Synapse: Difference between revisions

Latest revision as of 06:01, 24 October 2024

History

In the second half of the 19th century, there were two vigorously debated hypotheses about the structure of the brain. Proponents of the cell theory considered that the brain consisted of independent units (neurons), while others thought of as a continuous web-like reticulum (a syncytium). The debate was resolved when the new technique of electron microscopy revealed the cellular structure of the brain, and of the contacts between them. Ramon y Cajal, using the Golgi staining method, described differences between classes of neurons and precise connections between them. Later, electron microscopy and other techniques have showed that some neurons possess channels, called connexons, which permit electrical transmission between cells.

The first investigations of the properties of synapses were conducted on nerve-muscle synapse by Dale in 1936.^[1]

Structure

The nerve cell, transmitting the signal, is called the presynaptic cell; its target, receiving the signal, is called the postsynaptic cell. The presynaptic cell transmits the signal from the swollen tips of its axon’s branches, called presynaptic terminals, also called the synaptic boutons. The part of synapses where neurotransmitter is released is called the active zone. The presynaptic terminals usually end on the postsynaptic neuron’s dendrites, soma, or, less often, on the axon. The presynaptic cell does not make an anatomical contact with the postsynaptic cell since two cells are separated by a space, the synaptic cleft, which is about 20- 40 nm wide.^[2] Immediately behind the postsynaptic membrane is an elaborate complex of interlinked proteins called the postsynaptic density. Proteins in the postsynaptic density serve a myriad of roles, from anchoring and trafficking neurotransmitter receptors into the plasma membrane, to anchoring various proteins.

Chemical synapses can vary in size and shape. Under the electron microscope, synapses are seen either as symmetric or asymmetric. Asymmetric synapses are responsible for excitatory inputs, while symmetric ones transmit inhibitory inputs.

The number of synapses that one neuron can make varies greatly. The average neuron makes about 1000 synapses and can receive as many as 10,000 synapses; the Purkinje cell of the cerebellum receives up to 100,000. Early in development, neurons make many synapses, later the number declines, reaching the level of adulthood. The process is called activity dependent synapse elimination, when active synapses are reinforced and inactive ones are eliminated. The number of synapses can change even in the adult animals, contributing to synaptic plasticity. The adult human brain can have from 10¹⁵ to 5 × 10¹⁵ synapses.

Signaling across chemical synapses

Within the presynaptic nerve terminal, vesicles containing neurotransmitter sit "docked" at the synaptic membrane and ready to release the neurotransmitter. The release of neurotransmitter, the exocytosis, is triggered by the arrival of a nerve impulse (or action potential). The arriving action potential produces an influx of calcium ions through voltage-dependent, calcium-selective ion channels. Calcium ions then trigger a biochemical cascade which results in vesicles fusing with the presynaptic membrane and releasing their contents into the synaptic cleft. Vesicle fusion is driven by the action of a set of proteins, known as SNAREs. The membrane added by this fusion is later retrieved by endocytosis and recycled for the formation of fresh neurotransmitter-filled vesicles.

After a neurotransmitter is released into the synaptic cleft, it can bind ionotropic or metabotropic receptors at the postsynaptic membrane. Ionotropic receptors are themselves ion channels; when a neurotransmitter binds to these receptors, the receptor conformation changes. As a result, ion channels open and the ions flow in or out of the cell, changing the membrane potential. The resulting change in voltage is called a postsynaptic potential.

Whether an effect is excitatory or inhibitory depends on what type(s) of ion channel conduct the postsynaptic current, which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. The two most common neurotransmitters in the mammalian central nervous system are glutamate and GABA. Glutamate is an excitatory neurotransmitter, and can depolarise cells via its actions at any of three types of ionotropic receptor: kainate receptors; AMPA receptors; and NMDA receptors; activation of any of these allows the flow of K+, Na+ and sometimes Ca2+ into the postsynaptic cell. When GABA binds to GABA-A receptors, chloride channels open in the postsynaptic cell membrane. In adult neurons this usually results in chloride entering the postsynaptic cell and thus hyperpolarising it, but embryonic neurons and some adult cell types have a relatively high intracellular chloride concentration, and in these cases GABA actions may cause chloride to leave the cell, resulting in a depolarisation. Thus GABA can act as an excitatory neurotransmitter, but is mainly thought of as the most abundant inhibitory neurotransmitter in the adult.

Other important neurotransmitters in the mammalian CNS include purines, acetylcholine, serotonin, dopamine, serotonin and norepinephrine.

Synaptic transmission through ionotropic receptors is fast, taking just a few milliseconds to transmit the signal.

Neurotransmitter may also bind to metabotropic receptors, which are usually G-protein coupled receptors. When these receptors are activated, they produce intracellular second messengers, which subsequently may activate ion channels through phosphorylation. Such responses can last for several minutes.

Regulation of synaptic transmission

The last step in the synaptic transmission is the elimination of the neurotransmitter from the synaptic cleft. This removal prevents the desensitization of the post-synaptic receptors and ensures that succeeding action potentials will elicit the same size postsynaptic potential. The neurotransmitter can be removed because of diffusion, degradation or uptake by glial cells or nerve terminals.

The action of glutamate, glycine, GABA, dopamine, norepinephrine and 5-HT is terminated by uptake of transmitters by specific transport proteins, called transporters. Transporters neurotransmitter into nerve terminals can be packed into the vesicles and released again. ACh molecules in the synaptic cleft are degradated by a specific enzyme acetylcholinesterase, ATP is terminated by hydrolysis. Neuropetides are removed from the synaptic cleft by diffusion. Neurotransmitter degradation or removal is a prompt process, whereas diffusion is a slower one.

The necessity of removal of neurotransmitters and desensitization of receptors and ion channels means that the strength of a synapse may in effect diminish as a train of action potentials arriving in rapid succession. The phenomenon is called frequency dependence of synaptic transmission. The nervous system exploits this property for computational purposes, and can tune its synapses through such means as phosphorylation of the proteins involved. The size, number and replenishment rate of vesicles also are subject to regulation, as are many other elements of synaptic transmission.

Synaptic plasticity

The efficacy of chemical transmission is not fixed, but depends on the ongoing activity in the synapse. These changes can be a short-term, lasting from milliseconds to minutes, and long-term, lasting hours or days.^[3] Short periods of synaptic activation can lead in facilitation, depression or augmentation of neurotransmitter release. All these processes change the amount of neurotransmitter released, last seconds and have a presynaptic origin. Posttetanic facilitation also has a presynaptic origin, but it usually lasts for tens of minutes. Repetitive stimulation can result in long-term potentiation (LTP) or long-term depression (LTD) of synaptic strength. The mechanisms of LTP and LTD have both presynpatic and postsynaptic origins.

Integration of synaptic inputs

Generally, if an excitatory synapse is strong, an action potential in the presynaptic neuron will trigger another action potential in the postsynaptic cell; whereas at a weak synapse the excitatory post-synaptic potential (EPSP) will not reach the threshold for action potential initiation. In the brain, however, each neuron typically forms synapses with many others, and likewise each receives synaptic inputs from many others. When many synapses of a neuron receive excitatory inputs at the same time, the neuron may generate an impulse even though the synapses are weak. This process is known as spatial summation. If only one synapse is active, but it receives many impulses in a short period of time, impulses are also summated. This process is called temporal summation. On the other hand, a pre-synaptic neuron releasing an inhibitory neurotransmitter such as GABA can cause inhibitory postsynaptic potential in the postsynaptic neuron, decreasing its excitability and therefore decreasing the neuron's likelihood to fire an action potential. In this way the output of a neuron may depend on the inputs of many others, each of them may have a different degree of influence, depending on the strength of its synapse and the location on the neuron. John Carew Eccles performed some of the important early experiments on synaptic integration, for which he received the Nobel Prize for Physiology or Medicine in 1963. Complex input/output relationships form the basis of transistor-based computations in computers, and are thought to figure similarly in neural circuits.

Comparison with electrical synapses

An electrical synapse forms a narrow gap between the pre- and postsynaptic cells, known as a gap junction. At gap junctions, cells approach within about 3.5 nm of each other^[4], a much shorter distance than the 20 to 40 nm distance that separates cells at chemical synapses.^[2] As opposed to chemical synapses, the postsynaptic potential in electrical synapses is not caused by the opening of ion channels by chemical transmitters, but by direct electrical coupling between both neurons. Electrical synapses are therefore faster, current spreads instantaneously, whereas chemical synapses have a delay of about 1 ms. Electrical synapses conduct equally to both directions, while at the chemical synapse the impulse is send only from pre- to postsynaptic neuron. Electrical synapses are found throughout the nervous system, yet are less common than chemical synapses. Electrical and chemical transmission can coexist at a single synapse.^[3] Such combined synapses were first found avian ciliary ganglion cells.^[5]

References

↑ Dale HH et al. (1936) J Physiol 86:353-80
↑ ^2.0 ^2.1 Hormuzdi SG et al. (2004). "Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks". Biochim Biophys Acta 1662: 113–37. DOI:10.1016/j.bbamem.2003.10.023. PMID 15033583. Research Blogging.
↑ ^3.0 ^3.1 Martin A al. et (2001). From neuron to brain. Sunderland, Mass: Sinauer Associates. ISBN 0-87893-439-1.
↑ Jessell TM et al. (2000). Principles of neural science. New York: McGraw-Hill. ISBN 0-8385-7701-6.
↑ Martin AR, Pilar G (1963) J Physiol 168:443-63

[1] Dale HH et al. (1936) J Physiol 86:353-80

[pmid15033583-2] 2.0 ^2.1 Hormuzdi SG et al. (2004). "Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks". Biochim Biophys Acta 1662: 113–37. DOI:10.1016/j.bbamem.2003.10.023. PMID 15033583. Research Blogging.

[isbn0-87893-439-1-3] 3.0 ^3.1 Martin A al. et (2001). From neuron to brain. Sunderland, Mass: Sinauer Associates. ISBN 0-87893-439-1.

[4] Jessell TM et al. (2000). Principles of neural science. New York: McGraw-Hill. ISBN 0-8385-7701-6.

[5] Martin AR, Pilar G (1963) J Physiol 168:443-63

[1]

[2]

[3]

[4]

[5]

@@ Line 1: / Line 1: @@
-==Chemical synapse==
+{{subpages}}
-'''Chemical synapses''' are specialized junctions through which [[neuron]]s transmit information to each other or to non-neuronal cells such as [[muscle]]s or [[gland]]s. They are called chemical synapses because the electrical signal from the neuron to the target cell is transmitted via chemical messengers, called [[neurotransmitter]]s.
+{{Image|Synapse.gif|right|350px|Diagram of a synapse  between a presynaptic axon and a postsynaptic dendrite.}}
-Chemical synapses allow the neurons to communicate and to form interconnected neural circuits. They are thus crucial to the biological computations that underlie perception and thought. They also provide the means through which the nervous system connects to and controls the other systems of the body.
+A '''synapse''' is a specialized junction through which [[neuron]]s transmit information to each other or to non-neuronal cells such as [[muscle]]s or [[gland]]s. At ''chemical synapses'', neurons transmit information using chemical messengers, called [[neurotransmitter]]s. At ''electrical synapses'', the presynaptic and postsynaptic cell membranes are connected by channels that are capable of passing electrical current.
-== History of synapses ==
+The word "synapse" comes from "synaptein" which [[Charles Scott Sherrington]] and his colleagues coined from the [[Greek]] ''syn-'' ("together"( and ''haptein'' ("to clasp").
-In the second half of the nineteenth century there were two vigorously debated theories about the brain structure. Proponents of the [[cell theory]] considered that the brain consisted of independent units, which we now call the neurons; while others thought of as a continuous web-like reticulum, called syncytium. The debate remained until the late nineteenth century, when the [[electron microscopy]] eventually revealed the presence of the cells, which have their own plasma membrane and make contacts, which we now call the synapses. [[Ramon y Cajal]] with [[Golgi staining]] method was able to describe the differences between classes of neurons and precise connections between them. Later, however, electron microscopy and other techniques have showed that some neurons possess channels, called [[connexon]]s, which permit direct flow of ions and other small molecules through the membrane. This type of connection now is called [[electrical transmission]], and the contacts between the cells are called [[electrical synapse]]s.
-The word "synapse" comes from "synaptein" which Sir [[Charles Scott Sherrington]] and his colleagues coined from the [[Greek]] "syn-" meaning "together" and "haptein" meaning "to clasp". The "synapse" by itself most commonly refers to a chemical synapse.
+Synapses are crucial to the biological computations that underlie perception and thought. They also provide the means through which the nervous system connects to and controls the other systems of the body.
-The first synapse investigations were done on nerve-muscle synapse by Dale at 1936 (1).
+== History ==
+In the second half of the 19th century, there were two vigorously debated hypotheses about the structure of the brain. Proponents of the [[cell theory]] considered that the brain consisted of independent units (''neurons''), while others thought of as a continuous web-like reticulum (a ''syncytium''). The debate was resolved when the new technique of  [[electron microscopy]] revealed the cellular structure of the brain, and of the contacts between them. [[Ramon y Cajal]], using the [[Golgi staining]] method, described differences between classes of neurons and precise connections between them. Later, electron microscopy and other techniques have showed that some neurons possess channels, called [[connexon]]s, which permit  [[Electrical synapse|electrical transmission]] between cells.
-==Structure of the chemical synapse==
+The first investigations of the properties of synapses were conducted on nerve-muscle synapse by Dale in 1936.<ref>Dale HH ''et al.'' (1936) ''J Physiol'' 86:353-80</ref>
-The nerve cell, transmitting the signal, is called the '''presynaptic cell'''. Its target, receiving the signal, is called the '''postsynaptic cell'''. The presynaptic cell transmits the signal from the swollen tips of its axon’s branches, called '''presynaptic terminals''', also called the synaptic button or bouton. The part of synapses where neurotransmitter is released is called the '''active zone'''. The presynaptic terminals usually end on the postsynaptic neuron’s [[dendrite]]s, [[soma]], or, less often, on the [[axon]]. The presynaptic cell does not make an anatomical contact with the postsynaptic cell since two cells are separated by a space, the synaptic cleft, which is about 20- 40 nm wide (2). Immediately behind the postsynaptic membrane is an elaborate complex of interlinked proteins called the '''postsynaptic density'''. Proteins in the postsynaptic density serve a myriad of roles, from anchoring and trafficking neurotransmitter receptors into the plasma membrane, to anchoring various proteins.
-Chemical synapses can vary in the size and shape. Under the electron microscopy synapses are seen either as symmetric or asymmetric.  Asymmetric, or [[excitatory synapses]], are responsible for excitatory inputs, while symmetric ones are called [[inhibitory synapse]]s and transmit inhibitory inputs.
+==Structure==
+The nerve cell, transmitting the signal, is called the '''presynaptic cell'''; its target, receiving the signal, is called the '''postsynaptic cell'''. The presynaptic cell transmits the signal from the swollen tips of its axon’s branches, called '''presynaptic terminals''', also called the ''synaptic boutons''. The part of synapses where neurotransmitter is released is called the '''active zone'''. The presynaptic terminals usually end on the postsynaptic neuron’s [[dendrite]]s, [[soma]], or, less often, on the axon. The presynaptic cell does not make an anatomical contact with the postsynaptic cell since two cells are separated by a space, the synaptic cleft, which is about 20- 40 nm wide.<ref name="pmid15033583">{{cite journal |author=Hormuzdi SG ''et al.'' |title=Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks |journal=Biochim Biophys Acta |volume=1662 |pages=113–37 |year=2004 |pmid=15033583 |doi=10.1016/j.bbamem.2003.10.023}}</ref> Immediately behind the postsynaptic membrane is an elaborate complex of interlinked proteins called the '''[[postsynaptic density]]'''. Proteins in the postsynaptic density serve a myriad of roles, from anchoring and trafficking neurotransmitter receptors into the plasma membrane, to anchoring various proteins.
-Number of synapses one neuron makes varies greatly, reaching 1000 synapses for a neuron. Early during the development neurons make many synapses, later the number declines, reaching the level of adulthood. The process is called activity dependent synapse elimination, when active synapses are reinforced and inactive ones are eliminated. Number of synapses can change even in the adult animals, making conditions for synaptic plasticity. Adult human brain can have from 10<sup>15</sup> to 5 × 10<sup>15</sup> synapses.
+Chemical synapses can vary in size and shape. Under the electron microscope, synapses are seen either as symmetric or asymmetric.  Asymmetric synapses are responsible for excitatory inputs, while symmetric ones transmit inhibitory inputs.
+The number of synapses that one neuron can make varies greatly. The average neuron makes about 1000 synapses and can receive as many as 10,000 synapses; the [[Purkinje cell]] of the [[cerebellum]] receives up to 100,000. Early in development, neurons make many synapses, later the number declines, reaching the level of adulthood. The process is called '''activity dependent synapse elimination,''' when active synapses are reinforced and inactive ones are eliminated. The number of synapses can change even in the adult animals, contributing to synaptic plasticity. The adult human brain can have from 10<sup>15</sup> to 5 × 10<sup>15</sup> synapses.
 == Signaling across chemical synapses ==
+Within the presynaptic nerve terminal, vesicles containing neurotransmitter sit "docked" at the synaptic membrane and ready to release the neurotransmitter. The release of [[neurotransmitter]], the [[exocytosis]], is triggered by the arrival of a nerve impulse (or [[action potential]]). The arriving action potential produces an influx of calcium ions through voltage-dependent, calcium-selective ion channels. Calcium ions then trigger a biochemical cascade which results in vesicles fusing with the presynaptic membrane and releasing their contents into the synaptic cleft. Vesicle fusion is driven by the action of a set of proteins, known as SNAREs. The membrane added by this fusion is later retrieved by [[endocytosis]] and recycled for the formation of fresh neurotransmitter-filled vesicles.
-=== Direct synaptic transmission ===
+After a neurotransmitter is released into the synaptic cleft, it can bind [[ionotropic receptor|ionotropic]] or [[metabotropic receptor|metabotropic ]] receptors at the postsynaptic membrane. Ionotropic receptors are themselves ion channels; when a neurotransmitter binds to these receptors, the receptor conformation changes. As a result, ion channels open and the ions flow in or out of the cell, changing the membrane potential. The resulting change in voltage is called a ''postsynaptic potential''.
-Within the presynaptic nerve terminal, vesicles containing neurotransmitter sit "docked" at the synaptic membrane and ready to release the neurotransmitter. The release of [[neurotransmitter]], the [[exocytosis]], is triggered by the arrival of a nerve impulse (or [[action potential]]). The arriving action potential produces an influx of calcium ions through voltage-dependent, calcium-selective ion channels. Calcium ions then trigger a biochemical cascade which results in vesicles fusing with the presynaptic membrane and releasing their contents to the synaptic cleft. Vesicle fusion is driven by the action of a set of proteins, known as SNAREs. The membrane added by this fusion is later retrieved by endocytosis and recycled for the formation of fresh neurotransmitter-filled vesicles.
-After neurotransmitter is released to the synaptic cleft, it can bind [[ionotropic receptor|ionotropic]] or [[metabotropic receptor|metabotropic ]] postsynaptic receptors. During direct synaptic transmission, neurotransmitters bind ionotropic receptors which are themselves ion channels, and change the receptor conformation. As a result, ion channels open and the ions flow in or out of the cell, changing the membrane potential. The resulting change in voltage is called a postsynaptic potential.
+Whether an effect is excitatory or inhibitory depends on what type(s) of ion channel conduct the postsynaptic current, which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. The two most common neurotransmitters in the mammalian central nervous system are [[glutamate]] and [[GABA]]. Glutamate is an excitatory neurotransmitter, and can depolarise cells via its actions at any of three types of ionotropic receptor: kainate receptors; AMPA receptors; and NMDA receptors; activation of any of these  allows the flow of K+, Na+ and sometimes Ca2+ into the postsynaptic cell. When GABA  binds to GABA-A receptors, chloride channels open in the postsynaptic cell membrane. In adult neurons this usually results in chloride entering the postsynaptic cell and thus hyperpolarising it, but embryonic neurons and some adult cell types have a relatively high intracellular chloride concentration, and in these cases GABA actions may cause chloride to leave the cell, resulting in a depolarisation. Thus GABA can act as an excitatory neurotransmitter, but is mainly thought of as the most abundant inhibitory neurotransmitter in the adult.
-Whether an effect is excitatory or inhibitory depends on what type(s) of ion channel conduct the postsynaptic current, which in turn is a function of the type of receptors and neurotransmitter employed at the synapse. In the case of excitatory synapses, positively charged ions move into the postsynaptic cell, [[depolarization|depolarizing]] the cell and making it more excitable. At inhibitory synapses negatively charged ions pass through the membrane and [[hyperpolarization|hyperpolarize]] the cell. In the mammalian [[central nervous system]] the main excitatory neurotransmitter is [[glutamate]], while the [[glycine]] and [[GABA]] are the major inhibitory neurotransmitters. Other important neurotransmitters in the mammalian CNS, acting on ionotropic receptors, are [[purines]], [[acetylcholine]], [[serotonin]], [[dopamine]] and others.
+Other important neurotransmitters in the mammalian CNS include [[purines]], [[acetylcholine]], [[serotonin]], [[dopamine]], [[serotonin]] and [[norepinephrine]].
-Direct synaptic transmission through ionotropic receptors is fast, taking several milliseconds to transmit the signal.
+Synaptic transmission through ionotropic receptors is fast, taking just a few milliseconds to transmit the signal.
-===Indirect synaptic transmission===
-At indirect synaptic transmission, after neurotransmitter is being released, it binds to the metabotropic postsynaptic receptors, which are usually [[G-protein]] coupled receptors. When these receptors are activated, they produce intracellular second messangers, which usually are enzymes. Second messangers then activate ion channels through phosphorilation, letting the ions pass into the membrane. Metabotropic receptors can activate ion channels directly, they can also activate another enzymes, changing the neuron excitability. Usually potassium and calcium channels are targeted by such indirect action.
-Such responses may last seconds, minutes and hours. Indirect synaptic transmission provide a mechanism for an enormous signal amplification, since one G-protein coupled receptor can activate many ion channels.
+Neurotransmitter may also bind to metabotropic receptors, which are usually [[G-protein]] coupled receptors. When these receptors are activated, they produce intracellular second messengers, which subsequently may activate ion channels through phosphorylation. Such responses can last for several minutes.
 == Regulation of synaptic transmission ==
@@ Line 42: / Line 39: @@
 The action of [[glutamate]], [[glycine]], [[GABA]], [[dopamine]], [[norepinephrine]] and  [[Serotonin|5-HT]] is terminated by uptake of transmitters by specific transport proteins, called transporters. Transporters neurotransmitter into nerve terminals can be packed into the vesicles and released again. ACh molecules in the synaptic cleft are degradated by a specific enzyme acetylcholinesterase, ATP is terminated by hydrolysis. Neuropetides are removed from the synaptic cleft by diffusion. Neurotransmitter degradation or removal is a prompt process, whereas diffusion is a slower one.
- The necessity of  removal of neurotransmitters and desensitization of receptors and ion channels means that the strength of a synapse may in effect diminish as a train of action potentials arriving in rapid succession. The phenomenon is called frequency dependence of synaptic transmission. The nervous system exploits this property for computational purposes, and can tune its synapses through such means as phosphorylation of the proteins involved. The size, number and replenishment rate of vesicles also are subject to regulation, as are many other elements of synaptic transmission.
+The necessity of  removal of neurotransmitters and desensitization of receptors and ion channels means that the strength of a synapse may in effect diminish as a train of action potentials arriving in rapid succession. The phenomenon is called frequency dependence of synaptic transmission. The nervous system exploits this property for computational purposes, and can tune its synapses through such means as phosphorylation of the proteins involved. The size, number and replenishment rate of vesicles also are subject to regulation, as are many other elements of synaptic transmission.
 == Synaptic plasticity ==
-The efficacy of chemical transmission is not fixed, but depends on the ongoing activity in the synapse. These changes can be a short-term, lasting from milliseconds to minutes, and long-term, lasting hours or days (3). Short periods of synaptic activation can lead in '''facilitation''', '''depression''' or '''augmentation''' of neurotransmitter release. All these processes change the amount of neurotransmitter released, last seconds and have a presynaptic origin. Posttetanic facilitation also has a presynaptic origin, but it usually lasts for tens of minutes. Repetitive stimulation can result in '''long-term potentiation''' (LTP) or '''long-term depression''' (LTD) of synaptic strength. The mechanisms of LTP and LTD have both presynpatic and postsynaptic origins.
+The efficacy of chemical transmission is not fixed, but depends on the ongoing activity in the synapse. These changes can be a short-term, lasting from milliseconds to minutes, and long-term, lasting hours or days.<ref name="isbn0-87893-439-1">{{cite book |author=Martin A al.'' ''et |title=From neuron to brain |publisher=Sinauer Associates |location=Sunderland, Mass |year=2001 |pages= |isbn=0-87893-439-1 |oclc= |doi=}}</ref> Short periods of synaptic activation can lead in '''facilitation''', '''depression''' or '''augmentation''' of neurotransmitter release. All these processes change the amount of neurotransmitter released, last seconds and have a presynaptic origin. Posttetanic facilitation also has a presynaptic origin, but it usually lasts for tens of minutes. Repetitive stimulation can result in '''long-term potentiation''' (LTP) or '''long-term depression''' (LTD) of synaptic strength. The mechanisms of LTP and LTD have both presynpatic and postsynaptic origins.
 == Integration of synaptic inputs ==
-Generally, if an excitatory synapse is strong, an action potential in the presynaptic neuron will trigger another action potential in the postsynaptic cell; whereas at a weak synapse the excitatory post-synaptic potential (EPSP) will not reach the threshold for action potential initiation. In the brain, however, each neuron typically forms synapses with many others, and likewise each receives synaptic inputs from many others. When many synapses of a neuron receive excitatory inputs at the same time, the neuron may generate an impulse even though the synapses are weak. This process is known as '''spatial summation'''. If only one synapse is active, but it receives many impulses in a short period of time, impulses are also summated. This process is called '''temporal summation'''. On the other hand, a pre-synaptic neuron releasing an inhibitory neurotransmitter such as GABA can cause inhibitory postsynaptic potential in the postsynaptic neuron, decreasing its excitability and therefore decreasing the neuron's likelihood to fire an action potential. In this way the output of a neuron may depend on the inputs of many others, each of them may have a different degree of influence, depending on the strength of its synapse and the location on the neuron. [[John Carew Eccles]] performed some of the important early experiments on synaptic integration, for which he received the [[Nobel Prize for Physiology or Medicine]] in [[1963]]. Complex input/output relationships form the basis of transistor-based computations in computers, and are thought to figure similarly in neural circuits.
+Generally, if an excitatory synapse is strong, an action potential in the presynaptic neuron will trigger another action potential in the postsynaptic cell; whereas at a weak synapse the excitatory post-synaptic potential (EPSP) will not reach the threshold for action potential initiation. In the brain, however, each neuron typically forms synapses with many others, and likewise each receives synaptic inputs from many others. When many synapses of a neuron receive excitatory inputs at the same time, the neuron may generate an impulse even though the synapses are weak. This process is known as '''spatial summation'''. If only one synapse is active, but it receives many impulses in a short period of time, impulses are also summated. This process is called '''temporal summation'''. On the other hand, a pre-synaptic neuron releasing an inhibitory neurotransmitter such as GABA can cause inhibitory postsynaptic potential in the postsynaptic neuron, decreasing its excitability and therefore decreasing the neuron's likelihood to fire an action potential. In this way the output of a neuron may depend on the inputs of many others, each of them may have a different degree of influence, depending on the strength of its synapse and the location on the neuron. [[John Carew Eccles]] performed some of the important early experiments on synaptic integration, for which he received the [[Nobel Prize for Physiology or Medicine]] in 1963. Complex input/output relationships form the basis of transistor-based computations in computers, and are thought to figure similarly in neural circuits.
-==
+== Comparison with electrical synapses ==
-Comparison with electrical synapses ==
+An electrical synapse forms a narrow gap between the pre- and postsynaptic cells, known as a [[gap junction]]. At gap junctions, cells approach within about 3.5 nm of each other<ref>{{cite book |author=Jessell TM ''et al.''|title=Principles of neural science |publisher=McGraw-Hill |location=New York |year=2000 |pages= |isbn=0-8385-7701-6 |oclc= |doi=}}</ref>, a much shorter distance than the 20 to 40 nm distance that separates cells at chemical synapses.<ref name="pmid15033583"/> As opposed to chemical synapses, the postsynaptic potential in electrical synapses is not caused by the opening of ion channels by chemical transmitters, but by direct electrical coupling between both neurons. Electrical synapses are therefore faster, current spreads instantaneously, whereas chemical synapses have a delay of about 1 ms.  Electrical synapses conduct equally to both directions, while at the chemical synapse the impulse is send only from pre- to postsynaptic neuron. Electrical synapses are found throughout the nervous system, yet are less common than chemical synapses. Electrical and chemical transmission can coexist at a single synapse.<ref name="isbn0-87893-439-1"/> Such combined synapses were first found avian ciliary ganglion cells.<ref>Martin AR,  Pilar G (1963) ''J Physiol'' 168:443-63</ref>
-An electrical synapse forms a narrow gap between the pre- and postsynaptic cells, known as a [[gap junction]]. At gap junctions, cells approach within about 3.5 nm of each other (4), a much shorter distance than the 20 to 40 nm distance that separates cells at chemical synapses (2). As opposed to chemical synapses, the postsynaptic potential in electrical synapses is not caused by the opening of ion channels by chemical transmitters, but by direct electrical coupling between both neurons. Electrical synapses are therefore faster, current spreads instantaneously, whereas chemical synapses have a delay of about 1 ms.  Electrical synapses conduct equally to both directions, while at the chemical synapse the impulse is send only from pre- to postsynaptic neuron. Electrical synapses are found throughout the nervous system, yet are less common than chemical synapses. Electrical and chemical transmission can coexist at a single synapse (3). Such combined synapses were first found avian ciliary ganglion cells (5).
 ==References==
-# Dale, H. H., Feldberg, W. and Vogt, M. (1936). ''J.Physiol''. 86: 353- 380.
+{{Reflist}}
-# Hormuzdi SG, Filippov MA, Mitropoulou G, Monyer H, Bruzzone R. Electrical synapses: a dynamic signaling system that shapes the activity of neuronal networks. ''Biochim Biophys Acta''. 2004 Mar 23;1662(1-2):113-37. PMID 15033583.
-# {{cite book | author=J.G. Nicholls, A.R. Martin, B.G. Wallace, and P.A. Fuchs | year=2001 | title=From Neuron to Brain | edition = 4th edition | publisher=Sinauer Associates | location=Sunderland, MA | id = ISBN 0878934391 }}
+[[Category:Suggestion Bot Tag]]
-# Eric R. Kandel, James H. Schwartz, Thomas M. Jessell (2000). Principles of Neural Science, 4th edition, New York: McGraw-Hill. ISBN 0-8385-7701-6.
-# Martin, A. R, and Pilar, G. (1963). ''J.Physiol.'' 168: 443- 463.

Synapse: Difference between revisions

Latest revision as of 06:01, 24 October 2024

Contents

History

Structure

Signaling across chemical synapses

Regulation of synaptic transmission

Synaptic plasticity

Integration of synaptic inputs

Comparison with electrical synapses

References

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Synapse: Difference between revisions

Latest revision as of 06:01, 24 October 2024

History

Structure

Signaling across chemical synapses

Regulation of synaptic transmission

Synaptic plasticity

Integration of synaptic inputs

Comparison with electrical synapses

References

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