Neurons communicate through a combination of electrical impulses that travel within each cell and chemical signals that pass between cells. At rest, a neuron holds a negative electrical charge of about -60 millivolts compared to its surroundings. When stimulated enough, it fires a rapid electrical pulse down its length, and at the endpoint, it releases chemical messengers that drift across a tiny gap to influence the next neuron. This two-part system, electrical then chemical, is the foundation of everything your brain does.
The Electrical Signal Inside a Neuron
Every neuron maintains a baseline voltage called the resting potential, typically around -60 millivolts, though it can range from -80 to -40 millivolts depending on the type of neuron. This charge exists because the cell membrane carefully controls which charged particles (ions) sit inside versus outside. Think of it as a tiny battery, always slightly negative on the inside.
When a neuron receives enough stimulation, channels in its membrane snap open and positively charged sodium ions rush in. This flips the voltage rapidly from negative to positive, creating what’s called an action potential. The signal doesn’t fade as it travels. It regenerates at each point along the neuron’s long fiber (the axon), so it arrives at the far end just as strong as when it started. After firing, the neuron resets by pumping sodium back out and letting potassium flow in, restoring the negative resting charge.
A neuron can’t fire again immediately. For about 2 milliseconds after an action potential, it’s completely unresponsive. Over the next 3 milliseconds or so, it gradually regains the ability to fire but needs a stronger-than-normal stimulus. This brief cooldown period caps how rapidly a neuron can send signals and helps ensure that electrical pulses travel in one direction.
How Speed Varies Across Nerve Fibers
Not all neurons transmit signals at the same speed. Thin, bare nerve fibers conduct impulses at roughly 0.5 to 10 meters per second. That’s adequate for things like dull, aching pain signals from your organs. But neurons wrapped in a fatty insulating layer called myelin can conduct signals at up to 150 meters per second, fast enough to travel from your spinal cord to your foot and back in a fraction of a second. Myelin works by forcing the electrical signal to jump between exposed gaps along the axon rather than crawling continuously down its length.
What Happens at the Chemical Synapse
When an electrical signal reaches the end of an axon, it can’t jump directly to the next cell. Instead, the neuron converts its electrical message into a chemical one. Here’s the sequence: the arriving impulse opens calcium channels at the nerve terminal, and calcium ions flood in. Calcium acts as the trigger. It binds to a sensor protein, which then interacts with a set of molecular machinery that forces tiny storage bubbles (vesicles) filled with chemical messengers to merge with the cell membrane and spill their contents into the narrow gap between neurons. That gap, the synaptic cleft, is only about 20 nanometers wide.
The released molecules, called neurotransmitters, float across the cleft and lock onto receptor proteins on the receiving neuron. What happens next depends entirely on which neurotransmitter was released and which receptor catches it.
Excitatory vs. Inhibitory Signals
Glutamate is the brain’s primary excitatory messenger. When it binds to receptors on the receiving neuron, it opens channels that let positively charged ions flow in, pushing the cell’s voltage upward toward the firing threshold. This nudge toward firing is called an excitatory postsynaptic potential.
GABA is the brain’s primary inhibitory messenger. It opens channels that allow negatively charged chloride ions to flow in, pulling the voltage further from the firing threshold and making the neuron less likely to fire. Your brain relies on the balance between glutamate’s “go” signals and GABA’s “stop” signals for everything from muscle coordination to mood regulation. Disruptions in this balance are involved in conditions ranging from epilepsy to anxiety disorders.
How a Neuron Decides to Fire
A single neuron in the brain can receive input from thousands of other neurons simultaneously, some excitatory, some inhibitory. All of these signals converge at a region near the cell body called the axon hillock, which acts as the neuron’s decision point. If the combined input pushes the voltage past the firing threshold, an action potential launches. If not, nothing happens.
Two types of addition make this work. Spatial summation occurs when signals from many different neurons arrive at the same moment and combine their effects. Temporal summation occurs when one neuron fires repeatedly in quick succession, and each pulse arrives before the effect of the previous one fades. Synapses located physically closer to the axon hillock carry more influence over the outcome, simply because their signals lose less strength before reaching the decision point. This integration process means a neuron isn’t just relaying messages. It’s computing, weighing inputs, and producing an output based on the sum of everything it receives.
Clearing the Signal
Once a neurotransmitter has done its job, it needs to be removed from the synapse quickly. If it lingered, the receiving neuron would be stimulated (or inhibited) continuously, which would disrupt normal signaling. The brain uses two main strategies.
The first is reuptake: the sending neuron vacuums the neurotransmitter back up through specialized transport proteins and recycles it for future use. This is the primary clearance method for serotonin, norepinephrine, epinephrine, and most amino acid neurotransmitters. It’s also the mechanism targeted by common antidepressants, which block the reuptake of serotonin to keep it active in the synapse longer.
The second strategy is enzymatic breakdown. Acetylcholine, for instance, is split apart in the synapse by a dedicated enzyme called acetylcholinesterase. This destruction is nearly instantaneous, which is why acetylcholine signaling at your muscles can be so precisely timed. Blocking that enzyme amplifies acetylcholine’s effects, a principle used in treatments for conditions like myasthenia gravis and Alzheimer’s disease.
Electrical Synapses: The Fast Lane
Not all neuron-to-neuron communication uses chemicals. Some neurons connect directly through physical channels called gap junctions. Each gap junction is made of two interlocking rings of proteins, called connexons, that punch a tiny pore (about 1.5 nanometers wide) through the membranes of both cells. The membranes don’t actually touch. They’re separated by a gap of 2 to 4 nanometers, which is where the name comes from.
These channels allow ions and small molecules to pass straight from one neuron’s interior to the next, so the electrical signal transfers almost instantly with no chemical middleman. Electrical synapses are especially useful where groups of neurons need to fire in sync, such as in circuits that coordinate rhythmic breathing or rapid escape reflexes. The tradeoff is flexibility: unlike chemical synapses, electrical synapses don’t easily adjust their strength or switch between excitation and inhibition.
How Connections Strengthen or Weaken
Synapses aren’t fixed in strength. They change based on how much they’re used, a property called synaptic plasticity. This is the cellular basis of learning and memory.
When a synapse is stimulated intensely or repeatedly, calcium flows through a specific type of receptor channel on the receiving neuron. That calcium surge activates an enzyme inside the cell, which then triggers two changes. First, it causes additional receptor proteins to be inserted into the receiving neuron’s membrane, making the synapse more sensitive to future signals. Second, it modifies existing receptors so that each one lets more current through when activated. Some dormant synapses that previously had no functional receptors “wake up” and become active connections. This strengthening process is called long-term potentiation, and it can also work in reverse. When calcium levels rise modestly rather than sharply, receptors are pulled out of the membrane instead, weakening the connection in a process called long-term depression.
Over longer timescales, the neuron synthesizes new proteins to lock these changes in place, making the strengthening or weakening more permanent. This is why brief practice produces fleeting improvement, but repeated practice produces lasting skill.
Astrocytes: The Third Partner
Neurons don’t operate in isolation. Star-shaped support cells called astrocytes wrap their finger-like processes around synapses and actively participate in signaling. This arrangement, sometimes called the tripartite synapse, adds a third player to what was once thought to be a two-neuron conversation.
Astrocytes express receptors for neurotransmitters, so they can “listen” to the signals neurons exchange. When they detect neurotransmitter activity, their internal calcium levels rise, and they can respond by releasing their own signaling molecules (including glutamate and ATP) that modulate how the synapse behaves. They also carry specialized glutamate transporters that soak up excess glutamate from the synaptic cleft, preventing overstimulation that could damage or kill neurons. Neuronal activity can even recruit astrocyte processes to move closer to active synapses, fine-tuning the relationship over time.