8 & 9 - Synaptic Plasticity and Associative Learning Flashcards Preview

PSYC3014 - Behavioural & Cognitive Neuroscience > 8 & 9 - Synaptic Plasticity and Associative Learning > Flashcards

Flashcards in 8 & 9 - Synaptic Plasticity and Associative Learning Deck (21):

Explain the Hebbian synapse

Describes the neural mechanisms for learning

A US and UR have hard-wired synaptic connections

When a CS and US occur simultaneously, weak CS synapse are formed with neurons controlling the behaviour.

This connection is strengthened over time.


What are the three regions of the hippocampus?

CA1, CA2 and CA3 (cornu ammonis)


How is LTP demonstrated in the hippocampus?

- Weak stimulation of pre-synaptic input causes weak to no activity in post-synaptic neuron
- Strong, high frequency stimulation of pre-synaptic causes long-lasting increase in sensitivity of post-synaptic
- Weak stimulation of pre-synaptic now produces AP in post-synaptic


Explain why LTP is dose dependent

Weak HFS can produce short -lived potentiation, strong HFS produces long-ives.


What is Theta Burst Stimulation?

Bursts of stimulus at theta frequency.

E.g. 5 pulses in 50 ms repeated every 200ms

Duration on LTP depends on number of TBSs


What are the three properties of LTP that recommends it as a model of learning and memory?

Persistance (potentiation enduring, essential for LTM)

Synaptic Specificity (only stimulated pre-synaptic inputs show potentiation, memories are specific)

Associativity (Can get LTP at pre-synaptic inputs by weakly stimulating an input at the same time as a strong stimulus)


What is the evidence that demonstrates that plasticity is bi-directional?

Long-term depression

Reduce the effectiveness of a synapse with long-frequency stimulation.

Delivering one pulse every second that is low frequency


What is the evidence of LTP and learning sharing common mechanisms?

- Correlations; age-related decline in learning correlates with decline in LTP induction in hippocampus
- Saturation of LTP affects learning.
- Share common neurochemistry; pharmacological interventions that prevent LTP, disrupt learning


Why is LTP dependent on the release of glutamate?

1. Glu binding to AMPA receptors (fast depolarisation of recipient neurone)

2. Glu binding to NMDA receptors (responsible for plasticity processes)


Explain how glutamate functions in LTP

Glu from pre-synaptic terminal binds to AMPA receptors on post-synaptic neurone, causing depolarisation of post-synaptic neurone.
Sodium flows in and causes EPSP

Glu must bind to NMDA receptors, opening Ca2+ channels


What does the binding of Glutamate to NMDA receptors achieve?

NMDA receptor has Ca2+ channel, so when it binds Ca2+ enters the cell, cascade of processes occurs, leading to potentiation.

Increases number of AMPA receptors


What are the special properties of NMDA that underlie synaptic plasticity?

1. Admits Ca2+ into the neuron (cascade of changes within the cell causing increased sensitivity, also ncrease AMPA receptors, increasing Na+, increased excitability)

2. The Ca2+ channels on NMDA receptors are ligand and voltage gated which are responsible for specificity and associativity.


Explain the gating channels of NMDA receptors

Ligand-gated; Glu must bind to NMDA receptor

Voltage-gated; post-synaptic neurone must be depolarised to remove Mg2+ which clogs pore


What are post-translational changes?

Rapid-response changes that do not require translation as they use existing proteins.

Not very stable, but fast. Need other processes to stabilise.


What are the stages that convert initial learning into long-term memory?

1. Generating the Synaptic Change (constitutive trafficking, actin breakdown)

2. Stabilising Changes (rebuild and re-organise actin, cell-adhesion molecules)

3. Consolidating Changes (translation and transcription of mRNA, spine growth)

4. Maintaining Changes


Describe constitutive trafficking

Receptors are being continually recycled.

- AMPA receptors diffuse laterally
- Membrane absorbs AMPA R into dendritic spine through endocytosis
- Endosome forms to hold the R
- This gets delivered back to the membrane and pushed back into synapse


What can up regulate constitute trafficking?

Protein kinases


What occurs to actin during plasticity changes?

Ca2+ influx triggers an enzyme to disassemble actin filaments (cytoskeleton) in the dendritic spine, which otherwise obstruct AMPA trafficking.

Ca2+ influx then triggers myosin 2b to shear actin into short segments which are then polymerised into long filaments by coflin, and cross-linked with spectrin


What are the role of cell-adhesion molecules in plasticity?

Ca2+ dependent cell adhesion molecules form bridges between pre- and post-synaptic membranes.

Ca2+ influx through NMDA-R converts weakly-adhesive monomer to strong-adhesive dimer to stabilise the synapse


Why and how does spine growth occur in plasticity/

Sustained synaptic activity leads to long lasting polymerisation of actin cytoskeleton, increasing the dendritic spine.

Depends on brain-derived neurotrophic factor and transcription of mRNA

New cytoskeleton provides scaffold for routine trafficking


What are the outcomes for an enlarged dendritic spine?

More effective
More stable
May lose plasticity