Lecture 33-35: Neuroplasticity Flashcards
Short term potentiation is mainly due to
the delay of calcium release from synaptotagmin
Three ways to increase strength of synapses
- Increase in Pr (Probability of release) of vesicles 2. Increase in N (number of release sites) i.e. insertion of new active zones into synapse 3. Increase in q (quantal size)
How can you achieve an increase in probability of release of vesicles?
More Ca2+ flux into the presynaptic terminal More docked vesicles
How can you achieve an increase in N (number of release sites)?
Unsilencing of synapses (pre or postsynaptic) Production/synthesis of new synapses
How can you achieve an increase in q (quantal size)?
Increase in AMPA receptors (only if AMPA receptors of that synapse are saturated) Change in AMPA receptor kinetics
True or false: Most LTP is associative.
True.
True or false: Associative LTP only occurs if presynaptic neuron fires at the same time as the postsynaptic neuron
False, associative LTP occurs if presynaptic neuron fires just before postsynaptic neuron (within 1 millisecond)
True or false: Non-associative LTP requires NDMA receptors, but associative does not.
False, it is the associative that requires NDMA receptors.
The connection between the entorhinal cortex and the dentate gyrus is called the
Perforant pathway
The connection between the dentate gyrus and region CA3 is called the
Mossy fibre pathway
The connection between region CA3 and region CA1 is called the
Schafer collateral pathway
The connection between region CA1 and the entorhinal cortex is called the
Subicular return pathway
Which pathway does not follow the curvature of the hippocampus?
Perforant pathway (it perforates the two cell layers)
When a glutamate vesicle is released, how many glutamate molecules are released?
When a glutamate vesicle is released, 5000 glutamate molecules are released which bind to all 3 types of glutamate receptor
Effects of NMDA activation
Ca2+ entry via NMDA receptors leading to:
- Ca2+ release from intracellular stores through activation of PKC
- Ca2+ entry via VACCs, as at all synapses
- Activation of CaCam Kinase II (by Ca2+)
- Activation of PKA and PKC (by Ca2+ and DAG)