Neuron

Neuronum

Also known as: nerve cell, neurone

The excitable cell that is the structural and functional unit of the nervous system. It receives input on its dendrites and soma, integrates it at the axon hillock, and transmits action potentials along its axon to synapses on other cells.

Neuron & Action Potential

Overview

Neurons in human brain≈86 billion

Cerebellum / cerebral cortex≈69 bn / ≈16 bn

Soma diameter≈5–100 µm (granule cell → α motor neuron)

Longest axons≈1 m (sciatic motor/sensory fibres)

Fast axonal transport≈200–400 mm/day

The human brain contains about 86 billion neurons: ≈69 billion in the cerebellum (mostly granule cells) and ≈16 billion in the cerebral cortex. They are linked by an estimated 10¹⁴–10¹⁵ synapses. Neurons are highly polarised cells with distinct compartments. Dendrites are the receptive surface. The soma (perikaryon) is the metabolic centre. The axon hillock and initial segment form the trigger zone where action potentials begin. The axon conducts, and the axon terminals release neurotransmitter.

Neurons have three special properties. They are excitable, generating and propagating action potentials. They are largely post-mitotic (amitotic), so lost neurons are generally not replaced; limited adult neurogenesis is described in the hippocampal dentate gyrus and the olfactory system. And they have a very high metabolic rate, depending on a continuous supply of glucose and oxygen; consciousness is lost within ≈10 s of cerebral circulatory arrest. They can live as long as the person.

Because an axon may be up to a metre long and may hold >99% of the cell's volume, neurons depend on axonal transport. Kinesin carries cargo anterogradely along microtubules and dynein carries it retrogradely. This transport supplies the axon and returns trophic signals to the soma, and it is also the route by which some toxins and viruses reach the CNS.

Parts & subdivisions

Dendrites
Short, tapering, highly branched processes that receive most synaptic input. They are covered in dendritic spines, the sites of most excitatory (glutamatergic) synapses and of structural plasticity. They contain Nissl substance, mitochondria and microtubules, and conduct graded (electrotonic) potentials toward the soma.
Soma (perikaryon)
The cell body, containing a large, pale, euchromatic nucleus with a prominent nucleolus ("owl's eye"), abundant rough ER in clumps (Nissl bodies, basophilic), an extensive Golgi apparatus, many mitochondria, neurofilaments and microtubules, and lipofuscin with age. It is the biosynthetic centre of the neuron.
Axon hillock and initial segment
The cone-shaped origin of the axon from the soma. It lacks Nissl bodies, which is a histological identifier. The adjoining initial segment has the highest density of voltage-gated Na⁺ channels, so it has the lowest threshold and is the trigger zone where summated synaptic potentials initiate the action potential.
Axon
A single process of uniform diameter (≈0.2–20 µm) that may give off recurrent collaterals at right angles. Its plasma membrane is the axolemma and its cytoplasm the axoplasm. It contains microtubules and neurofilaments but no rough ER, so all proteins must be shipped from the soma.
Myelin sheath
A segmented lipid-rich wrapping formed by oligodendrocytes (CNS) or Schwann cells (PNS). It insulates the axon, raising membrane resistance and lowering capacitance, which enables saltatory conduction.
Nodes of Ranvier
Gaps (≈1 µm) between adjacent myelin segments, where the axolemma is exposed and packed with voltage-gated Na⁺ channels (Nav1.6). The paranodes and juxtaparanodes hold K⁺ channels. The action potential "jumps" from node to node.
Axon terminals (telodendria and boutons)
Terminal branches ending in synaptic knobs (boutons) that contain synaptic vesicles, mitochondria and voltage-gated Ca²⁺ channels at active zones. They release neurotransmitter by Ca²⁺-triggered exocytosis.

Anatomy

Histology: Stains: Nissl stains (cresyl violet) show rough ER and soma; silver stains (Golgi, Bielschowsky) show processes and neurofibrils; Luxol fast blue shows myelin. Ultrastructurally there are neurofilaments (intermediate filaments), microtubules (with MAPs such as tau in the axon and MAP2 in dendrites) and actin at spines and growth cones. After axotomy the soma undergoes chromatolysis: it swells, the Nissl bodies disperse and the nucleus moves to the periphery.
Development: Derived from neuroectoderm: neural tube (CNS neurons) and neural crest (sensory and autonomic ganglion neurons, enteric neurons). Neuroblasts migrate along radial glia to their destinations.

Function

Receives and integrates synaptic and sensory input (spatial and temporal summation).
Generates and conducts action potentials.
Transmits signals to other neurons, muscle or glands through synapses.
Stores information through synaptic plasticity (learning and memory).
Neurosecretion: some neurons release hormones into blood, for example hypothalamic neurons releasing ADH and oxytocin.

Physiology: Axonal transport: fast anterograde (kinesin, ≈200–400 mm/day) carries vesicles and membrane proteins. Slow anterograde (≈0.2–8 mm/day) carries cytoskeletal proteins and cytosolic enzymes. Retrograde (dynein, ≈100–200 mm/day) returns used material and trophic factors such as NGF. Neurons rely on oxidative metabolism of glucose and have minimal energy stores.

Clinical significance

Retrograde axonal transport as a route of infection

Rabies virus (from a bite), tetanus toxin, herpes simplex and varicella-zoster virus, and poliovirus travel retrogradely by dynein from peripheral terminals to the neuronal soma in the CNS or sensory ganglia. This explains the latent period of rabies, which is longer for bites far from the head.

Neurodegeneration and tau

Hyperphosphorylated tau detaches from axonal microtubules and aggregates into neurofibrillary tangles in Alzheimer disease, disrupting transport. α-synuclein aggregates (Lewy bodies) characterise Parkinson disease.

Hypoxic–ischaemic injury

Neurons are the most vulnerable cells to hypoxia, especially hippocampal CA1 pyramidal cells, cerebellar Purkinje cells and cortical layers 3, 5 and 6 (laminar necrosis). Irreversible injury begins after about 4–5 min of global ischaemia. "Red neurons" (eosinophilic, shrunken) appear 12–24 h after injury.

Test yourself

After a stroke, a patient has drooping of the left lower face but can wrinkle the forehead normally on both sides. What does this pattern indicate?

Left facial nerve lesion at the stylomastoid foramen
Bell palsy
Right upper motor neuron (corticobulbar) lesion
Left facial nucleus lesion in the pons

Answer: Right upper motor neuron (corticobulbar) lesion

The part of the facial nucleus that supplies the forehead receives corticobulbar input from both hemispheres, so a unilateral UMN lesion spares the upper face. The weakness is contralateral to the lesion. Any LMN facial lesion paralyses the entire half of the face, forehead included.

The rapid depolarising upstroke of a neuronal action potential is caused by:

Opening of voltage-gated K⁺ channels
Activity of the Na⁺/K⁺-ATPase
Opening of voltage-gated Na⁺ channels
Opening of ligand-gated Cl⁻ channels

Answer: Opening of voltage-gated Na⁺ channels

At threshold (≈ −55 mV), voltage-gated Na⁺ channels open. Na⁺ influx depolarises the membrane further, which opens more channels (positive feedback), and the potential overshoots to ≈ +30 mV. Repolarisation follows from Na⁺ channel inactivation and the opening of delayed-rectifier K⁺ channels.

Where are the cell bodies of preganglionic sympathetic neurons located?

Sympathetic chain ganglia
Sacral segments S2–S4
Ventral horn of all spinal segments
Lateral (intermediolateral) horn of spinal segments T1–L2

Answer: Lateral (intermediolateral) horn of spinal segments T1–L2

The sympathetic outflow is thoracolumbar. Its preganglionic neurons lie in the intermediolateral cell column of segments T1–L2 and leave through the ventral roots and white rami communicantes. The S2–S4 segments give parasympathetic outflow.