Imagine your nerves are like a row of dominoes. One good push, and the whole line falls in a chain reaction. That’s kind of how neurons send signals across your brain and body.

Let’s take a closer look at how all this works. 

Action Potentials

At rest, the inside of a neuron is about –70 millivolts compared to the outside. This difference, known as the resting membrane potential, is kept stable by the sodium-potassium pump. That pump constantly pushes out three sodium ions for every two potassium ions it brings in. This creates both a chemical gradient and an electrical one.

But neurons aren’t always resting. When a strong enough stimulus arrives, the cell responds with a sudden change. If the signal reaches a threshold (like the tipping point before a sneeze) the neuron fires. Voltage-gated sodium channels open, and sodium rushes in. This depolarizes the membrane, which makes the inside more positive. For a moment, the inside of the neuron can even swing past zero, heading toward approximately +30 mV.

Then just as quickly, the sodium channels close, and potassium channels open. Potassium flows out and pulls the voltage back down in a process called repolarization. These potassium channels take a bit longer to close, so the neuron briefly becomes more negative than it was at rest; this is called hyperpolarization. Finally, the sodium-potassium pump returns the membrane to its normal -70 mV resting state.

After each action potential, there’s a short recovery period. During the absolute refractory period, no new signal can be triggered, no matter how strong. The sodium channels are stuck in an inactive state. Soon after comes the relative refractory period, where a new action potential is possible, but only if the signal is stronger than usual, since the membrane is still slightly hyperpolarized and not quite ready.

How Signals Travel

Once initiated, an action potential travels down the axon toward the terminal, but the way it moves depends on the axon’s structure. In neurons wrapped in myelin, the signal “jumps” rather than inching forward continuously. This is because myelin acts as insulation, so the action potential jumps between exposed gaps called nodes of Ranvier, a process known as saltatory conduction. This allows the signal to move rapidly and efficiently, which is important for reflexes and motor coordination. In contrast, unmyelinated axons use continuous conduction, where the signal travels steadily along the entire membrane. It’s slower, but still effective. These fibers often carry pain or temperature signals.

Synaptic Transmission

When the electrical signal reaches the end of the neuron (the axon terminal) it needs to pass the message on. But the next neuron isn’t physically connected. Instead, there’s a narrow space between them called the synaptic cleft.

Here’s how the handoff works: the incoming action potential triggers voltage-gated calcium channels to open. Calcium ions enter the terminal, and their presence causes vesicles filled with neurotransmitters to fuse with the membrane and release their contents into the cleft. This process (exocytosis) turns an electrical signal into a chemical one.

The neurotransmitters diffuse across the synapse and bind to receptors on the next neuron. Depending on the type of neurotransmitter and the receptor it binds to, the signal can either be excitatory, encouraging the next neuron to fire, or inhibitory, making it less likely to fire.

For example, glutamate is a major excitatory neurotransmitter in the brain. It makes the postsynaptic membrane more positive by opening sodium channels, which pushes the neuron toward threshold. On the other hand, GABA (gamma-aminobutyric acid) opens chloride channels, which makes the inside more negative and calms the system down. This balance between excitation and inhibition is what keeps the nervous system running smoothly, where it’s fast enough to react, but not so fast that it spirals into chaos.

Not all synapses rely on chemicals. Some neurons connect through gap junctions, where they form electrical synapses, where ions flow directly from one cell to the next. These are fast and allow synchronized firing, like in some interneurons and retinal cells.

But most communication in the brain happens through chemical synapses, which is what we described above. This takes slightly more time than direct electrical connections but allows for more control, such as signals being weakened, strengthened, or even combined with others.

Some Important Neurotransmitters

Neurotransmitters sometimes get reduced to one-word descriptions, like “the memory chemical” or “the pleasure molecule.” So I’ll try to go in a little more detail here so you understand better what each actually does. 

Acetylcholine is the “go” signal. It’s what makes muscles contract when you decide to move, like lifting your arm to grab a cup. That part happens at the neuromuscular junction. But acetylcholine also plays a role in attention and learning. In the brain, it helps put the spotlight on important sensory information so it stands out against the background. If you’re trying to follow a lecture in a noisy classroom, acetylcholine is part of what lets you tune in. The signal is cleared almost immediately by an enzyme, acetylcholinesterase which prevents overstimulation. Otherwise, muscles would seize up and attention circuits would short-circuit.

Dopamine is all about motivation and movement. When something turns out better than expected, like finally solving a frustrating problem, dopamine gets released in the brain’s reward pathway. That burst helps reinforce the behaviour that led to the outcome, so you’re more likely to try it again. It also plays a role in motor control. In Parkinson’s disease, for example, dopamine-producing neurons in the midbrain degenerate, and people struggle with slow, rigid movement. On the other end of the spectrum, too much dopamine activity in certain areas is linked to symptoms of schizophrenia, like delusions or hallucinations.

Serotonin helps stabilize things like mood, appetite, sleep cycles. After eating, serotonin rises in the hypothalamus to reduce hunger. Later in the day, it helps nudge the brain toward sleep by influencing circadian rhythms. It also dampens excessive emotional reactivity, especially in brain areas like the amygdala. That’s one reason SSRIs (selective serotonin reuptake inhibitors) can help with anxiety and depression. They increase serotonin levels gradually over time, which give these circuits a chance to rebalance.

Norepinephrine kicks in when you need to focus or respond quickly. It’s part of the brain’s alert system. If you suddenly hear your name across a noisy room, norepinephrine helps shift your attention toward it. It also ramps up heart rate and blood pressure as part of the fight-or-flight response. In emotionally intense moments, it helps stamp memories more clearly, which can be useful or in the case of trauma, hard to unlearn. Too little can make it hard to get going in the morning. Too much can keep you stuck in a state of high alert long after the stressor is gone.

Synaptic Regulation

The nervous system has fine control over how long and how strongly these chemical messages last. One method is reuptake, where neurotransmitters are reabsorbed back into the presynaptic neuron. Blocking this process (like with SSRIs) lets the neurotransmitter linger longer. Another method is enzymatic breakdown. For example, MAOIs (monoamine oxidase inhibitors) prevent enzymes from degrading serotonin, dopamine, and norepinephrine, which boosts their overall levels.

There are also drugs that can mimic or block neurotransmitters directly. Agonists bind to receptors and activate them. For example, morphine activates opioid receptors, which mimics natural endorphins to dull pain. Antagonists do the opposite: they bind without activating, which effectively blocks the receptor. For example, naloxone is used to reverse opioid overdoses, and works this way by outcompeting opioids at their own receptors.