How the Nervous System Works: Signals, Reflexes, and the Brain-Body Connection

Touch a hot pan, and your hand withdraws in roughly 50–100 milliseconds — before your brain has consciously registered pain. Read this sentence, and millions of neurons fire in coordinated cascades across your cortex, translating light patterns into language and meaning in a fraction of a second. The nervous system is simultaneously the body's communication network, its data processor, and its executive decision-making system, running 100 billion neurons connected by approximately 100 trillion synapses. Understanding it requires understanding two things: the electrical language neurons use, and the architecture that organizes them into a coherent whole.

The Big Picture: CNS vs. PNS

The nervous system divides into two anatomically distinct divisions.

Central nervous system (CNS) — the brain and spinal cord. This is where sensory information is processed, decisions are made, and motor commands are generated. The CNS is enclosed in bone (skull and vertebral column) and surrounded by three protective membranes called meninges — the dura mater (outer), arachnoid mater (middle), and pia mater (inner). Between the arachnoid and pia floats cerebrospinal fluid (CSF), a clear liquid that cushions the brain against impact and helps clear metabolic waste via the glymphatic system (primarily active during sleep — see how the brain works explained).

Peripheral nervous system (PNS) — all nervous tissue outside the CNS: 12 pairs of cranial nerves (emerging from the brain), 31 pairs of spinal nerves (emerging from the spinal cord), and all the ganglia (clusters of nerve cell bodies) outside the brain and spinal cord. The PNS connects the CNS to every organ, muscle, and patch of skin in the body.

The PNS subdivides further:

Division	Function	Type of control
Somatic nervous system	Voluntary movement, conscious sensation	Voluntary
Autonomic nervous system — sympathetic	Fight-or-flight responses	Involuntary
Autonomic nervous system — parasympathetic	Rest-and-digest responses	Involuntary
Enteric nervous system	Gut function (500 million neurons)	Semi-autonomous

Source: Kandel, E.R. et al., Principles of Neural Science, 6th edition, McGraw-Hill (2021) — Standard reference for nervous system organization, neuron physiology, and circuit function.

The Neuron: Unit of the System

Neuron — a specialized cell that transmits electrical signals. There are roughly 100 billion neurons in the human nervous system, but neurons make up only about 10% of brain cells by number; the other 90% are glial cells (astrocytes, oligodendrocytes, microglia, and Schwann cells), which provide structural support, metabolic assistance, insulation, and immune function.

A typical neuron has three structural regions:

Cell body (soma) — contains the nucleus and most of the metabolic machinery. This is where the neuron's proteins are synthesized.

Dendrites — branching extensions from the soma that receive incoming signals from other neurons or from sensory receptors. A single neuron can have hundreds or thousands of dendritic branches.

Axon — a single long projection that carries the neuron's output signal. Axons can be millimeters (in the brain) or up to a meter long (the sciatic nerve runs from the spinal cord to the foot). At its far end, the axon branches into axon terminals that form synapses with the next neuron or target tissue.

Many axons are wrapped in myelin — a fatty insulating sheath produced by oligodendrocytes (in the CNS) or Schwann cells (in the PNS). Myelin is not continuous; it is interrupted at regular intervals by gaps called nodes of Ranvier. This architecture dramatically increases signal speed. Think of myelin as insulation on a wire with periodic relay stations.

Source: Nave, K.A., Nature Reviews Neuroscience (2010) — Myelination, oligodendrocyte function, and the consequences of demyelination in neurological disease.

The Action Potential: How Neurons Talk

The neuron's signal is a rapid, stereotyped reversal of electrical charge across its membrane — the action potential. Understanding it requires knowing the baseline state.

At rest, the inside of a neuron is electrically negative relative to the outside, by about -70 millivolts. This resting membrane potential is maintained by:

• The sodium-potassium ATPase pump, which continuously pumps 3 Na⁺ ions out for every 2 K⁺ ions in, at the cost of ATP.
• Leak channels that allow more K⁺ to leak out than Na⁺ to leak in at rest.

When a stimulus (a synaptic signal, a sensory input, or direct electrical stimulation) depolarizes the membrane to about -55 mV — the threshold — voltage-gated sodium channels snap open. Na⁺ rushes in down its electrochemical gradient, driven by both concentration and charge. The inside swings positive rapidly, reaching about +30 to +40 mV. This is depolarization.

Within milliseconds, the sodium channels inactivate and voltage-gated potassium channels open. K⁺ rushes out, repolarizing the membrane. Briefly, the membrane overshoots the resting potential (hyperpolarization), before the Na-K pump gradually restores the baseline.

The action potential has a critical property: it is all-or-nothing. Either the threshold is crossed and a full action potential fires, or it does not fire at all. The size of the stimulus affects only the frequency of action potentials per second (rate coding), not their individual amplitude. This is analogous to a gun trigger: no matter how gently you begin squeezing, the firing is binary — either the trigger breaks or it doesn't.

Source: Hodgkin, A.L. & Huxley, A.F., Journal of Physiology (1952) — Nobel Prize-winning mathematical model of the action potential in squid giant axons. For the full experimental story, see the Hodgkin-Huxley squid axon experiment.

How Fast Do Signals Travel?

Signal speed depends almost entirely on myelination and axon diameter.

Unmyelinated fibers (C fibers) — conduction velocity 0.5–2.0 m/s. These carry slow pain (the dull, burning ache after an initial injury) and some autonomic signals.

Lightly myelinated fibers (Aδ fibers) — 5–30 m/s. Fast pain (the sharp, immediate sensation of injury) and temperature travel here.

Heavily myelinated fibers (Aα fibers) — 70–120 m/s. Motor commands to skeletal muscle and proprioceptive signals (position sense from muscles and joints) use the fastest fibers.

In myelinated axons, the action potential does not travel as a continuous wave along the entire membrane. Instead, it jumps from node of Ranvier to node of Ranvier in a process called saltatory conduction (from Latin saltare, to jump). Because the electrical current jumps through the low-resistance myelinated segments rather than flowing through the membrane step by step, conduction is both faster and more energy-efficient. It is the nervous system's version of using an express bus that skips every intermediate stop.

Fiber type	Myelination	Signal speed	Carries
Aα	Heavy	70–120 m/s	Motor commands, proprioception
Aβ	Medium	30–70 m/s	Touch, pressure, vibration
Aδ	Light	5–30 m/s	Fast pain, cold, temperature
C	None	0.5–2 m/s	Slow pain, warmth, post-ganglionic autonomic

Source: NCBI Bookshelf, Neuroscience, 2nd edition (Purves et al.) — Fiber classification, conduction velocity ranges, and saltatory conduction mechanism.

Synapses: The Chemical Handoff

The action potential is electrical, but communication between most neurons is chemical. The junction between one neuron's axon terminal and the next neuron's dendrite (or cell body, or muscle fiber) is a synapse.

When an action potential reaches the axon terminal, it opens voltage-gated calcium channels. Ca²⁺ floods in and triggers vesicles (membrane-bound packages) filled with neurotransmitter molecules to fuse with the presynaptic membrane and release their contents into the synaptic cleft — a gap of roughly 20–40 nanometers.

Neurotransmitter molecules diffuse across the cleft in under a millisecond and bind to receptor proteins on the postsynaptic membrane. Depending on the receptor type, this either:

• Opens ion channels directly (ionotropic receptors) — fast, millisecond-scale effects
• Triggers a signaling cascade via a G protein (metabotropic receptors) — slower, seconds-to-minutes effects modulating excitability

The postsynaptic effect is either excitatory (making the next neuron more likely to fire — e.g., glutamate acting on AMPA receptors) or inhibitory (making it less likely to fire — e.g., GABA acting on GABA-A receptors). Whether a postsynaptic neuron fires depends on the sum of all excitatory and inhibitory inputs converging on it at any moment — a process of synaptic integration performed by the dendritic tree.

After neurotransmitter release, it is rapidly terminated: reuptake into the presynaptic terminal (the primary mechanism for dopamine, serotonin, and norepinephrine — the targets of most psychiatric drugs), enzymatic degradation in the cleft (as with acetylcholine, broken down by acetylcholinesterase), or diffusion away from the cleft.

Source: Bhaskaran, M.D. & Smith, B.N., Journal of Neurophysiology (2010) — Synaptic integration mechanisms in central neurons.

The Autonomic Nervous System: Running Without You

Most of the body's operations — heart rate, blood pressure, digestion, pupil dilation, sweating, erection, bladder control — are managed by the autonomic nervous system (ANS), which operates below conscious awareness. The ANS has two main branches that generally oppose each other.

Sympathetic nervous system — the "fight-or-flight" arm. Its preganglionic neurons originate in the thoracic and lumbar spinal cord (the thoracolumbar division). When activated — by threat, exercise, stress, or low blood pressure — sympathetic output increases heart rate, dilates pupils, redirects blood from the gut to skeletal muscle, releases adrenaline (epinephrine) from the adrenal medulla, and suspends digestion and sexual arousal. The primary neurotransmitter at the target organ is norepinephrine (noradrenaline).

Parasympathetic nervous system — the "rest-and-digest" arm. Preganglionic neurons originate in the brainstem and sacral spinal cord (craniosacral division). Activation slows the heart, promotes digestion (stimulates gastric secretion, intestinal motility; see how digestion works), constricts the pupils, and enables sexual arousal. The primary neurotransmitter is acetylcholine.

The two branches are not simply on-off switches; they more often operate with one dominant and the other permissive, with the balance shifting continuously. Resting heart rate, for example, reflects primarily the degree of parasympathetic tone — a highly fit athlete has strong vagal (parasympathetic) tone, producing resting heart rates of 40–50 bpm.

Enteric nervous system — sometimes called the "second brain," the enteric system is an extensive network of about 500 million neurons lining the gut. It can regulate peristalsis, secretion, and blood flow without any input from the CNS, though it communicates bidirectionally with the brain via the vagus nerve. Gut bacteria interact with enteric neurons and with the immune system in ways that researchers are beginning to understand.

Source: Furness, J.B., Nature Reviews Gastroenterology & Hepatology (2012) — Organization and function of the enteric nervous system and the gut-brain axis.

Reflex Arcs: Bypassing the Brain

The nervous system contains hardwired shortcuts for rapid protective responses that cannot wait for the brain's processing time. The reflex arc routes a sensory signal to the spinal cord and directly back to a motor response — bypassing the cortex.

The classic example: touching something sharp. Nociceptors (pain receptors) in the finger send an afferent signal up a sensory (afferent) nerve fiber to the dorsal horn of the spinal cord. In the spinal cord, an interneuron connects the sensory neuron to a motor (efferent) neuron in the anterior horn. The motor neuron immediately fires, causing the flexor muscles of the arm to contract and the limb to withdraw. All of this completes in 50–100 ms. Only later — after the reflex has already executed — does the signal reach the somatosensory cortex and you become conscious of the pain.

This is why you pull your hand away before you register "that was hot."

The withdrawal reflex is a polysynaptic reflex (involving interneurons). Simpler monosynaptic reflexes have only one synapse: the sensory neuron connects directly to the motor neuron. The classic example is the patellar (knee-jerk) reflex: tapping the patellar tendon stretches the quadriceps muscle, muscle spindle receptors fire, and the motor neuron directly contracts the quadriceps — producing the knee extension. This monosynaptic arc happens in about 25 ms.

Source: Pierrot-Deseilligny, E. & Burke, D., The Circuitry of the Human Spinal Cord (2012) — Comprehensive treatment of spinal reflex circuits and their modulation by descending pathways.

Neuroplasticity: The Rewiring Capacity

The nervous system is not static. Synaptic connections strengthen or weaken based on use in a process called neuroplasticity — famously summarized by the heuristic "neurons that fire together, wire together."

Long-term potentiation (LTP) — repeated co-activation of a presynaptic and postsynaptic neuron strengthens the synapse between them. LTP is the primary cellular mechanism underlying learning and memory, occurring predominantly through the insertion of more AMPA receptors into the postsynaptic membrane of glutamatergic synapses.

Long-term depression (LTD) — the reverse: weak or asynchronous activation leads to synapse weakening and receptor removal. LTD is essential for forgetting irrelevant information and for fine-tuning motor skills (extensive in the cerebellum).

Neuroplasticity is highest in childhood — the critical period for sensory development — but persists throughout life. Adult neuroplasticity underlies skill acquisition, recovery from brain injury, and the cognitive effects of experiences, stress, and sleep. It is also the mechanism exploited by rehabilitation after stroke: surviving neurons in adjacent cortical regions can be trained to take over functions previously handled by damaged tissue.

Source: Bliss, T.V.P. & Collingridge, G.L., Nature (1993) — LTP at glutamatergic synapses and its role in synaptic plasticity and memory.

What Goes Wrong: Neurological Conditions

When nervous system components fail, the consequences reveal the architecture's logic.

Multiple sclerosis (MS) — the immune system attacks and destroys myelin in the CNS. Without myelin, saltatory conduction fails; signals slow, distort, or fail to propagate. Depending on which white matter tracts are affected, MS produces motor weakness, sensory loss, visual disturbance, or cognitive symptoms.

Parkinson's disease — death of dopaminergic neurons in the substantia nigra (a midbrain structure) eliminates dopamine input to the basal ganglia, disrupting the motor control circuit that smooths voluntary movement. The result: resting tremor, rigidity, and bradykinesia (slowed movement).

ALS (amyotrophic lateral sclerosis) — degeneration of both upper motor neurons (in the cortex) and lower motor neurons (in the spinal cord), cutting off voluntary motor commands entirely. Sensation and cognition are typically preserved; movement is progressively lost.

Peripheral neuropathy — damage to peripheral nerves (from diabetes, alcohol, toxins, or autoimmune attack). Depending on which fiber types are affected, this produces numbness, burning pain, weakness, or autonomic dysfunction (postural hypotension, gastroparesis).

Source: Compston, A. & Coles, A., Lancet (2008) — Pathogenesis, clinical features, and management of multiple sclerosis.

Frequently Asked Questions

Q: How many neurons does the human brain actually have?
A: The most accurate estimate, derived from isotropic fractionation studies by Suzana Herculano-Houzel's group, is approximately 86 billion neurons in the human brain — not the often-cited 100 billion. About 69 billion of these are in the cerebellum; the cerebral cortex has roughly 16 billion.

Q: Is it true we only use 10% of our brain?
A: No. This is one of the most persistent neuromyths. Neuroimaging studies show that all brain regions are active during various tasks, and over a 24-hour period essentially all cortical regions show measurable activity. The myth may derive from misinterpretations of early neurology findings or misquoted statements about glial-to-neuron ratios.

Q: How does anesthesia work?
A: General anesthetics suppress consciousness and pain by modulating multiple ion channels and receptors. Most agents (propofol, barbiturates, volatile agents) enhance GABA-A receptor activity (increasing inhibitory signaling) and/or inhibit glutamate NMDA receptors (reducing excitatory signaling). The exact mechanism by which this produces unconsciousness remains an active area of research; the current best model involves disrupting corticothalamic feedback circuits that maintain conscious awareness.

Q: What happens to nerves after injury?
A: In the PNS, peripheral nerve axons can regenerate — the Schwann cell tube guides re-growing axons back toward their targets, at a rate of roughly 1–3 mm per day. Recovery is often incomplete, especially over long distances or for fine motor function. In the CNS, regeneration is far more limited: inhibitory factors in CNS myelin (including Nogo-A) and the glial scar formed at injury sites actively suppress axon regrowth. This is why spinal cord injury typically produces permanent deficits.

Q: What is the blood-brain barrier?
A: The blood-brain barrier (BBB) is formed by the tight junctions between endothelial cells lining the CNS capillaries, reinforced by astrocyte end-feet. It selectively restricts what can pass from blood into brain tissue — blocking most large molecules and pathogens while allowing glucose, oxygen, and lipid-soluble small molecules (including many drugs). The BBB protects the brain's chemical environment but also makes delivering drugs to the brain extremely challenging.

Q: How do neurotransmitters relate to mood?
A: Several neurotransmitter systems modulate mood and arousal. Serotonin (primarily from the raphe nuclei) influences mood, appetite, and sleep; SSRIs (selective serotonin reuptake inhibitors) elevate synaptic serotonin by blocking its reuptake. Dopamine (from the ventral tegmental area and substantia nigra) drives reward, motivation, and movement. Norepinephrine modulates arousal and stress response. These systems interact in complex, incompletely understood ways — the simple "low serotonin causes depression" model has been substantially revised in the literature over the past decade.

Source: Moncrieff, J. et al., Molecular Psychiatry (2022) — Systematic review of the serotonin hypothesis of depression and the evidence for its limitations.

The Takeaway

The nervous system is the body's only system that simultaneously perceives, processes, decides, and commands — doing all of it in real time, at speeds up to 120 m/s, across a network of 100 trillion connections. Its architecture reflects a history of evolutionary layering: the brainstem runs the most ancient survival functions; the limbic system handles emotion and memory; the cortex handles language, planning, and abstraction. Neurons communicate through a precise electrochemical language — action potentials converted to neurotransmitter signals and back again at synapses — and the whole network rewires itself continuously based on experience. When that architecture fails, whether through demyelination, neurodegeneration, or synaptic imbalance, the consequences map precisely onto the circuits involved. The nervous system is not a single organ; it is the body's most distributed, most complex, and most definitively human system.

---

Read next:

• How the Brain Works Explained
• How Muscles Work Explained
• The Hodgkin-Huxley Squid Axon Experiment