Table of Contents
Lecture 1. Systems consolidation....................................................................................... 2
Lecture 2. Learning and behaviour .................................................................................... 8
Lecture 3. Spatial memory .............................................................................................. 16
Lecture 4. Sleep .............................................................................................................. 23
Lecture 5. Sleep and memory .......................................................................................... 27
Lecture 6. Emotional memory ......................................................................................... 37
1
,Lecture 1. Systems consolidation
Why am I looking at what I am looking at?
How will I do that?
What will be the follow up?
System consolidation = small part of memory = ‘declarative’ memory. → stuff that you
constantly aware off.
Episodic memory = me experiences
something.
Semantic memory = You know Paris
is the capital of French, but you don’t
remember learning this experience.
→ this is the process of system consolidation.
Memory = network of neurons that is active at time of encoding. If this network of neurons is
active again you are retrieving a memory (whole brain activity). Input will come in, activate
your hub and that would cause an activation of the rest of the network. Through that you have
memory (retrieval).
Hippocampus: very detailed network (episodic memory) in contrast to the cortex.
Cellular consolidation = before we go in system consolidation, we have to consolidate the
network between neurons first.
Happens during LTP (long-term potentiation) = LTP is the opposite of long-term depression
(LTD). In LTP, after intense stimulation of the presynaptic neuron, the amplitude of the post-
synaptic neuron's response increases. The stimulus applied is generally of short duration (less
than 1 second) but high frequency (over 100 Hz).
2
,LTP: Long-term potentiation: if it is not enforced with another signal it will actually fade
away. Re-enforcement is the dopamine. After the initial cascade, dopamine (by attaching to
the dopamine receptor) leads to increase gene expression, gene translation, more protein
synthesis + lot of phosphorylation.
Long term synapse only works when A + B happens.
NMDA-R activation + dopamine activation → protein synthesis.
Showed that that are actually two separate processes: synaptic tagging experiment.
You can regulate the two synapses by two processes.
AB = LTP experiment: stimulation, and you see the potentiation will slowly fade away.
C = they remember where the food was in 30 min, but after 24 hours they don’t remember.
If you want the remembering last longer you need to give dopamine signal.
AB: one gets a light stimulation and one get a strong stimulation (+dopamine). Also, the
weak one last stronger → the weak stimulation can benefit by the dopamine production of the
other stimulation.
C: if you follow your weak with novelty, that released a larger amount of dopamine into the
hippocampus. → make the memory last longer. E: no memory enhancement if you block
dopamine.
3
, If you activate the LC (part of the brain for being aware/shock), then you get this memory
enhancing effect. But also looked at which NT is released upon LC activation.
If you block noradrenalin (PROP) → no differences.
If you block dopamine (SCH) → no you see differences.
Two forms of novelty-associated consolidation:
Common novelty: seeing the sea for the third time. (more semantic)
Distinct novelty: novelty that don’t fit at all in our past experiences. (for example, you
remember everything you did on 9/11/01) → ‘flashbulb memory’ (highly episodic)
You brain is down sampling all the information (otherwise it would be way too much to
handle for the brain).
Hippocampus = stored by time
Cortex = compares different events and put them together by content.
→ system consolidation.
4
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