Lecture 5 - Learning and Memory General Flashcards
Explain declarative or explicit memory.
Knowledge about facts and their meaning (recalled consciously).
What is non-declarative or implicit memory?
Knowledge about how to perform something (recalled unconsciously).
Implicit memory can be associative or non-associative.
What are examples of non-associative implicit memory?
Habituation = the decrease in response to a benign stimulus through repeated presentation of the stimulus e.g. wearing clothes. Sensitisation = an enhanced response to multiple different stimuli after presentation with a noxious or intense stimulus. (opposite of habituation).
Associative implicit memory is that the association between two stimuli is learned e.g. classical conditioning.
Explain classical conditioning.
In Pavlov’s paradigm the food, which elicits a salivation response, is the Unconditioned Stimulus (US) and the bell is the Conditioned Stimulus (CS).
When the bell (CS) is repeatedly paired with the food (US), the bell (CS) becomes able to elicit salivation, now called the Conditioned Response (CR).
Cellular studies in invertebrates indicate that forms of implicit memory involve … modulation of … strength and structure.
Cellular studies in invertebrates indicate that forms of implicit memory involve experience-dependent modulation of synaptic strength and structure.
Name the differences between short term, intermediate term and long term memory i.e. time, protein modification/synthesis and gene-expression.
Short term memory: lasts seconds to minutes and involves covalent modifications of pre-existing proteins at the synapse by kinases. Synaptic plasticity does not involve gene expression.
Intermediate term memory: last hours and involves new protein synthesis (but not mRNA synthesis). No gene expression.
Long term memory: lasts days, weeks or more and requires CREB-mediated gene expression, and new mRNA and protein synthesis. There is new gene expression.
What is the result of gene expression in long-term memory?
It results in longer-lasting changes at the synapse.
Describe the neuromodulation example of Aplysia that was mentioned during lectures. Think of sensitisation.
Aplysia are sea snails that respond to attack by closing their grill and syphon, and ejecting ink.
This behaviour is controlled by a simple reflex circuit.
Following an attack, the sea snail is sensitised to future attacks –> enhancement of response in any future attack.
Sensitisation to attack involves modulation of synapses at sensory neurons.
Sensitisation in Aplysia research: What happens if glutamate is replaced with serotonin?
Neuron is sensitised and you’ll get a bigger reaction.
Describe the cellular mechanisms of short- and intermediate-term memory formation in Aplysia.
Start with Serotonin and use: cAMP, PKA, adenyl cyclase, calcium, potassium channels.
Serotonin binds to sensory neurons. This activates adenyl cyclase, which promotes production of cAMP.
Increased cAMP results in short-term sensitisation:
Increase of synaptic strength of sensory to motor neuron connection (short-term facilitation).
In addition there is depression of potassium channels because of PKA, which helps increase sensory neuron excitability.
Also, influx of calcium (due to PKC).
The increase in cAMP, Potassium channels depression and Ca influx cause the sensory neuron to be more excitable.
Cellular mechanisms of long-term memory formation in Aplysia:
Repeated stimulus of tail results in repeated enhancement of … and PKA . Short-term learning is still happening (depression of …, elevation of …). But also, … is activated –> CREB-2/CREB-1 are activated, which produce a persistent kinase (more long-term). Also, CREB expresses …, which express …, which results in growth of … . More transcription factors, more protein synthesis, which means synaptic and formation of new … .
Repeated stimulus of tail results in repeated enhancement of *cAMP and PKA. Short-term learning is still happening (depression of potassium channels, elevation of calcium channels). But also, MAPK is activated –> CREB-2/CREB-1 are activated, which produce a persistent kinase (more long-term). Also, CREB expresses early genes, which express late genes, which results in growth of transcription factors. More transcription factors, more protein synthesis, which means synaptic growth and formation of new synapses.
What is an important factor in cellular mechanisms of long-term memory i.e. transport?
There is retrograde transport from the synapse to the nucleus, which causes activation of nuclear transcription factors.
Thus, induction of gene expression.
Associative olfactory learning and memory involves learning the contingency between an odour (CS) and an aversive or appetitive stimulus (US).
Which enzyme performs the integration of these two types of sensory information in the fly brain?
Adenyl cyclase performs this integration function in the mushroom body neurons of the fly brain.
Which neurons carry information about aversive stimuli and which neurons about appetitive stimuli.
Dopaminergic neurons carry information about aversive stimuli and octopaminergic neurons about appetitive stimuli to the MB neurons.
Describe the process of aversive olfactory conditioning: An odour (CS) is presented to ... neurons by PNs. The PNs release ... at the synapses with MB causing voltage-gated calcium channels to open. Increase in intracellular Ca concentration produces more ... bound with Ca, which then activates adenylyl cyclase, producing an elevation in ... . The aversive stimulus (US) is presented to the MB neurons by ... neurons, which release dopamine onto MB neurons. Activation of dopamine receptors also increase ... levels through G-protein signalling to adenylyl cyclase.
An odour (CS) is presented to *MB* neurons by PNs. The PNs release *ACh* at the synapses with MB causing voltage-gated calcium channels to open. Increase in intracellular Ca concentration produces more *calmodulin (CaM)* bound with Ca, which then activates adenylyl cyclase, producing an elevation in *cAMP*. The aversive stimulus (US) is presented to the MB neurons by *PPL1/PPL2ab* neurons, which release dopamine onto MB neurons. Activation of dopamine receptors also increase *cAMP* levels through G-protein signalling to adenylyl cyclase.
