An excitatory postsynaptic potential, or EPSP, represents a temporary shift in the electrical charge across a neuron’s membrane. This change makes the receiving neuron more likely to generate its own electrical signal. The term “excitatory” indicates that it encourages the neuron towards activity. “Postsynaptic” refers to its occurrence on the membrane of the neuron that receives a signal across a synapse, the tiny gap between two neurons. “Potential” simply denotes a change in the electrical voltage across the membrane.
The Synaptic Event
The process begins when an electrical signal, known as an action potential, reaches the end of a transmitting neuron, called the presynaptic terminal. This arrival prompts the release of neurotransmitters into the synaptic cleft, the space separating neurons. Glutamate serves as the primary excitatory neurotransmitter throughout the central nervous system.
Glutamate molecules then travel across this gap and bind to specific receptor proteins located on the membrane of the receiving neuron, the postsynaptic cell. Many of these receptors are ligand-gated ion channels, meaning their structure includes a pore that opens when a neurotransmitter attaches. When these channels open, they allow positively charged ions to flow into the postsynaptic neuron.
The influx of positive ions, predominantly sodium (Na+), causes a slight increase in the electrical charge inside the neuron, making the interior less negative. This localized change in membrane potential is termed depolarization. The resulting EPSP is a graded potential, meaning its strength is not fixed but varies depending on the amount of neurotransmitter released and the number of activated receptors.
From Small Change to Firing Signal
A single excitatory postsynaptic potential is insufficient to cause a neuron to generate its own electrical signal. For a neuron to “fire,” its membrane potential must reach a specific voltage level known as the threshold of excitation. This threshold initiates a rapid, all-or-nothing electrical pulse called an action potential.
Neurons achieve this threshold through the combination of multiple EPSPs, a process known as summation. One way this occurs is through temporal summation, where a single presynaptic neuron fires repeatedly and rapidly. Each successive release of neurotransmitter causes new EPSPs that add to the lingering effect of previous ones, progressively depolarizing the postsynaptic membrane.
Another method is spatial summation, which involves multiple different presynaptic neurons releasing neurotransmitters at approximately the same time. The EPSPs generated at various locations on the postsynaptic neuron’s dendrites and cell body converge and combine. If the combined effect of these multiple, near-simultaneous EPSPs pushes the membrane potential to or beyond the threshold of excitation, the postsynaptic neuron will then generate an action potential, propagating the signal onward.
The Counterpart to Excitation
While EPSPs increase a neuron’s likelihood of firing, another type of postsynaptic potential works in opposition: the Inhibitory Postsynaptic Potential (IPSP). IPSPs make a neuron less likely to generate an action potential, effectively dampening its excitability. This balance between excitation and inhibition is important for precise neural function.
Inhibitory neurotransmitters, such as gamma-aminobutyric acid (GABA) and glycine, are responsible for generating IPSPs. When these neurotransmitters bind to their specific receptors on the postsynaptic membrane, they typically cause ion channels to open that allow negative ions, primarily chloride (Cl-), to flow into the cell. Alternatively, some inhibitory receptors may open channels that allow positive ions, like potassium (K+), to exit the cell.
This inward flow of negative charge or outward flow of positive charge makes the inside of the neuron even more negative, a process called hyperpolarization. Hyperpolarization moves the neuron’s membrane potential further away from the threshold required for an action potential. A neuron’s ultimate decision to fire an action potential is a dynamic calculation, constantly integrating all incoming excitatory and inhibitory signals.
Role in Neural Plasticity and Function
Excitatory postsynaptic potentials are central to neural plasticity, the brain’s ability to change and adapt over time. An example is Long-Term Potentiation (LTP), a persistent strengthening of synaptic connections. LTP occurs when a synapse experiences repeated, high-frequency stimulation, leading to a long-lasting increase in the amplitude of subsequent EPSPs at that synapse.
This enhanced synaptic efficiency means the same neurotransmitter release from the presynaptic neuron will produce a stronger depolarization in the postsynaptic neuron. LTP is a cellular mechanism underlying learning and memory formation in the brain. It allows for the strengthening of frequently used neural pathways, consolidating information and skills.
However, imbalances in excitatory signaling can also contribute to pathological states. Excessive or prolonged activation of excitatory neurotransmitter receptors, particularly by glutamate, can lead to excitotoxicity. This overstimulation can damage or kill neurons, and it is implicated in conditions such as seizures and neurodegenerative diseases.