Neuron Anatomy

A neuron is a nerve cell that processes and transmits information through electrical and chemical signals in the nervous system.

Neurons consist of a cell body, dendrites (which receive signals), and an axon (which sends signals).

Synaptic connections allow communication between neurons, facilitating the relay of information throughout the body.

How do Neurons Work?

Neurons lie adjacent to each other but are not connected.

There is a tiny gap between neurons called a synapse.

A neuron’s job is simple.

It sends an impulse the length of its own axon, then passes the signal across the synapse into the next neuron.

The electrical signals transmitted by neurons are called action potentials.

Synaptic Transmission

Synaptic transmission is how one neuron talks to the next.

Information travels down the axon as an electrical impulse called an action potential. That signal has to cross the synaptic gap to continue its journey to or from the CNS.

This crossing happens chemically. Chemicals called neurotransmitters diffuse across the gap between the two neurons.

During synaptic transmission, the arriving action potential triggers the synaptic vesicles of the presynaptic neuron to release their neurotransmitter.

This chemical handoff is deceptively precise. The arriving impulse opens calcium channels in the terminal, and the calcium rush makes vesicles burst open against the membrane: a process called exocytosis.

The neurotransmitter has now arrived. It diffuses across the synaptic gap and binds to specialised receptor sites on the postsynaptic neuron.

The type of receptor on the other side then decides what happens next. An ionotropic receptor is a channel itself, so it opens immediately for a fast signal lasting about a millisecond.

The difference matters. A metabotropic receptor is not a channel: binding instead sets off a slower chemical cascade inside the cell. The same neurotransmitter can excite one synapse and calm another, depending only on which type of receptor it meets.

Binding like this changes the receiving neuron’s membrane potential.

It nudges the neuron toward firing, or not.

The central nervous system, which comprises the brain and spinal cord, and the peripheral nervous system, which consists of sensory and motor nerve cells, all contain these information-processing neurons.

What are the Parts of a Neuron?

A neuron has three main parts. The soma (cell body) is the core; from it extends the axon, a nerve fiber that conducts electrical impulses away from the soma. Dendrites are tree-like structures that receive signals from other neurons.

The myelin sheath is an insulating layer that forms around the axon and allows nerve impulses to transmit more rapidly along the axon.

The unique structure of neurons permits it to receive and carry messages to other neurons and throughout the body.

Dendrites

Dendrites are the tree-root-shaped part of the neuron which are usually shorter and more numerous than axons.

Their purpose is to receive information from other neurons and to transmit electrical signals to the cell body.

Dendrites are covered in synapses, which allow them to receive signals from other neurons. Some neurons have short dendrites, whilst others have longer ones.

For instance, cells called Purkinje cells, which are found in the cerebellum, have highly developed dendrites to receive signals from thousands of other cells.

Soma (Cell Body)

The soma, or cell body, is the neuron’s core.

Its job is simple: keep the cell alive. It does this by maintaining the neuron so it keeps functioning efficiently (Luengo-Sanchez et al., 2015).

A membrane encloses the soma, protecting it and letting it interact with its surroundings.

Inside sits the cell nucleus. It holds the genetic code and directs the synthesis of the proteins the rest of the neuron needs.

Most neurons have exactly one axon, which can range in length from about 0.1 millimetres to over a metre (Miller & Zachary, 2017).

Myelin covers some axons. This fatty substance insulates the axon and speeds up signal transmission.

Axoplasm is the cytoplasm within an axon.

It is responsible for transporting proteins, organelles, and other cellular components from the neuron’s cell body to the synaptic terminals and vice versa.

This transport is crucial for the maintenance and function of the axon.

Myelin Sheath

The myelin sheath is a fatty layer that wraps around the axon.

It does two jobs. It insulates each nerve cell from its neighbours.

Second, it dramatically speeds up conduction along the axon.

Glial cells called oligodendrocytes and Schwann cells build this sheath by wrapping around the axon.

Thanks to this wrapping, signals travel much faster than they would along an unmyelinated axon.

The sheath itself is not continuous. It is broken up into segments, leaving small gaps called the nodes of Ranvier.

Electrical signals jump between these nodes, which is what speeds up transmission.

Axon Terminals

Located at the end of the neuron, the axon terminals (terminal buttons) transmit signals to other neurons.

At the end of the terminal button is the synapse.

Terminal buttons hold vesicles that contain neurotransmitters.

Neurotransmitters are released from the terminal buttons into the synapse and carry signals across the synapse to other neurons.

The electrical signals convert to chemical signals during this process.

It is then the responsibility of the terminal buttons to reuptake the excess neurotransmitters that did not get passed onto the next neuron.

The Action Potential: How a Neuron Fires

The nerve impulse itself is called an action potential. It is generated by the movement of charged sodium (Na⁺) and potassium (K⁺) ions across the neuron’s membrane through tiny gated channels.

Resting Potential and Threshold

An inactive neuron sits at a resting potential of about −70 millivolts (mV): the inside of the cell is more negatively charged than the outside.

A pump keeps this balance.

It exports three Na⁺ ions for every two K⁺ ions it lets in, and at rest the membrane barely lets Na⁺ through at all.

This keeps the inside negative.

Incoming signals make the inside of the membrane less negative, a process called depolarisation. If it reaches a threshold of about −55 mV, voltage-gated sodium channels snap open and Na⁺ floods in.

The membrane flips positive.

It briefly reaches about +40 mV, and this triggers neighbouring channels to open in turn, so the impulse propagates down the whole axon without weakening.

Firing, Refraction and Saltatory Conduction

Sodium channels then close, and potassium channels open, letting K⁺ flow out and restoring the negative resting state. There is often a brief dip below resting level first.

A neuron either fires a full-strength impulse or it does not fire at all; there is no “firing weakly.” A stronger stimulus is coded as a higher frequency of identical impulses, not a bigger one.

Immediately after firing, the axon enters a refractory period.

Another impulse cannot occur at all for a moment, then can only occur weakly. This caps how fast a neuron can fire.

It also forces the impulse to travel only one direction.

Because the myelin sheath only exposes the axon at the nodes of Ranvier, the action potential jumps from node to node rather than travelling continuously.

This “saltatory” conduction is far faster and more energy-efficient than conduction along an unmyelinated fibre. Together, the refractory period and saltatory conduction explain both the impulse’s speed and its one-way direction.

The Key Study: Hodgkin and Huxley (1952)

The mechanism above was worked out by Alan Hodgkin and Andrew Huxley, using the unusually large giant axon of the squid, which was wide enough to thread electrodes down. Their 1963 Nobel Prize recognised the work.

Aim: To test whether the rising and falling phases of the action potential are produced by separate, voltage-dependent changes in the membrane’s permeability to sodium and potassium.

Method: Using the voltage clamp technique, they held the membrane potential at a chosen value. This measured the current needed to hold it steady. That current is a direct readout of the membrane’s ion conductance at each voltage.

Results: Stepping the membrane to different depolarised levels revealed a fast rise in sodium conductance, then a slower rise in potassium conductance. The timing matched a real impulse.

Conclusion: The action potential comes from sequential, voltage-gated changes in the membrane’s conductance to Na⁺ and then K⁺, not from one single change in permeability. This was a genuinely predictive theory. Its “gates” were later confirmed as real channel proteins.

Types of Neurons

Although there are billions of neurons and vast variations, neurons can be classified into three basic groups depending on their function: sensory neurons, motor neurons, and relay neurons.

Sensory Neurons

Sensory neurons (sometimes called afferent neurons) are nerve cells that carry impulses from sensory receptors toward the central nervous system and brain.

Sensory neurons have long dendrites and short axons.

When these impulses reach the brain, they are translated into ‘sensations’: vision, hearing, taste and touch.

The information can be physical (sound, heat, touch, light) or chemical (taste, smell).

Touching a hot surface is one example. The sensory neurons simply relay what they detected to the central nervous system.

Most sensory neurons are characterized as being pseudounipolar.

This means that they have one axon which is split into two branches.

Motor Neurons

Motor neurons (also referred to as efferent neurons) are the nerve cells responsible for carrying signals away from the central nervous system towards muscles to cause movement.

They release neurotransmitters to trigger responses leading to muscle movement.

Motor neurons have short dendrites and long axons.

Their cell bodies sit in the brainstem or spinal cord. From there, they connect out to muscles, glands and organs all over the body.

These neurons carry signals from the spinal cord and brainstem to skeletal and smooth muscle, controlling movement directly or indirectly.

For instance, after touching a hot surface, the sensory neurons pick up the message. The motor neurons then pull the hand away.

There are two types of motor neurons:

• Lower motor neurons – these are neurons that travel from the spinal cord to the muscles of the body.
• Upper motor neurons – these are neurons that travel between the brain and the spinal cord.

Motor neurons are characterized as being multipolar. This means they have one axon and several dendrites projecting from the cell body.

Relay Neurons

A relay neuron (also known as an interneuron) allows sensory and motor neurons to communicate with each other. Relay neurons connect various neurons within the brain and spinal cord.

Relay neurons have short dendrites and short or long axons.

Alike to motor neurons, interneurons are multipolar. This means they have one axon and several dendrites.

As well as acting as a connection between neurons, interneurons can also communicate with each other by forming circuits of differing complexities.

Interneuron communication helps the brain carry out complex functions such as learning and decision-making. It also plays a vital role in reflexes and in neurogenesis (the regeneration of new neurons).

Applications and Clinical Relevance

Virtually every psychoactive drug, and many neurological diseases, act at the synapse or on the axon. This mechanism is therefore the basis of a large part of clinical practice.

Agonists, Antagonists and Toxins

Drugs that mimic or boost a neurotransmitter’s action are called agonists. Drugs that block that action are antagonists.

L-DOPA boosts dopamine synthesis to treat Parkinson’s disease, and nicotine acts as an agonist at acetylcholine receptors. SSRIs block the reuptake of serotonin to treat depression, benzodiazepines enhance GABA to reduce anxiety, and curare blocks acetylcholine receptors, causing paralysis.

Several natural toxins work the same way.

Botulinum toxin blocks the release of acetylcholine, a mechanism used both cosmetically and medically. Organophosphate nerve agents block the enzyme that normally clears acetylcholine, so the transmitter builds up catastrophically at the synapse.

This same fit is what makes targeted drugs possible. A molecule shaped for one specific receptor can switch a single pathway on or off, with few side effects elsewhere.

Multiple Sclerosis and Psychoactive Medication

Myelin loss has real consequences. In multiple sclerosis (MS), the immune system attacks the myelin sheath in the central nervous system.

Without an intact sheath, saltatory conduction breaks down. Impulses slow or fail, producing the fatigue, numbness, weakness and visual disturbance that characterise the disease.

MS is a direct clinical demonstration of what myelin is for.

Medication works on this system too. Antidepressants, antipsychotics, anxiolytics and stimulants all act by altering synaptic transmission.

They change how much transmitter is released, how long it stays in the cleft, or which receptors it can reach. Understanding EPSPs, IPSPs, reuptake and enzymatic breakdown is therefore the foundation of psychopharmacology.

Not everyone responds the same way. Receptor density, transmitter levels and drug metabolism all vary between people.

Every one of these effects depends on exactly the same basic synaptic machinery described earlier: vesicles, receptors, reuptake and enzymatic breakdown. Shift any single step in that chain, and behaviour, mood or movement can shift with it.

That is why psychiatric drugs often carry side effects. The same neurotransmitter rarely does only one job in the brain.

References

Herculano-Houzel, S. (2009). The human brain in numbers: A linearly scaled-up primate brain. Frontiers in Human Neuroscience, 3, 31. https://doi.org/10.3389/neuro.09.031.2009

Luengo-Sanchez, S., Bielza, C., Benavides-Piccione, R., Fernaud-Espinosa, I., DeFelipe, J., & Larrañaga, P. (2015). A univocal definition of the neuronal soma morphology using Gaussian mixture models. Frontiers in Neuroanatomy, 9, 137. https://doi.org/10.3389/fnana.2015.00137

Miller, M. A., & Zachary, J. F. (2017). Mechanisms and morphology of cellular injury, adaptation, and death. In J. F. Zachary (Ed.), Pathologic basis of veterinary disease (6th ed., pp. 2–43). Elsevier.