Molecular mechanisms of learning and memory

24 important questions on Molecular mechanisms of learning and memory

Where in the brain is nondeclarative memory mediated?

Striatum

Nondeclarative memory can be dividen in associative and nonassociative memory

Associative: classical conditioning, pavlov, instrumental conditioning
nonasscociative:  habituation and sensitization

Research conducted instrumental learning on the Aplysia. They found that sensory/motor neurons become habituated

Motor
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Research conducted instrumental learning on the Aplysia, they found that there is habituation at the presynaptic/postsynaptic level due to ....-channels becoming less-sensitive

Presynaptic, calcium channels

Describe the presynaptic modification of the stimulation of the L29 neuron

Electrical stimulation L29 -> serotonine release in synaptic cleft -> serotonin binding post-synapse -> cAMP release -> PKA activation -> closure K+ -> activation calcium channels -> more transmitter release

If bot US and CS reach the motor neuron, what happens?

A huge release of cAMP -> phosphorylation of K channels -> more neurotransmitter in the synaptic cleft

Of which three layers exists the cortex?

Molecular layer -> Purkinje cell layer -> granule cell layer (-> white matter)

From which two fibres gets the Purkinje cell input?

Clmibing fibre and granule cell

What is the pathway of receiving information for the climbing fibre?

Muscle -> olive -> climbing fibre (-> Purkinje)

What is the pathway of receiving information for the Purkinje cells?

Motor cortex -> pontine nuclei -> mossy fibre (becoming granule cell) -> Purkinje fibre)

How responds the Purkinje cell upon stimulation by both parallel and climbing fibres?

It responds with decline: long term depression (molecular change thus happens postsynaptically = decrease in number of AMPA receptors, forgetting)

Which three synapses lie in the HC?

Synapse from entorhinal cortex, which goes to the dentate gyrus, which goes to CA3 region and splits to go to the fornix and CA1

How is hippocampal LTP achieved?

By high frequency stimulation.

What is co-operativity in synapses?

That you need more synapses to fire to get a sufficient signal, otherwise nothing will happen.

What is spatial summation?

That you need all synapses to work together simultaneously.

Describe the process of hippocampal LTP

Stimulus -> glutamate release -> AMPA receptor activation -> sodium influx -> activation

What does a tetanus stimulation to HC LTP?

Calcium influx -> attachment of kinases (CAMKII and PKA) and AMPA receptors to the membrane -> sensitization for glutamate (consolidation)

What will happen if you stimulate synapses with a low frequency? Describe how.

LTD will occur. Low level of calcium -> inducing protein phosphatases -> LTD

What does scaffold protein PSD-95 with AMPA?

It determines how much room there is for AMPA receptors on the membrane.

What does LTP to PSD-95?

LTP causes more PSD-95 which results in more room for AMPAr.

Why does phosphorylation for long-term memory not work?

1. Phosphorylation is not permanent
2. Protein molecules are not permanent (they are constantly replaced)

Of which exist the 10 subunits of CAMKII?

A regulatory (determines activity) and catalytic (does the trick) region.

How does autophosphorylation of CAMKII work and what does it do?

Upon LTP, the subunits of CAMKII kind of phosphorylate each other, which causes remained activity (for about an hour).

What do you need for permanent LTP?

CREB (which can be activated by cAMP), it binds to CRE on the genome and causes gene expression. If CREB is phosphorylated it will remain active and will thus remain causing gene expression.

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