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ArticlesPhysiologyNervous systemAction potential and synapsesPostsynaptic potentials

Postsynaptic potentials

Author: Spyridon K. Votis • Reviewer: Assist. Prof. Konstantinos Ι. Tsamis, MD
Last reviewed: November 21, 2024
Reading time: 11 minutes

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Overview of electrical and chemical synapses.

Synapse

Synapsis

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Synonyms: none

Postsynaptic potentials refer to changes observed in the resting potential of the neuronal cell membrane triggered by synaptic activation. In its resting state, the cell membrane maintains a polarized potential, with the inner surface negatively charged. This potential is dynamic and can decrease, leading to depolarization, or increase, resulting in hyperpolarization. These alterations can occur at synapse sites on the postsynaptic membrane, giving rise to excitatory or inhibitory postsynaptic potentials, respectively.

Key facts about postsynaptic potentials Definition   Postsynaptic potentials refer to changes in the potential difference across the postsynaptic membrane, prompted by synaptic activation.  
Types   Excitatory postsynaptic potentials (EPSPs)
Inhibitory postsynaptic potentials (IPSPs)  
Excitatory postsynaptic potentials (EPSPs)   Primarily generated by neurotransmitter binding to ionotropic receptors selective for Na+ and Ca2+.
Activation of these receptors leads to the influx of positive ions into the postsynaptic cell.
Results in depolarization of the postsynaptic membrane.
Depolarization propagates to adjacent membrane regions as a graded potential.  
Inhibitory postsynaptic potentials (IPSPs)
  Primarily generated by neurotransmitter binding to ionotropic receptors selective for K+ or Cl-.
Activation of these receptors leads to the outflux of positive ions or influx of negative ions.
Results in hyperpolarization of the postsynaptic membrane.
Hyperpolarization propagates to adjacent membrane regions as a graded potential
 

Contents

Overview of synaptic function

Graded membrane potentials

Excitatory postsynaptic potentials (EPSPs)

Inhibitory postsynaptic potentials (IPSPs)

Summation of synaptic potentials

Excitatory vs inhibitory

Clinical Notes

Excitatory/Inhibitory imbalance in neurodegenerative disorders

Sources

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Overview of synaptic function

Synapses serve as critical structures enabling neurons to transmit signals to other neurons or effector cells. While synapses can be either electrical or chemical, the majority in the human nervous system are chemical. In a chemical synapse, the presynaptic neuron initiates the signal transmission, with its specific membrane region involved in the synapse, the presynaptic membrane. Conversely, the postsynaptic neuron receives the signal, with its membrane engaged in the synapse known as the postsynaptic membrane.

Upon activation, the presynaptic membrane releases neurotransmitters into the synaptic cleft. The postsynaptic membrane is enriched with receptors, which can be either ligand-gated ion channels (ionotropic receptors) or coupled with G-proteins (metabotropic receptors). In the latter case, second messengers also influence ion channels. So, regardless of the receptor type, neurotransmitter binding alters the postsynaptic membrane's permeability to specific ions. Consequently, ions flow into or out of the cell, leading to membrane depolarization or hyperpolarization.

[Ligand-gated ion channels]
These channels are activated or deactivated by a chemical substance (ligand) binding to a receptor protein (ligand-binding site) on the channel.

Graded membrane potentials

In the human central nervous system, the majority of chemical synapses occur between an axon terminal (presynaptic membrane) and either a cell body, dendrite, or dendritic spine (postsynaptic membrane). These regions of the neuronal cell membrane typically lack voltage-gated ion channels and are unable to generate action potentials. Consequently, changes in the potential difference across the postsynaptic membrane generate graded potentials, which can propagate to neighboring membrane regions. However, these potentials vary in magnitude and decay exponentially over time and distance from their origin.

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Excitatory postsynaptic potentials (EPSPs)

Excitatory postsynaptic potentials are triggered when neurotransmitters released from the presynaptic cell bind to receptors on the postsynaptic membrane, leading to depolarization. The main excitatory neurotransmitter in the central nervous system is the glutamate. The depolarization of the postsynaptic membrane primarily occurs through the activation of ionotropic receptors that are selective for specific cations such as Na+ and Ca2+, leading to an inward flow of positively charged ions. As a result, the postsynaptic potential deviates from its resting state of approximately -70mV towards 0mV. Excitatory postsynaptic potentials are localized to specific areas of the neuronal membrane that establish synapses and propagate as graded potentials to neighboring regions, potentially reaching the cell body and the axonal hillock. If the depolarization there reaches the threshold, it triggers an action potential in the entire neuron. Consequently, synapses that induce depolarization are defined as excitatory, and their effect on the postsynaptic membrane is termed an excitatory postsynaptic potential. Additionally, metabotropic receptors can also generate excitatory postsynaptic potentials by activating secondary messengers that open or close cation channels on the postsynaptic membrane.

[Excitatory neurotransmitter mechanism] If EPSPs are not strong enough, then the depolarization at the membrane doesn't reach the threshold and it doesn't trigger an action potential. If on the other hand the EPSP is strong enough then a new action potential will be generated. 

Inhibitory postsynaptic potentials (IPSPs)

Similar to excitatory synapses, in inhibitory synapses, neurotransmitters released from the presynaptic membrane bind to receptors on the postsynaptic membrane, activating them. Ionotropic receptors in inhibitory synapses are principally ion channels permeable to Cl- or K+, and their activation allows ions to flow across the membrane according to their electrochemical gradient. The gradient for Cl- drives it inside the cell, while K+ moves outside the cell, leading to an increase in the negative charge on the inner surface of the postsynaptic membrane in both cases. This hyperpolarization spreads to neighboring areas of the membrane as a graded potential, gradually diminishing. When it arrives at the cell body and axon hillock, it reduces the likelihood of the postsynaptic cell reaching the threshold for generating an action potential. In addition to ionotropic receptors directly increasing ion permeability, inhibitory postsynaptic potentials can occur through the activation of metabotropic receptors, which indirectly influence other ion channels, resulting in hyperpolarization of the postsynaptic membrane.

[Inhibitory neurotransmitter mechanism (GABA)] In inhibitory synapses, the binding of the neurotransmitter in the receptor leads to an increase in the negative charge on the inner surface of the postsynaptic membrane (hyperpolarization). 

Summation of synaptic potentials

It's essential to recognize that the impact of any single synapse on a neuron in the brain isn't potent enough to individually activate or deactivate the neuron. While postsynaptic potentials propagate from the receptive field toward the cell body, they gradually weaken, typically falling well below the threshold for triggering postsynaptic action potentials by the time they reach the axon hillock. However, neurons in the central nervous system receive input from thousands of synapses, and the collective effect on a neuron depends on how postsynaptic potentials from active synapses integrate spatially and temporally. At any given moment, if the combined effect of all excitatory and inhibitory postsynaptic potentials arriving at the axonal hillock results in a depolarization of sufficient magnitude to surpass the threshold, then the postsynaptic neuron will generate an action potential. Conversely, if inhibition predominates, the postsynaptic cell will remain inactive.

[Temporal and spatial summation of synaptic potential]This illustration demonstrates the difference between spatial and temporal summation of excitatory postsynaptic potentials (EPSPs). Spatial summation (top) occurs when subthreshold signals from multiple neurons are received simultaneously by a single postsynaptic neuron. These signals combine to produce a cumulative effect, which may bring the membrane potential to the threshold level required to trigger an action potential. Temporal summation (bottom) involves consecutive signals from a single presynaptic neuron, arriving in quick succession. When these signals are closely spaced in time, they can accumulate and increase the membrane potential to threshold, leading to the initiation of an action potential.

Excitatory vs inhibitory

It's crucial to note that the classification of neurons, neurotransmitters, and synapses as excitatory or inhibitory is contingent upon the interaction of a neurotransmitter with a specific receptor. So, the functional outcome vastly depends on the specific receptor type and the postsynaptic response it elicits. For instance, when the neurotransmitter dopamine binds to D1 receptors, it produces excitatory postsynaptic potentials, whereas binding to D2 receptors results in inhibitory postsynaptic potentials.

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Clinical Notes Excitatory/Inhibitory imbalance in neurodegenerative disorders

The balance between excitation and inhibition in neurons and neuronal networks is essential for their proper functioning. Disruptions to this balance can initially cause alterations in neuronal firing patterns and, over time, may contribute to the pathological mechanisms underlying disorders characterized by neuronal circuit degeneration. Overexcitability, in particular, has been identified as a key factor leading to neuronal dysfunction and apoptosis, a process known as excitotoxicity.

In Alzheimer's disease, for instance, pyramidal neurons in the hippocampus and neocortex have been consistently observed to increase their firing rates during the early stages of the disease. Similarly, Parkinson's disease and Huntington's disease exhibit disturbances in the balance between excitatory and inhibitory signals within the striatum. This imbalance is characterized by abnormal excitatory input from corticostriatal pathways alongside diminished inhibition mediated by interneurons. Additionally, in patients with amyotrophic lateral sclerosis, there are indications of an imbalance between excitatory and inhibitory signaling, which is evident in increased intracortical facilitation observed in the motor cortex. These observations underscore the importance of maintaining a delicate balance between excitation and inhibition for normal neuronal function and highlight the significance of understanding these mechanisms in the context of neurological disorders.

Sources

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