Synopsis
Explain membrane excitability, synaptic transmission, sensory coding, motor control and nociceptive modulation, then apply them to localisation and pain mechanisms.
- Resting potential reflects selective permeability and maintained ion gradients; threshold opens regenerative voltage-gated channels, producing an all-or-none action potential.
- Myelin raises membrane resistance and lowers capacitance, allowing saltatory conduction between nodes; demyelination slows or blocks propagation by reducing current safety margin.
- Chemical synapses convert presynaptic depolarisation into calcium-dependent transmitter release, receptor activation and excitatory or inhibitory postsynaptic potentials.
Reasoning priorities
Predict the voltage toward which a selective conductance drives membrane.
Use ion gradient and charge direction together; opening a channel shifts voltage toward, not necessarily all the way to, that ion's equilibrium potential.
Worked reasoning
A model axon has normal ion gradients and nodal sodium channels, but one internodal segment loses myelin, increasing membrane capacitance and current leak.
- Recognise that local current leaving the upstream node must charge the downstream membrane to threshold.
- Loss of myelin increases the charge required and allows more current to escape across the exposed internode.
- The downstream node reaches threshold later or not at all, producing slowed conduction, temporal dispersion or block depending on safety margin.
- The final predicted physiological outcome is unreliable propagation despite intact upstream action-potential generation.
- Verify by distinguishing axonal loss: demyelination primarily disrupts conduction properties, whereas loss of axons reduces the number of conducting fibres.