Chemical synapse

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.

At a chemical synapse, one neuron releases neurotransmitter

molecules into a small space (the synaptic cleft) that is adjacent to
another neuron. The neurotransmitters are contained within small
sacs called synaptic vesicles, and are released into the synaptic cleft
by exocytosis. These molecules then bind to neurotransmitter
receptors on the postsynaptic cell. Finally, the neurotransmitters are
cleared from the synapse through one of several potential
mechanisms including enzymatic degradation or re-uptake by Artistic interpretation of the major
specific transporters either on the presynaptic cell or on some other elements in chemical synaptic
neuroglia to terminate the action of the neurotransmitter. transmission. An electrochemical
wave called an action potential
The adult human brain is estimated to contain from 1014 to 5 × travels along the axon of a neuron.
1014 (100–500 trillion) synapses.[1] Every cubic millimeter of When the action potential reaches
cerebral cortex contains roughly a billion (short scale, i.e. 109 ) of the presynaptic terminal, it provokes
them.[2] The number of synapses in the human cerebral cortex has the release of a synaptic vesicle,
separately been estimated at 0.15 quadrillion (150 trillion)[3] secreting its quanta of
neurotransmitter molecules. The
The word "synapse" was introduced by Sir Charles Scott neurotransmitter binds to chemical
Sherrington in 1897.[4] Chemical synapses are not the only type of receptor molecules located in the
biological synapse: electrical and immunological synapses also membrane of another neuron, the
exist. Without a qualifier, however, "synapse" commonly refers to postsynaptic neuron, on the opposite
chemical synapse. side of the synaptic cleft.

Contents
Structure
Signaling in chemical synapses
Overview
Neurotransmitter release
Receptor binding
Termination
Synaptic strength
Receptor desensitization
Synaptic plasticity
Homosynaptic plasticity
 Heterosynaptic plasticity
Integration of synaptic inputs
Volume transmission
Relationship to electrical synapses
Effects of drugs
History and etymology
See also
Notes
References
External links

Structure
Synapses are functional connections
between neurons, or between neurons
and other types of cells.[5][6] A typical
neuron gives rise to several thousand
synapses, although there are some
types that make far fewer.[7] Most
synapses connect axons to
dendrites, [8][9] but there are also other
types of connections, including axon-
to-cell-body,[10][11] axon-to-
axon, [10][11] and dendrite-to-
dendrite.[9] Synapses are generally too
small to be recognizable using a light Diagram of a chemical synaptic connection.
microscope except as points where the
membranes of two cells appear to
touch, but their cellular elements can be visualized clearly using an electron microscope.

Chemical synapses pass information directionally from a presynaptic cell to a postsynaptic cell and are
therefore asymmetric in structure and function. The presynaptic axon terminal, or synaptic bouton, is a
specialized area within the axon of the presynaptic cell that contains neurotransmitters enclosed in small
membrane-bound spheres called synaptic vesicles (as well as a number of other supporting structures and
organelles, such as mitochondria and endoplasmic reticulum). Synaptic vesicles are docked at the
presynaptic plasma membrane at regions called active zones.

Immediately opposite is a region of the postsynaptic cell containing neurotransmitter receptors; for synapses
between two neurons the postsynaptic region may be found on the dendrites or cell body. Immediately
behind the postsynaptic membrane is an elaborate complex of interlinked proteins called the postsynaptic
density (PSD).

Proteins in the PSD are involved in anchoring and trafficking neurotransmitter receptors and modulating the
activity of these receptors. The receptors and PSDs are often found in specialized protrusions from the main
dendritic shaft called dendritic spines.
Synapses may be described as symmetric or asymmetric. When examined under an electron microscope,
asymmetric synapses are characterized by rounded vesicles in the presynaptic cell, and a prominent
postsynaptic density. Asymmetric synapses are typically excitatory. Symmetric synapses in contrast have
flattened or elongated vesicles, and do not contain a prominent postsynaptic density. Symmetric synapses
are typically inhibitory.

The synaptic cleft —also called synaptic gap— is a gap between the pre- and postsynaptic cells that is
about 20 nm (0.02 μ) wide.[12] The small volume of the cleft allows neurotransmitter concentration to be
raised and lowered rapidly.[13]

An autapse is a chemical (or electrical) synapse formed when the axon of one neuron synapses with its own
dendrites.

Signaling in chemical synapses

Overview

Here is a summary of the sequence of events that take place in synaptic transmission from a presynaptic
neuron to a postsynaptic cell. Each step is explained in more detail below. Note that with the exception of
the final step, the entire process may run only a few hundred microseconds, in the fastest synapses.[14]

1. The process begins with a wave of electrochemical excitation

called an action potential traveling along the membrane of the
presynaptic cell, until it reaches the synapse.
2. The electrical depolarization of the membrane at the synapse
causes channels to open that are permeable to calcium ions.
3. Calcium ions flow through the presynaptic membrane, rapidly
increasing the calcium concentration in the interior.
4. The high calcium concentration activates a set of calcium-
sensitive proteins attached to vesicles that contain a
neurotransmitter chemical.
5. These proteins change shape, causing the membranes of some "docked" vesicles to fuse
with the membrane of the presynaptic cell, thereby opening the vesicles and dumping their
neurotransmitter contents into the synaptic cleft, the narrow space between the membranes
of the pre- and postsynaptic cells.
6. The neurotransmitter diffuses within the cleft. Some of it escapes, but some of it binds to
chemical receptor molecules located on the membrane of the postsynaptic cell.
7. The binding of neurotransmitter causes the receptor molecule to be activated in some way.
Several types of activation are possible, as described in more detail below. In any case, this
is the key step by which the synaptic process affects the behavior of the postsynaptic cell.
8. Due to thermal vibration, the motion of atoms, vibrating about their equilibrium positions in a
crystalline solid, neurotransmitter molecules eventually break loose from the receptors and
drift away.
9. The neurotransmitter is either reabsorbed by the presynaptic cell, and then repackaged for
future release, or else it is broken down metabolically.

Neurotransmitter release
The release of a neurotransmitter is triggered by the arrival of a
nerve impulse (or action potential) and occurs through an unusually
rapid process of cellular secretion (exocytosis). Within the
presynaptic nerve terminal, vesicles containing neurotransmitter are
localized near the synaptic membrane. The arriving action potential
produces an influx of calcium ions through voltage-dependent,
calcium-selective ion channels at the down stroke of the action
potential (tail current).[15] Calcium ions then bind to synaptotagmin
proteins found within the membranes of the synaptic vesicles,
allowing the vesicles to fuse with the presynaptic membrane.[16] Release of neurotransmitter occurs
The fusion of a vesicle is a stochastic process, leading to frequent at the end of axonal branches.
failure of synaptic transmission at the very small synapses that are
typical for the central nervous system. Large chemical synapses
(e.g. the neuromuscular junction), on the other hand, have a synaptic release probability, in effect, of 1.
Vesicle fusion is driven by the action of a set of proteins in the presynaptic terminal known as SNAREs. As
a whole, the protein complex or structure that mediates the docking and fusion of presynaptic vesicles is
called the active zone.[17] The membrane added by the fusion process is later retrieved by endocytosis and
recycled for the formation of fresh neurotransmitter-filled vesicles.

An exception to the general trend of neurotransmitter release by vesicular fusion is found in the type II
receptor cells of mammalian taste buds. Here the neurotransmitter ATP is released directly from the
cytoplasm into the synaptic cleft via voltage gated channels.[18]

Receptor binding

Receptors on the opposite side of the synaptic gap bind neurotransmitter molecules. Receptors can respond
in either of two general ways. First, the receptors may directly open ligand-gated ion channels in the
postsynaptic cell membrane, causing ions to enter or exit the cell and changing the local transmembrane
potential.[14] The resulting change in voltage is called a postsynaptic potential. In general, the result is
excitatory in the case of depolarizing currents, and inhibitory in the case of hyperpolarizing currents.
Whether a synapse is excitatory or inhibitory depends on what type(s) of ion channel conduct the
postsynaptic current(s), which in turn is a function of the type of receptors and neurotransmitter employed
at the synapse. The second way a receptor can affect membrane potential is by modulating the production
of chemical messengers inside the postsynaptic neuron. These second messengers can then amplify the
inhibitory or excitatory response to neurotransmitters.[14]

Termination

After a neurotransmitter molecule binds to a receptor molecule, it must be removed to allow for the
postsynaptic membrane to continue to relay subsequent EPSPs and/or IPSPs. This removal can happen
through one or more processes:

The neurotransmitter may diffuse away due to thermally-induced oscillations of both it and
the receptor, making it available to be broken down metabolically outside the neuron or to be
reabsorbed.[19]
Enzymes within the subsynaptic membrane may inactivate/metabolize the neurotransmitter.
Reuptake pumps may actively pump the neurotransmitter back into the presynaptic axon
terminal for reprocessing and re-release following a later action potential.[19]
Synaptic strength
The strength of a synapse has been defined by Sir Bernard Katz as the product of (presynaptic) release
probability pr, quantal size q (the postsynaptic response to the release of a single neurotransmitter vesicle, a
'quantum'), and n, the number of release sites. "Unitary connection" usually refers to an unknown number
of individual synapses connecting a presynaptic neuron to a postsynaptic neuron. The amplitude of
postsynaptic potentials (PSPs) can be as low as 0.4 mV to as high as 20 mV.[20] The amplitude of a PSP
can be modulated by neuromodulators or can change as a result of previous activity. Changes in the
synaptic strength can be short-term, lasting seconds to minutes, or long-term (long-term potentiation, or
LTP), lasting hours. Learning and memory are believed to result from long-term changes in synaptic
strength, via a mechanism known as synaptic plasticity.

Receptor desensitization
Desensitization of the postsynaptic receptors is a decrease in response to the same neurotransmitter
stimulus. It means that the strength of a synapse may in effect diminish as a train of action potentials arrive
in rapid succession – a phenomenon that gives rise to the so-called frequency dependence of synapses. The
nervous system exploits this property for computational purposes, and can tune its synapses through such
means as phosphorylation of the proteins involved.

Synaptic plasticity
Synaptic transmission can be changed by previous activity. These changes are called synaptic plasticity and
may result in either a decrease in the efficacy of the synapse, called depression, or an increase in efficacy,
called potentiation. These changes can either be long-term or short-term. Forms of short-term plasticity
include synaptic fatigue or depression and synaptic augmentation. Forms of long-term plasticity include
long-term depression and long-term potentiation. Synaptic plasticity can be either homosynaptic (occurring
at a single synapse) or heterosynaptic (occurring at multiple synapses).

Homosynaptic plasticity

Homosynaptic plasticity (or also homotropic modulation) is a change in the synaptic strength that results
from the history of activity at a particular synapse. This can result from changes in presynaptic calcium as
well as feedback onto presynaptic receptors, i.e. a form of autocrine signaling. Homosynaptic plasticity can
affect the number and replenishment rate of vesicles or it can affect the relationship between calcium and
vesicle release. Homosynaptic plasticity can also be postsynaptic in nature. It can result in either an increase
or decrease in synaptic strength.

One example is neurons of the sympathetic nervous system (SNS), which release noradrenaline, which,
besides affecting postsynaptic receptors, also affects presynaptic α2-adrenergic receptors, inhibiting further
release of noradrenaline.[21] This effect is utilized with clonidine to perform inhibitory effects on the SNS.

Heterosynaptic plasticity

Heterosynaptic plasticity (or also heterotropic modulation) is a change in synaptic strength that results from
the activity of other neurons. Again, the plasticity can alter the number of vesicles or their replenishment
rate or the relationship between calcium and vesicle release. Additionally, it could directly affect calcium
influx. Heterosynaptic plasticity can also be postsynaptic in nature, affecting receptor sensitivity.
One example is again neurons of the sympathetic nervous system, which release noradrenaline, which, in
addition, generates an inhibitory effect on presynaptic terminals of neurons of the parasympathetic nervous
system.[21]

Integration of synaptic inputs

In general, if an excitatory synapse is strong enough, an action potential in the presynaptic neuron will
trigger an action potential in the postsynaptic cell. In many cases the excitatory postsynaptic potential
(EPSP) will not reach the threshold for eliciting an action potential. When action potentials from multiple
presynaptic neurons fire simultaneously, or if a single presynaptic neuron fires at a high enough frequency,
the EPSPs can overlap and summate. If enough EPSPs overlap, the summated EPSP can reach the
threshold for initiating an action potential. This process is known as summation, and can serve as a high
pass filter for neurons.[22]

On the other hand, a presynaptic neuron releasing an inhibitory neurotransmitter, such as GABA, can cause
an inhibitory postsynaptic potential (IPSP) in the postsynaptic neuron, bringing the membrane potential
farther away from the threshold, decreasing its excitability and making it more difficult for the neuron to
initiate an action potential. If an IPSP overlaps with an EPSP, the IPSP can in many cases prevent the
neuron from firing an action potential. In this way, the output of a neuron may depend on the input of many
different neurons, each of which may have a different degree of influence, depending on the strength and
type of synapse with that 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.

Volume transmission
When a neurotransmitter is released at a synapse, it reaches its highest concentration inside the narrow
space of the synaptic cleft, but some of it is certain to diffuse away before being reabsorbed or broken
down. If it diffuses away, it has the potential to activate receptors that are located either at other synapses or
on the membrane away from any synapse. The extrasynaptic activity of a neurotransmitter is known as
volume transmission.[23] It is well established that such effects occur to some degree, but their functional
importance has long been a matter of controversy.[24]

Recent work indicates that volume transmission may be the predominant mode of interaction for some
special types of neurons. In the mammalian cerebral cortex, a class of neurons called neurogliaform cells
can inhibit other nearby cortical neurons by releasing the neurotransmitter GABA into the extracellular
space.[25] Along the same vein, GABA released from neurogliaform cells into the extracellular space also
acts on surrounding astrocytes, assigning a role for volume transmission in the control of ionic and
neurotransmitter homeostasis.[26] Approximately 78% of neurogliaform cell boutons do not form classical
synapses. This may be the first definitive example of neurons communicating chemically where classical
synapses are not present.[25]

Relationship to electrical synapses

An electrical synapse is an electrically conductive link between two abutting neurons that is formed at 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, rather than the 20 to 40  nm distance that separates cells at
chemical synapses.[27][28] As opposed to chemical synapses, the postsynaptic potential in electrical
synapses is not caused by the opening of ion channels by chemical transmitters, but rather by direct
electrical coupling between both neurons. Electrical synapses are faster than chemical synapses.[13]
Electrical synapses are found throughout the nervous system, including in the retina, the reticular nucleus of
the thalamus, the neocortex, and in the hippocampus.[29] While chemical synapses are found between both
excitatory and inhibitory neurons, electrical synapses are most commonly found between smaller local
inhibitory neurons. Electrical synapses can exist between two axons, two dendrites, or between an axon
and a dendrite.[30][31] In some fish and amphibians, electrical synapses can be found within the same
terminal of a chemical synapse, as in Mauthner cells.[32]

Effects of drugs
One of the most important features of chemical synapses is that they are the site of action for the majority of
psychoactive drugs. Synapses are affected by drugs, such as curare, strychnine, cocaine, morphine, alcohol,
LSD, and countless others. These drugs have different effects on synaptic function, and often are restricted
to synapses that use a specific neurotransmitter. For example, curare is a poison that stops acetylcholine
from depolarizing the postsynaptic membrane, causing paralysis. Strychnine blocks the inhibitory effects of
the neurotransmitter glycine, which causes the body to pick up and react to weaker and previously ignored
stimuli, resulting in uncontrollable muscle spasms. Morphine acts on synapses that use endorphin
neurotransmitters, and alcohol increases the inhibitory effects of the neurotransmitter GABA. LSD
interferes with synapses that use the neurotransmitter serotonin. Cocaine blocks reuptake of dopamine and
therefore increases its effects.

History and etymology

During the 1950s, Bernard Katz and Paul Fatt observed spontaneous miniature synaptic currents at the frog
neuromuscular junction.[33] Based on these observations, they developed the 'quantal hypothesis' that is the
basis for our current understanding of neurotransmitter release as exocytosis and for which Katz received
the Nobel Prize in Physiology or Medicine in 1970.[34] In the late 1960s, Ricardo Miledi and Katz
advanced the hypothesis that depolarization-induced influx of calcium ions triggers exocytosis.

Sir Charles Scott Sherringtonin coined the word 'synapse' and the history of the word was given by
Sherrington in a letter he wrote to John Fulton:

'I felt the need of some name to call the junction between nerve-cell and nerve-cell... I
suggested using "syndesm"... He [ Sir Michael Foster ] consulted his Trinity friend Verrall, the
Euripidean scholar, about it, and Verrall suggested "synapse" (from the Greek "clasp").'–
Charles Scott Sherrington[4]

See also
Acclimatisation (neurones)
Neuroscience
Ribbon synapse

Notes
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External links
Synapse Review for Kids (http://faculty.washington.edu/chudler/synapse.html)
Synapses (http://www.biologymad.com/NervousSystem/synapses.htm) Biologymad.com
(2004)
Synapse – Cell Centered Database (http://ccdb.ucsd.edu/sand/main?stype=lite&keyword=s
ynapse&Submit=Go&event=display&start=1)
Atlas of Ultrastructure Neurocytology (http://synapses.clm.utexas.edu/atlas/contents.stm) A
great electron microscope picture gallery assembled by Kristen Harris' lab of synapses and
other neuronal structures.

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