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This is an example of EPSP's depolarization effects on membrane potential and IPSP's hyper-polarization effects on membrane potential.
EPSP/IPSP example

Synaptic potential refers to the difference in voltage between the inside and outside of a postsynaptic neuron. In other words, it is the “incoming” signal of a neuron. There are two forms of synaptic potential: excitatory and inhibitory. Excitatory post-synaptic potentials (EPSPs) depolarize the membrane and move it closer to the threshold for an action potential. Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the membrane and move it farther away from the threshold. In order to depolarize a neuron enough to cause an action potential, there must be enough EPSPs to both counterbalance the IPSPs and also depolarize the membrane from its resting membrane potential to its threshold. As an example, consider a neuron with a resting membrane potential of -70 mV (millivolts) and a threshold of -50 mV. It will need to be raised 20 mV in order to pass the threshold and fire an action potential. The neuron will account for all the many incoming excitatory and inhibitory signals via neural integration, and if the result is an increase of 20 mV or more, an action potential will occur.

Both EPSP and IPSPs generation is contingent upon the release of neurotransmitters from a terminal bouton of the presynaptic neuron. The first phase of synaptic potential generation is the same for both excitatory and inhibitory potentials. As an action potential travels through the presynaptic neuron, the membrane depolarization causes voltage-gated calcium channels to open. Consequently, calcium ions flow into the cell, promoting neurotransmitter-filled vesicles to travel down to the terminal bouton. These vesicles fuse with the membrane, releasing the neurotransmitter into the synaptic cleft. EPSPs on the postsynaptic neuron result from the main excitatory neurotransmitter, glutamate, binding to its corresponding receptors on the postsynaptic membrane. By contrast, IPSPs are induced by the binding of GABA or glycine.

Synaptic potentials are small and many are needed to add up to reach the threshold. The two ways that synaptic potentials can add up to potentially form an action potential are spatial summation and temporal summation. Spatial summation refers to several excitatory stimuli from different synapses converging on the same postsynaptic neuron at the same time to reach the threshold needed to reach an action potential. Temporal summation refers to successive excitatory stimuli on the same location of the postsynaptic neuron. Both types of summation are the result of adding together many excitatory potentials. The difference being whether the multiple stimuli are coming from different locations at the same time (spatial) or at different times from the same location (temporal). Summation has been referred to as a “neurotransmitter induced tug-of-war” between excitatory and inhibitory stimuli. Whether the effects are combined in space or in time, they are both additive properties that require many stimuli acting together to reach the threshold. Synaptic potentials, unlike action potentials, degrade quickly as they move away from the synapse. This is the case for both excitatory and inhibitory postsynaptic potentials.

Synaptic potentials are not static. The concept of synaptic plasticity refers to the changes in synaptic potential. A synaptic potential may get stronger or weaker over time depending on a few factors. The quantity of neurotransmitters released can play a large role in the future strength of that synapse’s potential. The receptors on the post-synaptic side also play a role, both in their numbers, composition, and physical orientation.

In recent years, there has been an abundance of research on how to prolong the effects of a synaptic potential, and more importantly, how to enhance or reduce its amplitude. The enhancement of synaptic potential would mean that fewer would be needed to have the same or larger effect, which could have far-reaching medical uses. The research indicates that this long term potentiation or in the case of inhibitory synapses, long term depression of the synapse occurs after prolonged stimulation of two neurons at the same time. Long term potentiation is known to have a role in memory and learning, which could be useful in treating diseases like Alzheimers.