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Lecture 14: The Biology of Learning

Lecture 14: The Biology of Learning. References: H Shouval, M F Bear, L N Cooper, PNAS 99 , 10831-10836 (2002) H Shouval, G Castellani, B Blais, L C Yeung, L N Cooper, Biol Cybernetics 87 , 383-391 (2002) W Senn, H Markram, M Tsodyks, Neural Computation 13 , 35-67 (2001)

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Lecture 14: The Biology of Learning

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  1. Lecture 14: The Biology of Learning References: H Shouval, M F Bear, L N Cooper, PNAS99, 10831-10836 (2002) H Shouval, G Castellani, B Blais, L C Yeung, L N Cooper, Biol Cybernetics87, 383-391 (2002) W Senn, H Markram, M Tsodyks, Neural Computation13, 35-67 (2001) Dayan and Abbott, Sects 8.1, 8.2

  2. Learning = long-term synaptic changes Long-term potentiation (LTP) and long-term depression (LTD)

  3. Learning = long-term synaptic changes Long-term potentiation (LTP) and long-term depression (LTD) CA1 region of rat hippocampus

  4. Learning = long-term synaptic changes Long-term potentiation (LTP) and long-term depression (LTD) CA1 region of rat hippocampus Requires NMDA receptors, postsynaptic depolarization (not necessarily postsynaptic firing)

  5. Timing dependence Spike-timing dependent plasticity (STDP)

  6. Timing dependence Spike-timing dependent plasticity (STDP) (Markram et al, 1997)

  7. Timing dependence Spike-timing dependent plasticity (STDP) (Markram et al, 1997) (Zhang et al, 1998)

  8. Model I: Ca control model Shouval et al:

  9. Model I: Ca control model Shouval et al: Everything depends on Ca concentration

  10. Model I: Ca control model Shouval et al: Everything depends on Ca concentration Ca flows in through NMDA channels

  11. Model I: Ca control model Shouval et al: Everything depends on Ca concentration Ca flows in through NMDA channels “Back-propagating” action potential (BPAP) after postsynaptic spike (with slow tail)

  12. Model I: Ca control model Shouval et al: Everything depends on Ca concentration Ca flows in through NMDA channels “Back-propagating” action potential (BPAP) after postsynaptic spike (with slow tail) Ca dynamics:

  13. Ca control model (2) NMDA channel current (after spike at t = 0):

  14. Ca control model (2) NMDA channel current (after spike at t = 0):

  15. Ca control model (2) NMDA channel current (after spike at t = 0):

  16. Ca control model (2) NMDA channel current (after spike at t = 0):

  17. Ca control model (3) Synaptic strength (conductance) obeys

  18. Ca control model (3) Synaptic strength (conductance) obeys

  19. Ca control model (3) Synaptic strength (conductance) obeys Back-propagating action potential:

  20. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive)

  21. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations:

  22. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations:

  23. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations:

  24. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations:

  25. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations:

  26. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations: where

  27. Possible basis of equation for synaptic changes AMPA receptors – in membrane (active) and in cytoplasm (inactive) Kinetic equations: where

  28. How it works

  29. Need the slow tail of the BPAP

  30. LTD if presynaptic spike is too far in advance of postsynaptic one

  31. LTD if presynaptic spike is too far in advance of postsynaptic one (unavoidable consequence of model assumptions)

  32. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001)

  33. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc):

  34. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release

  35. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release (recall (Lect 6) treatment of synaptic facilitation: y = P(release|vesicle)

  36. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release (recall (Lect 6) treatment of synaptic facilitation: y = P(release|vesicle) Here (SMT notation): call it

  37. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release (recall (Lect 6) treatment of synaptic facilitation: y = P(release|vesicle) Here (SMT notation): call it Actual changes in build up slowly over ca 20 min,

  38. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release (recall (Lect 6) treatment of synaptic facilitation: y = P(release|vesicle) Here (SMT notation): call it Actual changes in build up slowly over ca 20 min,

  39. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release (recall (Lect 6) treatment of synaptic facilitation: y = P(release|vesicle) Here (SMT notation): call it Actual changes in build up slowly over ca 20 min, But changes faster, on the scale of ~1 s or less

  40. Model II (2 second messengers) (Senn, Markram, Tsodyks, 2001) Markram-Tsodyks experiments (rat barrel cortex, exc-exc): What is changed, (at least on the 1-hour timescale) is the probability of transmitter release (recall (Lect 6) treatment of synaptic facilitation: y = P(release|vesicle) Here (SMT notation): call it Actual changes in build up slowly over ca 20 min, But changes faster, on the scale of ~1 s or less Here we try to describe the dynamics of

  41. 2-messenger model (2)

  42. 2-messenger model (2) NMDA receptors Have 3 states

  43. 2-messenger model (2) 2nd messenger #1 NMDA receptors Have 3 states

  44. 2-messenger model (2) 2nd messenger #1 NMDA receptors Have 3 states 2nd messenger #2

  45. NMDA receptors Kinetic equations:

  46. NMDA receptors Kinetic equations:

  47. NMDA receptors Kinetic equations:

  48. NMDA receptors Kinetic equations:

  49. NMDA receptors Kinetic equations:

  50. 2nd messengers Activation driven by Nu,d

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