Electrical Excitabilty (5) Flashcards
Via what mechanism are neurotransmitter released from vesicles?
- Ca channels open and Ca influx occurs
- Ca binds to synaptotagmin
- Vesicles brought close to membrane
- Snare complex makes a fusion pore
- Transmitter released through this pore
What happens at the nerve terminal?
- Depolarisation open voltage gated Ca channels
- Ca entry
- Increase in Ca conc inside
- Causing release of neurotransmitter
ACh is released from the vesicles what does this do to stimulate an AP in the post synaptic axon?
- ACh binds to nicotinic ACh receptor channels
- Na/K channel is ligand gated to ACh.
What is the end plate potential?
- Depolarisation caused by binding of neurotransmitters to axon.
- Activation of nAChR by ACh
What may cause a decrease in end plate potential?
- Transmitter release is dependent on Ca entry
- If external Ca is lowered the end plate potential decreases in amplitude
How is ACh degraded?
- ACh esterase in synaptic cleft
How does a depolarising blocker work?
- Maintained depolarisation will fail to activate adjacent Na channels as they’ve become inactivated.
What are miniature end plate potentials?
Spontaneous release of vesicles without stimulus (~1/s)
What is myasthenia gravis?
- Autoimmune disease targeting nAChR
What are the symptoms of Myasthenia gravis?
- Profound weakness
- Weakness increases with exercise
What are the causes of Myasthenia gravis?
- Antibodies directed against nAChR on post-synaptic membrane of skeletal muscle
- Antibodies lead to loss of functional nAChR by complement mediated lysis and receptor degradation
- Leads to end plate potentials decreasing in amplitude -> muscle weakness and fatigue
What is the possible treatment of Myasthenia gravis?
- Inhibit ACh-esterase to allow more ACh
What does ACh also bind to other than nAChR?
- Muscarinic AChR
- mAChR produces a slower response as they’re coupled to G proteins which trigger a cascade of events in the cell.
Outline what happens in an action potential in an axon.
- Some K channels are open to establish resting potential via electrochemical gradient, so K influx until eqm is reached
- Threshold value is reached, voltage gated Na channels open leading to depolarisation as Na influx occurs. Up to +30mv
- At +30mv Na voltage gated channels become inactivated and are blocked until hyperpolarisation
- K voltage gated channels open due to potential causing K efflux and repolarisation.
- K permeability increases, all K voltage gated channels are open
- Na are free from inactivation, no K voltage gated channels open - hyperpolarisation
- Return to start, Na/K ATPase helps re-establish the ionic conc.
Why do we have unmyelinated axons?
- Unmylinated is faster but dissipates over a long distance
- So for pain unmyelinated is used as quick reactions are needed
- But for long nerves such as musculo-cutaneous can’t use unmyelinated as would dissipate
