exactly how thousands of these new connections hold our memories.

jake
Download Presentation

The physical basis of memory formation

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Connect those neurons The physical basis of memory formation

  2. The Role of the neuron in memory formation • We know that there is a neuronal basis to memory formation, what we do not know is exactly how thousands of these new connections hold our memories. • New memories (either short or long term) are NOT stored in individual synapses but in the pattern of thousands of new interrelated connections • Looking for memories in a single nerve cell or synapse is a dead end • http://www.youtube.com/watch?v=90cj4NX87Yk&NR=1

  3. The role of the neuron in memory formation • Eric Kandel studied the sea slug Aplysia Californica • Very simple nervous system • 20,000 neurons • Largest neurons in the world that can be seen with the naked eye SIPHON GILL

  4. Kandel’s experiments • Stimulated the siphon which caused it to contract and to withdraw gill to prevent from danger. • The process was repeated moments later and the Aplysia would withdraw gill more and more quickly • Forgetting – an hour later the withdrawal was again slow, progressively faster with continued stimulation • Habituation – eventually the slug stopped responding to the stimulation as it caused no damage, it had ‘learned’ that the shock was harmless.

  5. Kandel’s experiments • Each day the slug would habituate more quickly than the day before • This suggests some kind of LTM lasting days or even weeks • By studying the neurons involved in this process he identified the changes that allowed the learning to take place • The neurons were physically changing! • These changes are called collectively Long Term Potentiation

  6. Long Term Potentiation • Neural basis for memory formation • Synapse strength can increase in 3 ways • 1/ Release extra neurotransmitters (Function -STM) • 2/ Growth of dendrites (Structure-LTM) • 3/ Increased synaptic connections (LTM) • http://www.youtube.com/watch?v=yLa-cXg8BwM&feature=email

  7. Long Term Potentiation –STM New Receptor Formation Stronger neural impulse in post synaptic neuron

  8. Long Term Potentiation Short Term Memory New Receptor Formation Late LTP Long Term Memory New Synapse Formation

  9. Long Term Potentiation

  10. Activity: Write theory on a cut out of a candle (Kandel) to remind the students of the theorist and the theory

  11. The Hippocampus

  12. The hippo on campus lives on memory lane

  13. The Temporal Lobe

  14. The Medial Temporal Lobe • Includes: • (Medial) middle of the Temporal Lobe • Amygdala • Hippocampus • Other cortical tissue

  15. The Hippocampus & Medial Temporal Lobe – damage and memory • Henry Molaison • Severe epilepsy • Radical surgery removes hippocampus and parts of the medial temporal lobe • Success in preventing seizures • Left with permanent anterograde amnesia (Cant form new LTM’s) • Other mental abilities and STM fine http://www.youtube.com/watch?v=uCTw1MZ-uF8 Henry Molaison

  16. The Hippocampus & Medial Temporal Lobe – damage and memory • H.M provided researchers evidence on the roles of the hippocampus and temporal lobe they found that: • 1/ These areas are important in encoding and forming DECLARATIVE memories (Semantic and episodic) but not PROCEDURAL memories. • 2/ These areas play role in memory formation, but not storage for existing LTM’s. • 3/ LTM is a distinct sub system of memory. • 4/ STM or working memory is unaffected by damage to these areas

  17. Deep within the temporal lobe- the amygdala • Involved in remembering the emotional significance of an event • Involved in processing IMPLICIT memories

  18. Consolidation theory • Physical changes (LTP) in neurons occur when something is being learned and during a period of time immediately after the learning process has been completed. • If memory is disrupted during the period of consolidation (which is about 30 minutes) memory loss will occur • Hippocampus and Medial Temporal Lobe involved • Think of wet concrete

  19. Consolidation experiment– Rats in a maze • Rats learned to run a maze to find a food reward • 4 groups A – ECT immediately B – ECT 20 seconds after C – ECT 30 minutes after D – ECT 60 minutes after Results A – all rats forgot completely B – partial recall C – partial recall (better than B) D – total recall Consolidation seemed to be complete after about 1 hour

  20. Amnesia • Brain trauma – damage inflicted through injury interferes with functioning • E.g. Brain injury, stroke, drug abuse etc • Neurodegenerative disease – decline in structure and function of neurons • E.g. Alzheimer's disease • Amnesia– Loss of memory, partial or complete, temporary or permanent

  21. Amnesia AnterogrageAmnesia Inability to form new memories. Unable to transfer from STM to LTM Korsakoffssyndrome • Caused by chronic alcoholism • Symptoms include anterograde amnesia Retrograde Amnesia • Inability to remember old information, events before the injury lost.

  22. Dementia • Large group of neurodegenerative diseases • Loss of mental capacity • Loss of memory – interfering severely with the ability to function independently • Develops progressively

  23. Alzheimer’s Disease • The most common form of dementia • Accounts for 50 – 70% of dementia • Neurodegenerative disease that causes wide spread cell death • Causes decline in all aspects of cognitive function • 100,000 Australians effected • 1 in 25 over 60 • 1 in 8 over 80

  24. Alzheimer’s Disease – CAUSES • Show high levels of the protein Amyloid • Not usually in the brain • Highly toxic – causes cell death • Causes the development of plaques and tangles • These plaques and tangles effect neural transmission and eventually kill brain cells • Brains also have a massive lack of acetylcholine (an important neurotransmitter) • http://www.youtube.com/watch?v=9Wv9jrk-gXc

  25. Alzheimer’s Disease - SYMPTOMS • Typical memory loss includes: • Events • Words and names • Written and verbal directions • Stories, TV, Movies, Books • Semantic memory decline • Procedural memories • Personality changes also occur

  26. Memory decline over the lifespan • Not necessarily inevitable, some natural decline is normal, amount of decline depends on, how measured • motivation to remember, self confidence, nervous system slowing are possible explanations for the decline. • Older people DO take longer to learn new info • STM – depends on the task, easy task same, harder task decline. • LTM - Episodic down, Procedural same, Semantic Same

  27. Age related Memory Decline

More Related