Anatomy
Neuron Structure
Dendrites, soma, axon, myelin — the architecture of a signaling cell
A neuron is the excitable cell that processes and transmits information through electrical and chemical signals. Three regions: dendrites (input — branched, covered with thousands of synapses, integrate signals), soma (cell body — contains nucleus, organelles; sums inputs at axon hillock), axon (output — single, can be >1 m long; conducts action potentials). Many axons are myelinated by oligodendrocytes (CNS) or Schwann cells (PNS) — wrapped in lipid sheaths interrupted by nodes of Ranvier (~1 μm), allowing saltatory conduction up to 120 m/s vs ~0.5-2 m/s unmyelinated. Adults have ~86 billion neurons (Herculano-Houzel 2009), each forming ~1,000-10,000 synapses on average. Demyelinating disease (MS, GBS), neuronal loss (ALS, Alzheimer, Parkinson), and axonal injury (peripheral neuropathy from diabetes, chemotherapy) define many neurological disorders.
- Total neurons (brain)~86 billion
- Synapses per neuron~1,000-10,000 average
- Longest axon~1 m (sciatic nerve to foot)
- Resting potential~−70 mV (inside relative to outside)
- Myelinated conductionUp to 120 m/s
- Action potential threshold~−55 mV
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Why neuron structure matters
- Signal conduction. Neuron architecture determines speed and reliability.
- Demyelinating disease. MS, GBS, CMT — defined by myelin damage.
- Neurodegeneration. ALS, Alzheimer, Parkinson — distinct neuron classes lost.
- Stroke. Penumbra and ischemic core determine recovery; neurons die in minutes.
- Peripheral neuropathy. Diabetic, chemo, alcoholic — distal axonal die-back.
- Drug pharmacology. Receptors and channels at synapses are key targets.
- Neural prosthetics. Cochlear, retinal, BCI exploit electrical activity.
Common misconceptions
- Neurons fire continuously. Most fire intermittently; rate encodes information.
- Bigger neurons fire faster. Myelination matters more than size; some big axons are slow if unmyelinated.
- Action potential amplitude varies. All-or-nothing; signal strength is in firing rate.
- Glia are just support cells. Astrocytes, oligodendrocytes, microglia actively shape signaling and immunity.
- All synapses are chemical. Electrical (gap junction) synapses also exist.
- Damaged CNS axons regenerate like PNS. CNS regeneration largely fails; major therapeutic target.
Frequently asked questions
What does each part of the neuron do?
Dendrites — receive synaptic input from thousands of other neurons; covered with spines hosting receptors. Soma — contains nucleus, ER, Golgi, mitochondria; protein synthesis hub. Axon hillock — summation point; if depolarization reaches threshold (~−55 mV), action potential initiates. Axon — propagates AP to terminal. Synaptic terminal (bouton) — releases neurotransmitter onto next cell. Most neurons are multipolar (one axon, many dendrites); pseudo-unipolar (DRG sensory) and bipolar (retina) are special cases.
How is the action potential generated?
Resting potential ~−70 mV maintained by Na/K ATPase and K leak. Depolarization to threshold (~−55 mV) opens voltage-gated Na⁺ channels — rapid Na⁺ influx (rising phase, peaks ~+30 mV). Inactivation of Na channels and opening of voltage-gated K⁺ channels — K⁺ efflux drives repolarization. Brief hyperpolarization (afterhyperpolarization). Refractory period (Na channels recover) prevents backward propagation. Whole AP: ~1-2 ms. All-or-nothing: amplitude is constant; information is encoded in firing rate and pattern.
What is myelin and saltatory conduction?
Myelin is a lipid-rich (~70-80% lipid) insulating sheath wrapped around axons. CNS — formed by oligodendrocytes, each ensheathing ~50 axon segments. PNS — Schwann cells, one per internodal segment. Nodes of Ranvier (~1 μm gaps every ~1 mm) concentrate voltage-gated Na channels. AP "jumps" from node to node (saltare = "to leap"), bypassing myelinated segments — much faster (up to 120 m/s vs 0.5-2 m/s unmyelinated) and energy-efficient (less Na/K pumping required to restore gradients). Loss of myelin (MS, GBS) slows or blocks conduction.
How are signals transmitted at synapses?
Electrical synapses (gap junctions) — direct cytoplasmic continuity; ultra-fast, bidirectional; rare in mammalian CNS but in retina, brainstem, cardiac/smooth muscle. Chemical synapses (most) — AP arrives at terminal, opens voltage-gated Ca²⁺ channels, Ca²⁺ triggers vesicle fusion via SNARE proteins, neurotransmitter (glutamate, GABA, glycine, dopamine, serotonin, norepinephrine, ACh, neuropeptides) crosses ~20 nm cleft, binds receptors. Ionotropic receptors gate ion channels (fast, ms); metabotropic receptors couple to G proteins (slower, longer effects).
What's white matter vs gray matter?
Gray matter — predominantly cell bodies, dendrites, unmyelinated axons, glia, capillaries; brownish-pink in life, gray in fixed tissue. Located cortically (cerebral cortex, cerebellar cortex) and in deep nuclei (basal ganglia, thalamus, brainstem nuclei) and dorsal horn of cord. White matter — myelinated axon tracts; whitish from myelin lipid. Internally in cerebrum and cerebellum, externally in spinal cord. Tracts: corpus callosum (~200 million axons interconnect hemispheres), corticospinal, dorsal columns, spinothalamic. DTI on MRI maps tract integrity.
How do neurons communicate at thousands of synapses?
Each cortical pyramidal neuron has ~10,000 synapses on its dendritic tree. EPSPs (excitatory, mostly glutamate via AMPA/NMDA) depolarize; IPSPs (inhibitory, mostly GABA via GABA-A) hyperpolarize. Spatial summation — inputs at different sites add. Temporal summation — repeated inputs at same site add over time. Active dendritic conductances (Na, Ca channels in dendrites) amplify or filter. If integrated potential at axon hillock exceeds threshold, AP fires. Plasticity — LTP, LTD — adjusts synaptic strength; basis of learning.
What happens when neurons or axons are damaged?
Wallerian degeneration — distal axon segment (cut from soma) breaks down within days. PNS: axons can regenerate (~1 mm/day) along Schwann cell tubes; functional recovery possible if proximal stump aligns with distal nerve sheath. CNS: regeneration largely fails — inhibitory glycoproteins (Nogo, MAG, OMgp), glial scar, and reduced intrinsic neuronal growth state; clinical disability after stroke, spinal cord injury. Demyelination (MS, GBS) — affects conduction without axonal loss initially; remyelination possible. Some demyelinating injuries progress to axonal loss.