Excitable cells 16: synaptic plasticity Flashcards
What is synaptic plasticity?
Synaptic plasticity is the biological process by which specific patterns of synaptic activity result in changes in synaptic strength
What happens in homosynaptic short term plasticity? Examples?
Amplitude of synaptic potential varies greatly depending on preceding activity
- occurs mainly at high frequency stimulation i.e. APs fired at short intervals
e.g. synaptic depression in climbing fibres to cells-> proceeding signals are weaker
synaptic facilitation in parallel fibres to purkinje cells -> proceeding signals are stronger
Schaffer collateral -> facilitation followed by depression
Describe mechanism of paired-pulse facilitation
1st action potential arrives -> results in release of neurotransmitter as normal
1st action potential causes an increase in the number of primed neurotransmitter vesicles ready for release
Upon arrival of 2nd AP, more vesicles primed -> more neurotransmitter released -> larger response
Which protein is essential for homosynaptic facilitation and why?
Synaptotagmin 7
-> calcium sensor important for vesicular release
This particular protein important in synaptic facilitation, but not regular vesicle release
Explain ‘spike broadening’
After significant repeated stimulation, neuron begins to ‘fatigue’
- > synaptic terminal takes longer to hyperpolarise, meaning it is depolarised for longer
- > results in an increase in signal
Describe the mechanism of homosynaptic depression
1st action potential arrives -> results in release of neurotransmitter as normal
1st action potential causes a depletion in synaptic vesicles
at 2nd AP, fewer vesicles available for release -> less neurotransmitter release -> reduction in response amplitude
Describe difference between low p and high p synapses
low p -> low number of initially primed vesicles, increases in 2nd AP (facilitation)
high p -> high number of initially primed vesicles, decreases in 2nd AP (depression)
Describe in detail 2 examples of post synaptic modulation
1) GABAa receptor modulation by phosphorylation
- In addition to GABAa receptors in post synaptic membrane, serotonin GPCR also present
serotonin GPCR activated -> activates PKA
PKA targets GABAa -> phosphorylation affects GABAa channel activity (can enhance or repress depending on phosphorylation site)
2) GABAa receptors assembled in ER and packaged into vesicles in golgi
- insulin promotes insertion of GABAa receptors into membrane
- brain derived neurotrophic factor (BDNF) promotes removal of GABAa receptors
Higher or lower response depending on receptor number
Describe mechanism of presynaptic heterosynaptic inhibition
Inhibitory input synapse output on activation releases neurotransmitter which activates inhibitory pre-synaptic channels for the main synapse
Results in reduced neurotransmitter output and decreased amplitude of response
Example of well studied case of heterosynaptic facilitation?
Sensitisation of gill withdrawal reflex in Sea Hare (mollusc)
Touch of siphon alone produces weak gill withdrawal response
Touch of siphon briefly after electric shock of tail enhances gill withdrawal response i.e. touch response sensitised
-> shock stimulates facilitating interneuron which acts on motor neuron, facilitating synaptic response
Describe long-term potentiation (LTP) Why is it important?
Synapse receives a stimulus -> normal
Synapse receives multitude of stimuli over a short time -> produces larger response
Another single stimulus some time after -> synapse produces similar high response to previous multitude of stimuli - this is LPT
Important in hippocampus for long term memory
