Title: Psychology / Biopsychology / 13_Learning
Tags: Biopsychology::13_Learning Biopsychology::Semester_2

Q: How is long term memory roughly established on a molecular level?
A: Cell assemblies change their synaptic strengths.

Q: What two forms of procedural learning are there?
A: non-associative learning
associative learning

Q: What is the difference between associative and non-associative learning?
A: non-associative learning: no combination of different stimuli (habituation, sensitisation)
associative learning: combination of different stimuli or between stimulus and behavior (classical conditioning, instrumental/operant conditioning)

Q: Why is the aplysia californica used for studying "learning" processes?
A: The functions of its neurons are well studied and understood.

Q: Where does Habituation take place?
A: At the synapse between sensory and motor neurons. It works by attenuating the neurotransmitter release at the pre synapse.

Q: Where does Sensitisation take place?
A: <On a serotonergic synapse on the (excitatory presynapse between a sensory neuron and a motor neuron)> → modulating the synapse

Q: Why does Sensitisation last for days?
A: The protein kinase A lasts that long.

Q: What is the first step of Sensitisation?
A: Action potential arrives at the terminal button of the neuron L29 → Serotonin gets released

Q: What effect does the release of serotonin have during Sensitistion?
A: Serotinin receptors are activated → "molecular dynamics" → Protein Kinase A happens in sensory neuron

Q: What effect does the Protein Kinase A in the sensory neuron have during sensitisation?
A: Some Potassium (K+) channels get blocked.

Q: What effect does the blocking of Potassium channels have during Sensitisation?
A: Any arriving action potential gets prolonged.

Q: What effect does the prolonged action potential have during Sensitisation?
A: more calcium influx → more vesicles will release neurotransmitters → stronger response on the postsynaptic motor neuron

Q: What 2 things do Sensitisation and Classical Conditioning have in common?
A: Same neurocircuit/synapse
Same basic mechanism

Q: What is the difference between Sensitisation and Classical Conditioning on a molecular level?
A: In Classical conditioning, the sensory neuron (cs) and L29 (us) activate at the same time, as opposed to the L29 (us) alone
→ CA2+ streams into terminal button of sensory neuron (because ca2+ channels are open on the depolarized membrane) → much more Protein Kinase A than during Sensitisation → even more K+ channels blocked, even longer AP → stronger response on the motor neuron

Q: What neurotransmitter plays the most important role during Sensitisation and Classical Conditioning?
A: Serotonin

Q: What neurotransmitter plays the most important role in long-term potentiation (LTP)?
A: Glutamate

Q: What two types of glutamate-gated ion channels can be found on the postsynaptic membrane?
A: AMPA receptors (sodium)
NMDA receptors (sodium and calcium)

Q: How do NMDA receptors work?
A: They are blocked by a magnesium atom UNLESS
1. glutamate binds to the receptor
2. the postsynaptic membrane is depolarized

Q: What 2 kinds of ions can flow through NMDA receptors?
A: sodium and calcium

Q: What are the 2 possible sources of depolarization for NMDA receptors?
A: 1. a lot of repeated activations
2. activations on neighbouring synapses

Q: What happens when the NMDA channels open during long-term potentiation?
A: An influx of calcium, which leads to a relocation of AMPA receptors to the postsynaptic membrane → synapse is much more efficient

Q: What happens without strong NMDA receptor activity?
A: Less influx of calcium → AMPA receptors are lost → synapse becomes less effective → long-term depression

Q: Why is long term depression important during learning?
A: It improves the signal-to-noise-ratio by weakening less important synapses.

Q: What is the difference between Sensitation and Habituation?
A: Habituation: the reaction to a stimulus decreases upon repeated presentation.
Sensitation: the reaction to a stimulus is increased by a reaction to a second stimulus.