Anatomy and Physiology of Nerves

🧠 Nerve Cells (Neurons): Anatomy & Physiology

Neurons are highly specialised excitable cells designed for rapid communication within the nervous system. They receive, integrate, and transmit electrical signals over long distances and convert these signals into chemical messages at synapses. This capability underpins sensation, voluntary movement, autonomic regulation, cognition, and higher cortical function.

Unlike most cells, neurons are post-mitotic and must function for a lifetime. Structural damage, metabolic failure, or disruption of ion channel function therefore has immediate and often irreversible clinical consequences.

🔬 Basic Anatomy of a Neuron

The anatomy of a neuron is tightly coupled to its function. Each component contributes to signal reception, integration, propagation, or transmission.

Figure: Typical neuron showing dendrites, soma, axon, myelin sheath, nodes of Ranvier, and axon terminals. This structural layout explains both rapid conduction and directional signalling.

• Dendrites: Branched processes receiving synaptic input; allow spatial and temporal summation of thousands of signals.
• Cell body (soma): Contains nucleus and metabolic machinery; integrates incoming excitatory and inhibitory signals.
• Axon hillock: Trigger zone with high density of voltage-gated sodium channels where action potentials are initiated.
• Axon: Long projection specialised for rapid electrical conduction over distance.
• Myelin sheath: Lipid-rich insulation (oligodendrocytes in CNS, Schwann cells in PNS) that increases conduction speed.
• Nodes of Ranvier: Gaps in myelin rich in ion channels enabling saltatory conduction.
• Axon terminals: Presynaptic endings releasing neurotransmitters into the synaptic cleft.

⚙️ Neuronal Physiology: Resting Membrane Potential

At rest, neurons maintain a stable electrical gradient across their membrane known as the resting membrane potential (approximately −70 mV). This polarity is essential for excitability and action potential generation.

• High intracellular potassium (K⁺) and low intracellular sodium (Na⁺).
• High extracellular sodium (Na⁺) and chloride (Cl⁻).
• Na⁺/K⁺ ATPase: Pumps 3 Na⁺ out and 2 K⁺ in, maintaining ionic gradients.
• Potassium leak channels: Allow passive K⁺ efflux, the main determinant of resting potential.

Small changes in extracellular potassium can significantly alter neuronal excitability, explaining neurological features of hypo- and hyperkalaemia.

⚡ Action Potential: Electrical Signalling

An action potential is a rapid, stereotyped reversal of membrane polarity that propagates along the axon without decrement. It obeys the all-or-nothing principle once threshold is reached.

Figure: Phases of the action potential showing depolarisation, repolarisation, and hyperpolarisation driven by voltage-gated sodium and potassium channels.

• Threshold (~−55 mV): Achieved when depolarising inputs exceed inhibitory influences.
• Depolarisation: Rapid opening of voltage-gated Na⁺ channels → Na⁺ influx.
• Peak (~+30 mV): Na⁺ channels inactivate.
• Repolarisation: Voltage-gated K⁺ channels open → K⁺ efflux.
• Hyperpolarisation: Continued K⁺ efflux temporarily overshoots resting potential.
• Return to rest: Gradients restored by pumps and leak channels.

⛔ Refractory Periods

Refractory periods ensure unidirectional propagation and limit the maximum firing frequency of neurons.

• Absolute refractory period: Na⁺ channels are inactivated; no action potential can occur.
• Relative refractory period: Stronger stimulus required due to ongoing hyperpolarisation.

🚀 Conduction of Action Potentials

Action potentials propagate along the axon without loss of amplitude. Conduction velocity depends on axon diameter and myelination.

• Continuous conduction: Seen in unmyelinated fibres; slow and energy-intensive.
• Saltatory conduction: Action potentials jump between nodes of Ranvier in myelinated fibres.
• Myelination increases speed and reduces metabolic cost.
• Larger diameter axons conduct faster due to reduced internal resistance.

Demyelination slows or blocks conduction, explaining weakness, sensory loss, and fatigue in disorders such as multiple sclerosis.

🔄 Synaptic Transmission

At synapses, electrical signals are converted into chemical signals, allowing precise and modifiable communication between cells.

• Action potential reaches presynaptic terminal.
• Voltage-gated Ca²⁺ channels open → Ca²⁺ influx.
• Ca²⁺ triggers neurotransmitter vesicle fusion.
• Neurotransmitters bind postsynaptic receptors.
• Postsynaptic potentials may be excitatory (EPSP) or inhibitory (IPSP).

🧬 Sensory Nerve Fibres

• Ia (A-alpha): Proprioception from muscle spindles; fastest conduction (70–120 m/s).
• Ib (A-alpha): Golgi tendon organs; monitor muscle tension.
• II (A-beta): Touch, pressure, vibration.
• III (A-delta): Fast, sharp pain; cold temperature.
• IV (C fibres): Slow, dull pain; heat; itch; unmyelinated.

🦵 Motor & Autonomic Fibres

• A-alpha: Voluntary skeletal muscle contraction.
• A-gamma: Muscle spindle sensitivity and tone.
• B fibres: Preganglionic autonomic fibres (myelinated).
• C fibres: Postganglionic autonomic fibres (unmyelinated).

🩺 Clinical Integration & Exam Pearls

• Loss of myelination affects fast fibres first → early proprioceptive and motor deficits.
• Sharp pain precedes dull pain due to A-delta then C fibre activation.
• Autonomic neuropathies predominantly involve small C fibres.
• Channelopathies alter excitability rather than structure.

References

• StatPearls: Neuroanatomy – Nerve Fibers