Postsynaptic potential

These neurotransmitters bind to receptors on the postsynaptic terminal, which may be a neuron, or a muscle cell in the case of a neuromuscular junction.

Postsynaptic potentials are important mechanisms by which neurons communicate with each other allowing for information processing, learning, memory formation, and complex behavior within the nervous system.

The opposite can happen when the opening of ion channels results in the flow of negatively charged ions, like chloride (Cl−), into the cell, or positively charged ions, like potassium (K+), to flow out of the cell, creating inhibitory postsynaptic potentials (IPSP) that hyperpolarize the cell membrane, decreasing the likelihood of an action potential by bringing the neuron's potential further away from its firing threshold.

[7] EPSPs resulting from neurotransmitter release at a single synapse are generally too small to trigger an action potential spike in the postsynaptic neuron.

[9] Spatial summation: When inputs are received simultaneously at nearby synapses, their postsynaptic potentials combine.

[10] Postsynaptic potentials are essential in how the brain processes information, integrates signals, and coordinates complex behaviors.

[11] Long-term potentiation (LTP) is one mechanism where repeated EPSPs occur, strengthening neural circuits involved in learning, allowing the brain to store information more effectively.

Long-term depression (LTD) is another mechanism where IPSPs occur weakening less-used synapses, refining learning by filtering out unnecessary information.

During voluntary movement, EPSPs activate motor neurons, while IPSPs inhibit opposing muscle groups to make sure smooth motion occurs.

[14] Pharmacology and Neurological Treatments: Improved understanding of postsynaptic potentials has guided the development of drugs that modulate synaptic strength to help in neurodegenerative diseases, depression, anxiety, etc.

Two stages of activity at an excitatory glutamatergic synapse. A. Active synapse generating an EPSP. The presynaptic terminal releases glutamate into the synaptic cleft, shown binding to ionotropic glutamate receptors (e.g., AMPA receptors) on the postsynaptic membrane. Sodium ions (Na + ) flow into the postsynaptic neuron through the open receptor channels depolarizing the membrane and generating an EPSP. B. Termination of synaptic activity via reuptake. Glutamate unbinds from the AMPA receptor and is then cleared from the synaptic cleft by glutamate transporters (e.g., EAATs) located on the presynaptic membrane. Glutamate molecules are shown being actively transported back into the presynaptic terminal for recycling or breakdown. The postsynaptic membrane is no longer depolarized, and the ionotropic receptors are inactive, indicating termination of the EPSP.