Exam 4: Learning & Memory 3 (**heavily tested in exam**)

Wednesday, April 11, 2012 4:04 AM

1. Consolidation--when we learn something, we keep that information as a short term memory, and then that memory needs to be consolidated into long term memory to keep that memory for a long time. a. Learn something and first hold it in short term memory (hours or minutes, strong for a little bit but decays fast) b. Working memory (lasts a couple of seconds/minutes) 2. When we are actively studying, we first have to hold it into short term memory and the goal is to put it into long term memory, so that when you're taking an exam, you can retrieve it back into short term memory 3. Retrieve/recall information stored in long term memory back in to short term memory form to us the information. After this information is used, it has to be reconsolidated from short term memory into long term memory. Reconsolidation. 4. When reconsolidating, the information is susceptible to changes. Manipulation of memory while it is being consolidated, can lead to consolidation as a completely different memory. a. Example: eyewitness testimony 5. Study: Fear conditioned rats (receiving tone and shock pairing), when the rats are getting this tone and shock pairing, it's learning phase (learning about active association btwn. tone and shock)-->back into home cage (consolidation occurring) a. CS--US (learning)--> put back into home cage for 4 hours --> presented with tone paired with shock. Time frame, 4 hours, tests short term memory--> animals freeze b. Learning-->home cage-->20 hours later (consolidation has occurred) i. (??) What is the time frame at which consolidation occurs c. Learning--> after, animals were infused with mRNA synthesis blocker (blocks transcription process) into basal lateral amygdala (where fear conditioning occurs)--> basal lateral was not able to consolidate memory d. Does a similar process work with reconsolidation? Learning--> 4 hours later--> intact memory. Memory has been consolidated into long term memory-->tone ("do you remember this?")-->mRNA infused--> intact memory-->after 24 hours--> lower freezing level (didn't remember as well) 6. Brain changes a. What fires together, wires together i. "when an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth p rocess or metabolic change takes place in one or both cells such that A's efficiency, as one of the cells firing B is increased." --Donald Hebb b. How does L&M occur? i. Physiological changes at the synapse may store information ii. Structural changes at the synapse may provide long term storage iii. Different stages of memory may require different genes iv. Formation of memory requires protein synthesis c. Physiological changes i. After training (use particular pathway over and over again)--> several things can happen 1) Synaptic area can be more efficient at releasing NT, instead of releasing three, release five when you hear "amygdala" 2) Post synaptic area will be more efficient at receiving information, even if pre synaptic area sends 3 vesicles, the post synaptic area is more receptive 3) Combination of both ii. End result: bigger PSP iii. Changes in synaptic potential can last a long time and increase in potential/decrease in potential can last days, months --Long term potentiation (LTP) iv. LTP potentiated size of potential and lasted for a long time v. LTP: long lasting increase in neuronal activity induced by afferent activation (activation of the input to the neurons) vi. After repeated stimulation: increase in release of NT and increased receptors in post synaptic cell d. Inducing LTP i. Baseline: one AP through neuronal cell ii. Stimulate (v. fast AP) over and over and over again, cramming information into brain, a lot of stimulation, take a break, giv e a simple AP: EPSP magnitude increases. 1) Synaptic specific, even if other axons are near it, it doesn't happen to the second cell. 2) To induce this, the axon has to be specifically and massively stimulated. e. Synaptic level i. Presynaptic activation with sufficient post synaptic depolarization 1) Normal stimulation-->glutamate is released-->binds to receptors in post synaptic cell 2) Receptors that play crucial role in LTP induction: a) NMDA: glutamate binds to NMDA receptor, but NMDA has a hard time opening up because Mg is stuck in channel. Mg is voltage sensitive, i.e. if enough depolarization doesn't occur, then the Mg isn't removed. High frequency stimulation-->Mg gets kicked out of NMDA receptor channel-->Ca2+ goes through NMDA receptor channels b) LTP HAPPENS THROUGH NMDA receptors c) AMPA: glutamate binds-->opens-->Na+ goes in i) Repeated stimulation-->gradual depolarization 7. Properties of LTP
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7. Properties of LTP a. Associativity: the post synaptic neuron must be sufficiently depolarized for the LTP to occur. Pre synaptic and post synaptic cells need to work together. The post synaptic neuron must be sufficiently depolarized for the pre synaptic neuron's effects to be enhanced (i.e. NMDA receptor activation only occurs if there is already sufficient depolarization) b. Cooperativity: You cannot produce LTP by stimulating only one axon's input (axon terminal). Requires concurrent stimulation of at least several axons. c. Specificity: LTP is specific to the post synaptic neurons that have been stimulated by high frequency activation 8. Physiological & Structural changes from LTP a. Presynaptic change: After induction: retrograde signal goes back to presynaptic cell and this causes it to release more NT b. Post synaptic change: 2nd messenger system: post synaptic area, reserved ampa receptors that haven't been expressed at synaptic level (being held nearby). After LTP, internal AMPA receptors come up to the surface of synaptic area. More ampa receptors, when glutamate is released--> less time to depolarize cells 9. Structural changes a. Recruit unused post synaptic cell b. If two synaptic areas are not being used, but another one is being actively used, can kick out the other synaptic connection to withdraw and will make connection with post synaptic cell 10. Is long term potentiation learning? a. Study--> if long term potentiation is L&M, whatever you can do to interfere with long term potentiation, should have same process on L&M. Manipulate NMDA receptors (crucial in forming LTP)-->inactivated/blocked--> ask animals to learn something i. NMDA blocker-->water maze--> canula implant into head targeting hippocampus--> didn't learn at all (dose dependent) ii. Blocking NMDA-->block learning and LTP b. Saturate your brain with LTP, bombarded hippocampus with stimulation, tested to see if there was any LTP i. Some animals were still able to induce LTP ii. Tested memory--> animals that had <10% room for LTP didn't learn as much c. Behavioral LTP i. Can you see LTP after you learn something? 1) Animals went through learning first (inhibitory avoidance task, confined to one area, step into one area, shocked, spatial component)--> inhibitory avoidance learning-->LTP measured a) First group: active learning--> a lot of bright colors, a lot more potentiation seen. Once you go through active learning process-->have LTP in brain b) Control animals, nothing c) Random shock d) Exposed to environment

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