Postsynaptic potential

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Postsynaptic potentials are changes in the membrane potential of the postsynaptic terminal of a chemical synapse. Postsynaptic potentials are graded potentials, and should not be confused with action potentials although their function is to initiate or inhibit action potentials. Postsynaptic potentials occur when the presynaptic neuron releases neurotransmitters into the synaptic cleft. 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. [1] These are collectively referred to as postsynaptic receptors, since they are located on the membrane of the postsynaptic cell. 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. [2]

Contents

Ion Involvement

Ions can create excitatory or inhibitory potentials due to their unique reversal potentials and the membrane's permeability to each ion. The Nernst equation and Goldman equation can calculate membrane potential differences based on ion concentration, offering predictions into how ions can affect postsynaptic potentials. [3] Ions are subject to two main forces, diffusion and electrostatic repulsion. Ions will tend towards their equilibrium potential, which is the state where the diffusion force cancels out the force of electrostatic repulsion. When a membrane is at its equilibrium potential, there is no longer a net movement of ions. [4]

Neurons have a resting potential of about −70 mV. When a neurotransmitter binds to a postsynaptic receptor, this can lead to the opening or closing of ion channels, allowing ions to flow inside or outside of the cell, changing the membrane potential. When an ion channel opens and there is a net gain of positively charged ions, like sodium (Na+) and calcium (Ca2+), that flow into the cell, this creates excitatory postsynaptic potentials (EPSP) that depolarize the cell membrane increasing the likelihood of an action potential by bringing the neuron's potential closer to its firing threshold (about -55 mV).

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. [5]

It is important to note that neurotransmitters are not inherently excitatory or inhibitory. A single neurotransmitter can bind to different types of receptors on the postsynaptic neuron, opening or closing specific ion channels coupled to the receptor. [6]

Relation to Action Potentials

EPSPs and IPSPs are transient changes in the membrane potential. These changes in membrane potential occur at the postsynaptic membrane located on the dendrites or cell body of a neuron, specifically at the synapse where it receives signals from a presynaptic neuron. [7] EPSPs resulting from neurotransmitter release at a single synapse are generally too small to trigger an action potential spike in the postsynaptic neuron. However, a neuron may receive synaptic inputs from hundreds, if not thousands, of other neurons, with varying amounts of simultaneous input, so the combined activity of afferent neurons can cause large fluctuations in membrane potential or subthreshold membrane potential oscillations. If the postsynaptic cell is sufficiently depolarized, an action potential will occur. For example, in low-threshold spikes depolarizations by the T-type calcium channel occur at low, negative, membrane depolarizations resulting in the neuron reaching the threshold. Action potentials are not graded; they are an all-or-none response.

Algebraic summation

Postsynaptic potentials are graded potentials, meaning that signals don't fully propagate down the neuron and decrease in strength as they spread along the membrane. Graded potentials can summate in space or in time to generate a large enough response to reach action potential threshold. [8] Postsynaptic potentials undergo spatial and temporal summation due to their graded nature. [9]

Spatial summation : When inputs are received simultaneously at nearby synapses, their postsynaptic potentials combine. Multiple excitatory inputs combine resulting in greater membrane depolarization (more positive). Multiple inhibitory inputs combine and deepen hyperpolarization of the membrane (more negative). If the cell is receiving both inhibitory and excitatory postsynaptic potentials, they can cancel each other out, or one can be stronger than the other, and the membrane potential will change by the difference between them.

Temporal summation : When a single synapse inputs that are close together in time, their potentials are also added together. Thus, if a neuron receives an excitatory postsynaptic potential, and then the presynaptic neuron fires again, creating another EPSP, then the membrane of the postsynaptic cell is depolarized by the total sum of all the EPSPs fired, potentially bringing it closer to threshold for firing an action potential.

Termination

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. Excitatory Synapse Termination Figure.png
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.  

Termination of postsynaptic potentials begins when the neurotransmitter detaches from its receptor, allowing the receptor to return to its resting state. After the neurotransmitter detaches from the receptor, the neurotransmitters in the synaptic cleft can either be degraded by enzymes (e.g., acetylcholinesterase for acetylcholine) or can be taken back into the presynaptic neuron through reuptake mechanisms (e.g., EEAT glutamate transporters). Once the neurotransmitter is no longer bound to the receptor, the ion channels that were opened by receptor binding close, stopping ion flow. The membrane potential then returns to its resting membrane potential as ion concentrations normalize by diffusion and active transport mechanisms like the sodium-potassium pump. [10]

Postsynaptic Potential Applications

Postsynaptic potentials are essential in how the brain processes information, integrates signals, and coordinates complex behaviors. These temporary changes in a neuron's membrane potential determine if a neuron will fire an action potential which allows neurons to communicate within neural circuits. The balance between EPSPs and IPSPs are necessary for maintaining neural stability and function. There are many different applications of postsynaptic potentials.

Neural Communication and Integration: Postsynaptic potentials allow neurons to integrate inputs from thousands of synapses, functioning as a "decision-making unit" within the brain. [11]

Learning and Memory: Neuroplasticity is the key mechanism whereby learning and memory happens. When neurons consistently fire together, their synaptic connections strengthen, a principle known as Hebbian theory. [12] 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. [13]

Motor Control: Postsynaptic potentials in motor neurons integrate signals from the brain and spinal cord to coordinate muscle movement. During voluntary movement, EPSPs activate motor neurons, while IPSPs inhibit opposing muscle groups to make sure smooth motion occurs. [14]

Neurodevelopment and Recovery: In neurodevelopmental and recovery processes, postsynaptic plasticity abilities allow neural pathways to rewire, leading to improved motor skills, language recovery, and adapted cognitive strategies. [15]

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. [16] [17]

See also

Related Research Articles

<span class="mw-page-title-main">Chemical synapse</span> Biological junctions through which neurons signals can be sent

Chemical synapses are biological junctions through which neurons' signals can be sent to each other and to non-neuronal cells such as those in muscles or glands. Chemical synapses allow neurons to form circuits within the central nervous system. They are crucial to the biological computations that underlie perception and thought. They allow the nervous system to connect to and control other systems of the body.

<span class="mw-page-title-main">Synaptic plasticity</span> Ability of a synapse to strengthen or weaken over time according to its activity

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity. Since memories are postulated to be represented by vastly interconnected neural circuits in the brain, synaptic plasticity is one of the important neurochemical foundations of learning and memory.

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential. The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP), which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell-to-cell signalling. EPSPs and IPSPs compete with each other at numerous synapses of a neuron. This determines whether an action potential occurring at the presynaptic terminal produces an action potential at the postsynaptic membrane. Some common neurotransmitters involved in IPSPs are GABA and glycine.

<span class="mw-page-title-main">Excitatory postsynaptic potential</span> Process causing temporary increase in postsynaptic potential

In neuroscience, an excitatory postsynaptic potential (EPSP) is a postsynaptic potential that makes the postsynaptic neuron more likely to fire an action potential. This temporary depolarization of postsynaptic membrane potential, caused by the flow of positively charged ions into the postsynaptic cell, is a result of opening ligand-gated ion channels. These are the opposite of inhibitory postsynaptic potentials (IPSPs), which usually result from the flow of negative ions into the cell or positive ions out of the cell. EPSPs can also result from a decrease in outgoing positive charges, while IPSPs are sometimes caused by an increase in positive charge outflow. The flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC).

In neuroscience, a silent synapse is an excitatory glutamatergic synapse whose postsynaptic membrane contains NMDA-type glutamate receptors but no AMPA-type glutamate receptors. These synapses are named "silent" because normal AMPA receptor-mediated signaling is not present, rendering the synapse inactive under typical conditions. Silent synapses are typically considered to be immature glutamatergic synapses. As the brain matures, the relative number of silent synapses decreases. However, recent research on hippocampal silent synapses shows that while they may indeed be a developmental landmark in the formation of a synapse, that synapses can be "silenced" by activity, even once they have acquired AMPA receptors. Thus, silence may be a state that synapses can visit many times during their lifetimes.

<span class="mw-page-title-main">Graded potential</span> Changes in membrane potential varying in size

Graded potentials are changes in membrane potential that vary according to the size of the stimulus, as opposed to being all-or-none. They include diverse potentials such as receptor potentials, electrotonic potentials, subthreshold membrane potential oscillations, slow-wave potential, pacemaker potentials, and synaptic potentials. The magnitude of a graded potential is determined by the strength of the stimulus. They arise from the summation of the individual actions of ligand-gated ion channel proteins, and decrease over time and space. They do not typically involve voltage-gated sodium and potassium channels, but rather can be produced by neurotransmitters that are released at synapses which activate ligand-gated ion channels. They occur at the postsynaptic dendrite in response to presynaptic neuron firing and release of neurotransmitter, or may occur in skeletal, smooth, or cardiac muscle in response to nerve input. These impulses are incremental and may be excitatory or inhibitory.

<span class="mw-page-title-main">Excitatory synapse</span> Sort of synapse

An excitatory synapse is a synapse in which an action potential in a presynaptic neuron increases the probability of an action potential occurring in a postsynaptic cell. Neurons form networks through which nerve impulses travels, each neuron often making numerous connections with other cells of neurons. These electrical signals may be excitatory or inhibitory, and, if the total of excitatory influences exceeds that of the inhibitory influences, the neuron will generate a new action potential at its axon hillock, thus transmitting the information to yet another cell.

<span class="mw-page-title-main">Electrotonic potential</span>

In physiology, electrotonus refers to the passive spread of charge inside a neuron and between cardiac muscle cells or smooth muscle cells. Passive means that voltage-dependent changes in membrane conductance do not contribute. Neurons and other excitable cells produce two types of electrical potential:

<span class="mw-page-title-main">Neural circuit</span> Network or circuit of neurons

A neural circuit is a population of neurons interconnected by synapses to carry out a specific function when activated. Multiple neural circuits interconnect with one another to form large scale brain networks.

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<span class="mw-page-title-main">Neurotransmission</span> Impulse transmission between neurons

Neurotransmission is the process by which signaling molecules called neurotransmitters are released by the axon terminal of a neuron, and bind to and react with the receptors on the dendrites of another neuron a short distance away. A similar process occurs in retrograde neurotransmission, where the dendrites of the postsynaptic neuron release retrograde neurotransmitters that signal through receptors that are located on the axon terminal of the presynaptic neuron, mainly at GABAergic and glutamatergic synapses.

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<span class="mw-page-title-main">Synapse</span> Structure connecting neurons in the nervous system

In the nervous system, a synapse is a structure that allows a neuron to pass an electrical or chemical signal to another neuron or a target effector cell. Synapses can be classified as either chemical or electrical, depending on the mechanism of signal transmission between neurons. In the case of electrical synapses, neurons are coupled bidirectionally with each other through gap junctions and have a connected cytoplasmic milieu. These types of synapses are known to produce synchronous network activity in the brain, but can also result in complicated, chaotic network level dynamics. Therefore, signal directionality cannot always be defined across electrical synapses.

<span class="mw-page-title-main">Synaptic potential</span> Potential difference across the postsynaptic membrane

Synaptic potential refers to the potential difference across the postsynaptic membrane that results from the action of neurotransmitters at a neuronal synapse. In other words, it is the “incoming” signal that a neuron receives. There are two forms of synaptic potential: excitatory and inhibitory. The type of potential produced depends on both the postsynaptic receptor, more specifically the changes in conductance of ion channels in the post synaptic membrane, and the nature of the released neurotransmitter. Excitatory post-synaptic potentials (EPSPs) depolarize the membrane and move the potential closer to the threshold for an action potential to be generated. Inhibitory postsynaptic potentials (IPSPs) hyperpolarize the membrane and move the potential farther away from the threshold, decreasing the likelihood of an action potential occurring. The Excitatory Post Synaptic potential is most likely going to be carried out by the neurotransmitters glutamate and acetylcholine, while the Inhibitory post synaptic potential will most likely be carried out by the neurotransmitters gamma-aminobutyric acid (GABA) and glycine. In order to depolarize a neuron enough to cause an action potential, there must be enough EPSPs to both depolarize the postsynaptic membrane from its resting membrane potential to its threshold and counterbalance the concurrent IPSPs that hyperpolarize the membrane. 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 summative neural integration, and if the result is an increase of 20 mV or more, an action potential will occur.

<span class="mw-page-title-main">Synaptic gating</span>

Synaptic gating is the ability of neural circuits to gate inputs by either suppressing or facilitating specific synaptic activity. Selective inhibition of certain synapses has been studied thoroughly, and recent studies have supported the existence of permissively gated synaptic transmission. In general, synaptic gating involves a mechanism of central control over neuronal output. It includes a sort of gatekeeper neuron, which has the ability to influence transmission of information to selected targets independently of the parts of the synapse upon which it exerts its action.

<span class="mw-page-title-main">Summation (neurophysiology)</span>

Summation, which includes both spatial summation and temporal summation, is the process that determines whether or not an action potential will be generated by the combined effects of excitatory and inhibitory signals, both from multiple simultaneous inputs, and from repeated inputs. Depending on the sum total of many individual inputs, summation may or may not reach the threshold voltage to trigger an action potential.

Cellular neuroscience is a branch of neuroscience concerned with the study of neurons at a cellular level. This includes morphology and physiological properties of single neurons. Several techniques such as intracellular recording, patch-clamp, and voltage-clamp technique, pharmacology, confocal imaging, molecular biology, two photon laser scanning microscopy and Ca2+ imaging have been used to study activity at the cellular level. Cellular neuroscience examines the various types of neurons, the functions of different neurons, the influence of neurons upon each other, and how neurons work together.

<span class="mw-page-title-main">Nonsynaptic plasticity</span> Form of neuroplasticity

Nonsynaptic plasticity is a form of neuroplasticity that involves modification of ion channel function in the axon, dendrites, and cell body that results in specific changes in the integration of excitatory postsynaptic potentials and inhibitory postsynaptic potentials. Nonsynaptic plasticity is a modification of the intrinsic excitability of the neuron. It interacts with synaptic plasticity, but it is considered a separate entity from synaptic plasticity. Intrinsic modification of the electrical properties of neurons plays a role in many aspects of plasticity from homeostatic plasticity to learning and memory itself. Nonsynaptic plasticity affects synaptic integration, subthreshold propagation, spike generation, and other fundamental mechanisms of neurons at the cellular level. These individual neuronal alterations can result in changes in higher brain function, especially learning and memory. However, as an emerging field in neuroscience, much of the knowledge about nonsynaptic plasticity is uncertain and still requires further investigation to better define its role in brain function and behavior.

Neurotransmitters are released into a synapse in packaged vesicles called quanta. One quantum generates a miniature end plate potential (MEPP) which is the smallest amount of stimulation that one neuron can send to another neuron. Quantal release is the mechanism by which most traditional endogenous neurotransmitters are transmitted throughout the body. The aggregate sum of many MEPPs is an end plate potential (EPP). A normal end plate potential usually causes the postsynaptic neuron to reach its threshold of excitation and elicit an action potential. Electrical synapses do not use quantal neurotransmitter release and instead use gap junctions between neurons to send current flows between neurons. The goal of any synapse is to produce either an excitatory postsynaptic potential (EPSP) or an inhibitory postsynaptic potential (IPSP), which generate or repress the expression, respectively, of an action potential in the postsynaptic neuron. It is estimated that an action potential will trigger the release of approximately 20% of an axon terminal's neurotransmitter load.

References

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  2. ↑ "Postsynaptic Potential (PSP)". JoVE. Retrieved 2024-10-27.
  3. ↑ Purves, Dale; Augustine, George J.; Fitzpatrick, David; Katz, Lawrence C.; LaMantia, Anthony-Samuel; McNamara, James O.; Williams, S. Mark (2001), "The Forces that Create Membrane Potentials", Neuroscience. 2nd edition, Sinauer Associates, retrieved 2024-10-28
  4. ↑ Chrysafides, Steven M.; Bordes, Stephen J.; Sharma, Sandeep (2024), "Physiology, Resting Potential", StatPearls, Treasure Island (FL): StatPearls Publishing, PMID   30855922 , retrieved 2024-10-28
  5. ↑ Harvey, Victoria L.; Dickenson, Anthony H. (2010), "EPSPs and IPSPs", in Stolerman, Ian P. (ed.), Encyclopedia of Psychopharmacology, Berlin, Heidelberg: Springer, p. 489, doi:10.1007/978-3-540-68706-1_618, ISBN   978-3-540-68706-1 , retrieved 2024-10-28
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  7. ↑ Henley, Casey (2021-01-01). "Postsynaptic Potentials".{{cite journal}}: Cite journal requires |journal= (help)
  8. ↑ "Graded Potential - an overview | ScienceDirect Topics". www.sciencedirect.com. Retrieved 2024-10-27.
  9. ↑ Bennett, M. V. L. (2009-01-01), "Gap Junctions and Electrical Synapses", in Squire, Larry R. (ed.), Encyclopedia of Neuroscience, Oxford: Academic Press, pp. 529–548, ISBN   978-0-08-045046-9 , retrieved 2024-10-30
  10. ↑ Purves, Dale; Augustine, George J.; Fitzpatrick, David; Katz, Lawrence C.; LaMantia, Anthony-Samuel; McNamara, James O.; Williams, S. Mark (2001), "Neurotransmitter Release and Removal", Neuroscience. 2nd edition, Sinauer Associates, retrieved 2024-10-30
  11. ↑ Henley, Casey (2021-01-01). "Postsynaptic Potentials".{{cite journal}}: Cite journal requires |journal= (help)
  12. ↑ "Hebbian Theory - an overview | ScienceDirect Topics". www.sciencedirect.com. Retrieved 2024-12-07.
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  15. ↑ Zotey, Vaishnavi; Andhale, Amol; Shegekar, Tejas; Juganavar, Anup (2023-09-24). "Adaptive Neuroplasticity in Brain Injury Recovery: Strategies and Insights". Cureus. 15 (9): e45873. doi: 10.7759/cureus.45873 . ISSN   2168-8184. PMC   10598326 . PMID   37885532.
  16. ↑ Zhang, Jifa; Zhang, Yinglu; Wang, Jiaxing; Xia, Yilin; Zhang, Jiaxian; Chen, Lei (2024-08-23). "Recent advances in Alzheimer's disease: mechanisms, clinical trials and new drug development strategies". Signal Transduction and Targeted Therapy. 9 (1): 1–35. doi:10.1038/s41392-024-01911-3. ISSN   2059-3635. PMID   39174535.
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