Week 9 Flashcards
What is the difference between LTP and LDP in terms of function, memory and frequency of stimulation?
LTP:
- Long lasting strengthening of synapses
- Crucial for memory
- Is induced by high frequency stimulation
LDP:
- Weakening of synapses due to low frequency stimulation or synaptic inactivity
- Involved in pruning, also aiding memory
How does GABA mediate visual development / how is inhibition related to monocular deprivation?
- Neurons receiving information from the left eye receive excitatory input from the left eye but ALSO inhibitory input from the right eye (and vice versa)
- Left eye deprivation = lack of excitatory input AND strengthening of inhibitory input from the right eye
- GABA mediates this
- GABA agonists cause the sensitive period to start and finish earlier
What do NMDA and mGlu produce that are required for plasticity?
CAMKII
MAPK
PKA
PLC-beta1
What are some mechanisms of LDP/LTP expression?
- Altering NT release
- Addition/removal of receptors
- Altering receptor kinetics
- Addition of removal of synapses
How does NMDA activity affect AMPA activity? (2 WAYS)
AMPA Trafficking:
- NMDA activates PKA
- PKA increases number of AMPA receptors in the postsynaptic cell
- No PKA activity = removal of AMPA receptors
Receptor Kinetics:
- PKA acts on AMPA receptors directly to increase the time for which they are open
In addition to altering the receptor kinetics and number of ampa receptors in the postsynaptic cell, NMDA activity also stimulates the production of retrograde messengers.
What are these? and give an example of a class of retrograde messengers
- Chemicals that are released from the postsynaptic cell that work on the presynaptic cell to INREASE subsequent NT release
- Example = Endocannabinoids
- this only happens in some areas, such as the L3 of the visual system
What is meant by spike-dependent plasticity?
- The frequency/timing of incoming potentials has a bearing on whether or not the synapse will undergo LTP or LDP
- Due to back-propagating action potentials
What is metaplasticity?
The ability of neurons to alter the frequencies that induce LTP/LDP. I.e., the ability to change the modification threshold
What is the modification threshold and what happens to it during dark rearing?
- The frequency of input that causes neither LTP or LTD
- In dark reared animals, the MT shifts down, so lower frequencies cause LTP
How is homeostatic plasticity different from Hebbian plasticity?
Homeostatic:
- Homeostatic plasticity is a mechanism that aims to maintain/stabilise the strength of synapses in response to prolonged changes in neural activity.
- Has multiple mechanisms, changing distribution of channels, balance of excitatory and inhibitory input, shortening of the AIS
Hebbian:
- More synapse based! Firing and wiring n all that
What is the difference between excitability and and excitable cell?
Excitable cell:
A cell that can self-propagate electrical signals (neurons and muscle cells)
Excitability
The ability to regulate current flow (ions) across a membrane
How are cell proliferation and migration, and axon guidance regulated by cell excitability?
Cell proliferation and migration:
- Excitatory inputs inhibit progenitor cell proliferation
Axon guidance:
- Ability to respond to netrin gradient is mediated by Ca2+ influx
What are some qualities of the axon initial segment?
- Contain many Na+ channels
- Is plastic and can change with signal it receives
- If the cell is receiving too much excitatory input, the AIS can move away from the soma, making it more difficult to generate an axon potential
How is the action potential different in young animals compared to older animals?
- Mediated by Ca2+ in young, Na+ in old
- Ca2+ channels are slower to close than Na+ channels, so young animals have longer AP than adults
Explain why there is a switch in GABA function from excitatory when young to inhibitory
In adults:
- There is high chloride content OUTSIDE the cell due to the potassium-chloride transporter KCC2
- When GABA receptors open, Cl- flows into the cell, hyperpolarising it
In Young:
- KCC2 is not expressed yet and NKCC1 IS expressed, this increases the amount of Cl- WITHIN the cell
- therefore, when GABA opens, Cl flows out the cell causing depolarisation
