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Neurons and Synapses: How Nerve Signals Travel

Learn how an electrical signal travels down a neuron and passes on to the next cell.

The basic structure of a neuron

The neuron, the basic cell of the nervous system, is made up of a cell body, dendrites, and an axon. The cell body houses the nucleus and organelles; dendrites are branch-like extensions that receive signals from other neurons; the axon is a long fiber that carries the signal generated in the cell body over distance to the next neuron, muscle, or gland, handing it off at the axon terminal.

Resting membrane potential (-70mV)

When there is no stimulus, the inside of a neuron's cell membrane sits at a voltage roughly -70mV lower than the outside. This voltage difference comes from the concentration gradient of sodium (Na+) and potassium (K+) ions across the membrane, which the sodium-potassium pump continuously maintains using ATP energy. This baseline voltage, held while there's no stimulus, is called the resting membrane potential.

How an action potential (nerve impulse) arises

When a stimulus crosses a threshold, sodium channels open and the membrane potential briefly reverses β€” this is the action potential. Sodium ions rushing into the cell cause depolarization, flipping the potential positive, followed quickly by potassium ions flowing out, repolarizing it back to negative. Once triggered, this electrical signal doesn't weaken β€” it travels the full length of the axon at constant strength.

The myelin sheath and saltatory conduction

Thanks to the myelin sheath wrapping the axon, the signal jumps only between the gaps called nodes of Ranvier, traveling much faster. New action potentials only form at these unmyelinated nodes, while the signal leaps across the covered stretches in between. This saltatory conduction makes myelinated nerves transmit signals far faster than unmyelinated ones.

The synapse and the synaptic cleft

Where one neuron meets another is called a synapse, and it includes a very narrow gap β€” the synaptic cleft β€” roughly 20-40 nanometers wide. In most synapses, the two neurons' cell membranes don't touch directly; they're separated by this tiny gap. Since the electrical signal (action potential) can't leap across this gap on its own, a chemical method is needed to carry the signal across.

The role of neurotransmitters

When an action potential reaches the axon terminal, vesicles containing neurotransmitters burst and release their contents into the synaptic cleft. The released neurotransmitters (dopamine, serotonin, acetylcholine, and others) cross the gap and bind to receptors on the next neuron, and this binding generates a new electrical signal in that neuron β€” at the synapse, the electrical signal essentially converts to a chemical signal and then back to an electrical one.

Excitatory and inhibitory signals

Depending on the type of neurotransmitter, the next neuron can be excited or, conversely, inhibited. Excitatory signals make the next neuron more likely to fire an action potential, while inhibitory signals make it less likely. A single neuron receives both types of signals simultaneously from many other neurons and decides whether to fire based on the combined sum.

The reflex arc: a response that bypasses the brain

Like instantly pulling your hand away from something hot, some responses are handled directly by the spinal cord without going all the way to the brain. The pathway where a sensory neuron's signal passes through an interneuron in the spinal cord straight to a motor neuron is called a reflex arc. Because it skips the round trip up to the brain and back, it allows a much faster reaction to dangerous stimuli.

Glial cells: the supporting cast

Neurons are not the only cells in nervous tissue. Glial cells outnumber or at least rival neurons in many regions and do essential jobs: astrocytes help regulate the chemical environment around synapses and clear excess neurotransmitter, oligodendrocytes wrap axons in myelin in the brain and spinal cord, Schwann cells do the same for peripheral nerves, and microglia act as the resident immune cells. Without them, neurons could not signal reliably.

Ion channels and the sodium-potassium pump

Signals depend on proteins embedded in the cell membrane. Voltage-gated channels open when the membrane voltage crosses a threshold, letting sodium in or potassium out within a fraction of a millisecond. The sodium-potassium pump works more slowly and in the background, moving three sodium ions out for every two potassium ions in using ATP, which restores the gradients the channels spend. A neuron can fire many times before the pump needs to catch up, but over the long run the pump is what keeps the cell ready.

The refractory period

Right after an action potential, sodium channels are inactivated for a short time and the neuron cannot fire again, or can fire only in response to an unusually strong stimulus. This refractory period makes the impulse travel in one direction along the axon, since the stretch behind it is temporarily unable to respond, and it limits how often a neuron can fire.

How strength is encoded: frequency, not size

Because every action potential has the same size, a neuron signals a stronger stimulus by firing more often, and a weaker one by firing less often. Information also depends on which neurons fire and when. A brighter light, for example, is not carried by taller impulses but by faster trains of identical impulses from more cells.

Two families of receptors

Neurotransmitter receptors fall into two broad groups. Ionotropic receptors are channels that open directly when the transmitter binds, producing fast effects within milliseconds. Metabotropic receptors work through internal chemical messengers and produce slower, longer-lasting changes in how a cell responds. Many drugs act on one of these families.

Ending the signal: reuptake and breakdown

A synaptic signal must be switched off or the receiving cell would stay stimulated. Some transmitters are pumped back into the sending neuron or into nearby glia, which is called reuptake. Others are broken down by enzymes in the cleft, for example acetylcholine by acetylcholinesterase. Many medications work by interfering with these clean-up steps, which prolongs the transmitter's effect.

Synaptic plasticity and learning

Synapses can strengthen or weaken depending on how they are used, which researchers call synaptic plasticity. A widely studied form is long-term potentiation, in which repeated activity makes a synapse respond more strongly afterward. Changes of this kind are thought to be part of how memories and skills are stored, although the full picture of learning involves much more than a single mechanism.

Do neurotransmitter imbalances relate to disease?

Yes. When the release or action of neurotransmitters like dopamine and serotonin falls outside the normal range, it is known to be linked to various neurological and mental health conditions. That said, any specific diagnosis or treatment should always be discussed with a medical professional.

Following one signal from fingertip to muscle

Imagine touching a hot pan. Receptors in the skin convert heat into electrical changes in a sensory neuron. If the change passes threshold, an action potential starts and travels along the axon into the spinal cord. There it can pass through a synapse to an interneuron and then to a motor neuron whose axon runs to a muscle in the arm. At the neuromuscular junction the motor neuron releases acetylcholine, the muscle fiber contracts, and the hand pulls away. Meanwhile other branches of the same signal climb to the brain, which is why you feel pain a moment after the hand has already moved. The whole chain is a series of the same steps repeated: threshold, impulse, release, binding, and a new impulse.

Why myelin matters when it is damaged

When myelin is lost or damaged, signals slow down or fail to cross the affected stretch. In multiple sclerosis the immune system attacks myelin in the brain and spinal cord, and the resulting symptoms depend on which pathways are affected. In peripheral nerves, conditions that damage the myelin can cause numbness or weakness. This is a good illustration of how structure and function are tied together in the nervous system. This page is general educational information, not medical advice, and anyone with symptoms should see a clinician.

Frequently Asked Questions

Why does the action potential travel the full distance without shrinking?

The action potential follows an "all-or-none" rule. Once the threshold is crossed, an action potential of the same size is always generated, and it regenerates fresh at each point along the axon as it travels β€” which is why the signal doesn't weaken before reaching the end.

Are there electrical synapses too?

Most synapses are chemical synapses that rely on neurotransmitters, but some circuits β€” including heart muscle and certain neural pathways β€” have electrical synapses, where ions move directly through channels for an even faster signal.

Can neurons regenerate after injury?

It depends. Peripheral nerves can regrow slowly if the cell body survives and conditions are favorable, but recovery is often incomplete. In the brain and spinal cord regeneration is far more limited, and research on repair is ongoing. Specific injuries should be discussed with a medical professional.

How fast do nerve signals travel?

Speeds depend on axon thickness and myelination: thin unmyelinated fibers conduct slowly, while large myelinated fibers conduct many times faster, which is why reflex and motor signals reach muscles quickly while some dull pain signals arrive later.