An excitatory postsynaptic potential (EPSP) is a small, temporary voltage change in a neuron that makes it more likely to fire. When one neuron sends a chemical signal to another, the receiving neuron’s membrane becomes slightly more positive, nudging it closer to the threshold needed to generate its own electrical impulse. A single EPSP is tiny, roughly one millivolt, but neurons rely on combining many of these small signals to communicate.
How an EPSP Is Generated
Neurons communicate at junctions called synapses. When a signal arrives at the sending neuron’s terminal, it releases a chemical messenger (a neurotransmitter) into the gap between the two cells. That neurotransmitter binds to receptors on the receiving neuron, opening channels in its membrane that allow positively charged ions to flow in.
At rest, a neuron’s interior sits at about -60 millivolts relative to the outside. When glutamate, the brain’s primary excitatory neurotransmitter, binds to its receptors, the channels that open are permeable to both sodium and potassium ions. Because of the electrical and chemical forces at play, the net effect is a rush of positive charge into the cell. This shifts the membrane voltage upward, toward 0 mV. That upward shift is the EPSP.
The whole event is brief. A typical EPSP peaks within about 4 to 6 milliseconds and fades back toward the resting voltage within roughly 15 to 20 milliseconds. It’s a quick nudge, not a sustained push.
Two Types of Receptors, Two Speeds
Glutamate activates more than one kind of receptor, and each contributes differently to the EPSP. AMPA receptors open quickly and are responsible for the initial, fast component of the voltage change. NMDA receptors contribute a slower, secondary component. The EPSP you’d measure at a synapse is actually a combination of these two waves rather than a single uniform event.
NMDA receptors have a special property: they only allow ions through when the membrane is already partially depolarized. This means they respond most strongly when the neuron is already receiving excitatory input, making them particularly important for strengthening connections between neurons over time.
Why One EPSP Isn’t Enough
A single EPSP of about one millivolt is far too small to push a neuron from its resting voltage of -60 mV to the firing threshold of roughly -40 mV. To bridge that 20 mV gap, the neuron needs many EPSPs to combine. This process is called summation, and it happens in two ways.
Spatial summation occurs when multiple synapses on the same neuron fire at roughly the same time. If synapse A and synapse B both produce an EPSP simultaneously, those two voltage changes add together. Temporal summation occurs when the same synapse fires repeatedly in quick succession. Because an EPSP lasts several milliseconds, a second EPSP arriving before the first has fully decayed stacks on top of it. Both forms of summation allow subthreshold signals to combine into a voltage change large enough to trigger an action potential.
A typical neuron in the brain receives input from thousands of synapses. At any given moment, some are excitatory and some are inhibitory. The neuron essentially tallies all of these inputs. If the combined depolarization crosses the threshold, the neuron fires.
EPSPs vs. IPSPs
The counterpart to an EPSP is an inhibitory postsynaptic potential, or IPSP. While an EPSP makes a neuron more likely to fire, an IPSP makes it less likely. The difference comes down to which ions flow through the channels that open.
At inhibitory synapses, the neurotransmitter GABA typically opens channels permeable to chloride ions, which carry a negative charge. When chloride flows into the cell, the interior becomes more negative, pushing the voltage further from the firing threshold. This hyperpolarizing shift is the classic IPSP.
Interestingly, the distinction between excitation and inhibition isn’t simply “depolarization vs. hyperpolarization.” What actually matters is where the voltage change sits relative to the firing threshold. An IPSP can technically depolarize the membrane slightly and still be inhibitory, as long as it keeps the voltage below threshold. The defining question is always: does this signal move the neuron closer to firing, or further away?
The Role of EPSPs in Learning
EPSPs aren’t just momentary signals. They play a central role in how the brain strengthens or weakens connections, the process underlying learning and memory. When a synapse is stimulated at high frequency, the resulting EPSPs can trigger long-term potentiation (LTP), a lasting increase in how effectively that synapse drives the receiving neuron. After LTP, the same input produces a larger response, and the neuron becomes more likely to fire in response to a given EPSP.
This enhanced coupling between the EPSP and the neuron’s firing is sometimes called E-S potentiation, and it can persist for long periods, making it a candidate mechanism for how memories are encoded. The reverse also happens: low-frequency stimulation can weaken the connection, producing long-term depression (LTD) and reducing the neuron’s responsiveness. Both directions of change depend on calcium entering the cell through NMDA receptors, linking these plasticity mechanisms directly back to the ion channels that help generate EPSPs in the first place.
This bidirectional flexibility is considered essential for how neural networks store and update information. Without the ability to both strengthen and weaken synaptic responses, the brain would lack the capacity to form new memories while retaining old ones.