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. They are caused by the presynaptic neuron releasing neurotransmitters from the terminal bouton at the end of an axon into the synaptic cleft. The neurotransmitters bind to receptors on the postsynaptic terminal, which may be a neuron or a muscle cell in the case of a neuromuscular junction. These are collectively referred to as postsynaptic receptors, since they are on the membrane of the postsynaptic cell.

Contents

The role of ions

One way receptors can react to being bound by a neurotransmitter is to open or close an ion channel, allowing ions to enter or leave the cell. It is these ions that alter the membrane potential. 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. Two important equations that can determine membrane potential differences based on ion concentrations are the Nernst Equation and the Goldman Equation. [1] [2]

Relation to action potentials

Neurons have a resting potential of about −70 mV. If the opening of the ion channel results in a net gain of positive charge across the membrane, the membrane is said to be depolarized, as the potential comes closer to zero. This is an excitatory postsynaptic potential (EPSP), as it brings the neuron's potential closer to its firing threshold (about −55 mV).

If, on the other hand, the opening of the ion channel results in a net gain of negative charge, this moves the potential further from zero and is referred to as hyperpolarization. This is an inhibitory postsynaptic potential (IPSP), as it changes the charge across the membrane to be further from the firing threshold.

Neurotransmitters are not inherently excitatory or inhibitory: different receptors for the same neurotransmitter may open different types of ion channels. [3]

EPSPs and IPSPs are transient changes in the membrane potential, and EPSPs resulting from transmitter release at a single synapse are generally far too small to trigger a 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 all-or-none responses.

Termination

Postsynaptic potentials begin to be terminated when the neurotransmitter detaches from its receptor. The receptor is then free to return to its previous structural state. Ion channels that had been opened by the receptor when the neurotransmitter was bound to it will now close. Once the channels are closed, ions return to their equilibrium states, and the membrane is returned to its equilibrium potential.

Algebraic summation

Postsynaptic potentials are subject to summation, spatially and/or temporally.

Spatial summation : If a cell is receiving input at two synapses that are near each other, their postsynaptic potentials add together. If the cell is receiving two excitatory postsynaptic potentials, they combine so that the membrane potential is depolarized by the sum of the two changes. If there are two inhibitory potentials, they also sum, and the membrane is hyperpolarized by that amount. If the cell is receiving both inhibitory and excitatory postsynaptic potentials, they can cancel out, or one can be stronger than the other, and the membrane potential will change by the difference between them.

Temporal summation : When a cell receives inputs that are close together in time, they are also added together, even if from the same synapse. 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 of the EPSPs.

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.

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential. IPSPs were first investigated in motorneurons by David P. C. Lloyd, John Eccles and Rodolfo Llinás in the 1950s and 1960s. 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. Inhibitory presynaptic neurons release neurotransmitters that then bind to the postsynaptic receptors; this induces a change in the permeability of the postsynaptic neuronal membrane to particular ions. An electric current that changes the postsynaptic membrane potential to create a more negative postsynaptic potential is generated, i.e. the postsynaptic membrane potential becomes more negative than the resting membrane potential, and this is called hyperpolarisation. To generate an action potential, the postsynaptic membrane must depolarize—the membrane potential must reach a voltage threshold more positive than the resting membrane potential. Therefore, hyperpolarisation of the postsynaptic membrane makes it less likely for depolarisation to sufficiently occur to generate an action potential in the postsynaptic neurone.

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

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<span class="mw-page-title-main">Membrane potential</span> Type of physical quantity

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<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">End-plate potential</span>

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

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

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

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.

Low-threshold spikes (LTS) refer to membrane depolarizations by the T-type calcium channel. LTS occur at low, negative, membrane depolarizations. They often follow a membrane hyperpolarization, which can be the result of decreased excitability or increased inhibition. LTS result in the neuron reaching the threshold for an action potential. LTS is a large depolarization due to an increase in Ca2+ conductance, so LTS is mediated by calcium (Ca2+) conductance. The spike is typically crowned by a burst of two to seven action potentials, which is known as a low-threshold burst. LTS are voltage dependent and are inactivated if the cell's resting membrane potential is more depolarized than −60mV. LTS are deinactivated, or recover from inactivation, if the cell is hyperpolarized and can be activated by depolarizing inputs, such as excitatory postsynaptic potentials (EPSP). LTS were discovered by Rodolfo Llinás and coworkers in the 1980s.

<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.

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<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

  1. Henley, Casey (2021-01-01). "Postsynaptic Potentials".{{cite journal}}: Cite journal requires |journal= (help)
  2. Powell, Carolyn L.; Brown, Angus M. (2021-03-01). "A classic experiment revisited: membrane permeability changes during the action potential". Advances in Physiology Education. 45 (1): 178–181. doi: 10.1152/advan.00188.2020 . ISSN   1043-4046.
  3. Spitzer, Nicholas C. (2015). "Neurotransmitter Switching? No Surprise". Neuron. Elsevier BV. 86 (5): 1131–1144. doi: 10.1016/j.neuron.2015.05.028 . ISSN   0896-6273.