Nerve Membrane – Physiology · FCPS Part 1

Final FCPS rapid-revision sheet

Topic	One-line answer
Na⁺/K⁺ pump	3 Na⁺ out, 2 K⁺ in, using ATP
Main determinant of RMP	High resting K⁺ permeability
Nernst equation	Equilibrium potential of one ion
Goldman equation	Membrane potential considering multiple ions and their permeabilities
Action potential upstroke	Voltage-gated Na⁺ channel opening
Repolarization	Na⁺ channel inactivation plus K⁺ efflux
After-hyperpolarization	Delayed closure of K⁺ channels
All-or-none principle	Threshold triggers a full action potential
Absolute refractory period	Na⁺ channel inactivation
Relative refractory period	Incomplete recovery plus elevated K⁺ conductance
Saltatory conduction	Regeneration at nodes of Ranvier
Fastest fibres	Aα
Slowest fibres	C
Fast pain	Aδ
Slow pain	C
CNS myelin	Oligodendrocytes
PNS myelin	Schwann cells
Hypocalcaemia	Increased excitability and tetany
Hyperkalaemia	Depolarization followed by possible Na⁺ channel inactivation
Local anaesthetics	Voltage-gated Na⁺ channel blockade

Electrically active cell membrane

The cell membrane is a phospholipid bilayer. Because its core is hydrophobic, charged ions cannot freely cross it and require specific membrane proteins.

Membrane protein / channel	Stimulus or function	Example
Ligand-gated channel	Opens when a chemical messenger binds	Postsynaptic receptors
Mechanically gated channel	Opens in response to stretch, pressure or deformation	Touch receptors
Voltage-gated channel	Opens or changes state in response to membrane voltage	Na⁺ channels during action potentials
Leak channel	Permits passive ion movement at rest	K⁺ leak channels
Na⁺/K⁺-ATPase	Uses ATP to maintain Na⁺ and K⁺ concentration gradients	3 Na⁺ out, 2 K⁺ in per ATP

FCPS pearl: Ion channels permit passive movement down an electrochemical gradient; the Na⁺/K⁺ pump uses ATP to maintain the gradients needed for electrical activity.

Important electrical values

Parameter	Typical value	Significance
Resting membrane potential	−70 mV	Baseline neuronal voltage
Threshold potential	−55 mV	Approximate voltage at which regenerative depolarization begins
Action potential peak	+30 mV	Inside becomes positive
Na⁺ equilibrium potential	+60 to +61 mV	Electrical balance for Na⁺
K⁺ equilibrium potential	−90 to −94 mV	Electrical balance for K⁺
Extracellular Na⁺	142 mEq/L	High outside the cell
Intracellular Na⁺	14 mEq/L	Low inside the cell
Intracellular K⁺	140 mEq/L	High inside the cell
Extracellular K⁺	4 mEq/L	Low outside the cell

Diffusion potentials: Nernst vs Goldman

Feature	Nernst equation	Goldman-Hodgkin-Katz equation
Determines	Equilibrium potential of one ion	Membrane potential influenced by multiple ions
Main factors	Ion concentration gradient and charge	Ion concentrations, membrane permeabilities and ion charges
Application	Calculates (E_K) or (E_Na)	Estimates resting membrane potential
FCPS pearl	One ion at equilibrium	K⁺ dominates at rest because of high permeability

Phase	Main mechanism	Voltage change
Resting	K⁺ leak conductance; voltage-gated channels at rest	Approximately −70 mV
Depolarization	Rapid opening of voltage-gated Na⁺ channels; Na⁺ enters	−55 mV toward +30 mV
Peak / overshoot	Na⁺ channels inactivate; K⁺ conductance rises	Inside becomes positive
Repolarization	K⁺ exits; Na⁺ channels remain inactivated	Returns toward −70 mV
After-hyperpolarization	K⁺ channels close slowly	Becomes temporarily more negative than rest

Threshold and all-or-none principle

Concept	Explanation
Threshold	Approximate voltage needed to initiate a regenerative action potential
Positive feedback	Na⁺ entry causes depolarization, opening more voltage-gated Na⁺ channels
All-or-none response	Once threshold is reached, a full action potential occurs
Stronger stimulus	Generally increases action potential frequency, not the amplitude of each spike
Subthreshold stimulus	Produces a graded response but no propagated action potential

Refractory periods

Feature	Absolute refractory period	Relative refractory period
Can another action potential occur?	No	Yes, with a stronger stimulus
Main mechanism	Most voltage-gated Na⁺ channels are inactivated	Some Na⁺ channels have recovered, but K⁺ conductance may remain elevated
Membrane state	During depolarization and much of repolarization	Usually during late repolarization and after-hyperpolarization
Significance	Limits maximum firing frequency	Reduces excitability temporarily

Propagation of action potentials

Feature	Continuous conduction	Saltatory conduction
Fibre type	Unmyelinated	Myelinated
Propagation	Sequential regeneration along the membrane	Regeneration at nodes of Ranvier
Speed	Slower	Faster
Energy requirement	Relatively higher	Relatively lower
Mechanism	Local currents depolarize adjacent membrane	Local currents travel beneath myelin to the next node
FCPS pearl	No myelin insulation	Myelin increases membrane resistance and decreases capacitance

Why is propagation normally unidirectional?

The membrane immediately behind the advancing action potential is refractory, preventing immediate re-excitation in the backward direction.

Conduction velocity

In myelinated fibres, velocity increases with fibre diameter.
In unmyelinated fibres, velocity also increases with diameter, but remains much slower at comparable diameters.

Nerve fibre classification

Fibre	Myelination	Diameter (approx.)	Velocity (approx.)	Main function
Aα	Heavy	12–20 μm	70–120 m/s	Somatic motor, proprioception
Aβ	Heavy	5–12 μm	30–70 m/s	Touch, pressure
Aγ	Myelinated	3–6 μm	15–30 m/s	Motor supply to intrafusal muscle fibres
Aδ	Thin myelin	2–5 μm	12–30 m/s	Fast pain, cold
B	Thin myelin	Usually under 3 μm	3–15 m/s	Preganglionic autonomic
C	Unmyelinated	0.4–1.2 μm	0.5–2 m/s	Slow pain, warmth, postganglionic sympathetic

Must-know comparisons

Question	Answer
Fastest nerve fibres?	Aα
Slowest nerve fibres?	C
Fast pain?	Aδ
Slow, dull pain?	C
Preganglionic autonomic fibres?	B
Postganglionic sympathetic fibres?	Mostly C
Motor supply to muscle spindles?	Aγ
Touch and pressure?	Aβ

Demyelinating disorders

Feature	Multiple sclerosis (MS)	Guillain–Barré syndrome (GBS)
Site	CNS	PNS
Myelin-producing cell	Oligodendrocyte	Schwann cell
Mechanism	Immune-mediated CNS demyelination	Immune-mediated peripheral nerve injury
Typical presentation	Neurological deficits separated in time and anatomical location	Acute progressive weakness, commonly ascending
Reflexes	Variable	Often reduced or absent
FCPS pearl	CNS myelin disease	Peripheral neuropathy; axonal variants also occur

Effects of electrolytes on excitability

Disturbance	Membrane effect	Clinical consequence
Hyperkalaemia	Resting membrane depolarizes	Initially may increase excitability; sustained depolarization inactivates Na⁺ channels and impairs conduction
Hypokalaemia	Often hyperpolarizes the resting membrane	Muscle weakness and altered excitability
Hypocalcaemia	Lowers the threshold for neuronal excitation	Tetany, paraesthesia, Chvostek and Trousseau signs
Hypercalcaemia	Generally increases threshold for excitation	Reduced neuromuscular excitability

Important distinction: Hyperkalaemia does not always increase excitability. Mild depolarization may initially do so, but severe or sustained depolarization can cause weakness, conduction block and life-threatening cardiac arrhythmias.

Local anaesthetics

Local anaesthetics prevent action potential propagation by blocking voltage-gated Na⁺ channels.

Feature	Key fact
Site of action	Intracellular side of voltage-gated Na⁺ channels
Main effect	Prevents rapid Na⁺ influx and action potential propagation
Use-dependent block	Frequently active channels are blocked more readily
Pain fibres	Small Aδ and C fibres are often blocked before larger motor fibres under suitable clinical conditions
Clinical variation	Fibre type, firing frequency, myelination, drug concentration and nerve anatomy all influence block