   #copyright

Chemical synapse

2007 Schools Wikipedia Selection. Related subjects: General Biology

   Illustration of the major elements in a prototypical synapse. Synapses
   allow nerve cells to communicate with one another through axons and
   dendrites, converting electrical impulses into chemical signals.
   Enlarge
   Illustration of the major elements in a prototypical synapse. Synapses
   allow nerve cells to communicate with one another through axons and
   dendrites, converting electrical impulses into chemical signals.

   Chemical synapses are specialized junctions through which cells of the
   nervous system signal to one another and to non-neuronal cells such as
   muscles or glands. A chemical synapse between a motor neuron and a
   muscle cell is called a neuromuscular junction.

   Chemical synapses allow the neurons of the central nervous system 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.

   The human brain contains a huge number of chemical synapses, with young
   children having about 10^16 synapses (10,000 trillion.). This number
   declines with age, stabilizing by adulthood. Estimates for an adult
   vary from 10^15 to 5 × 10^15 synapses (1,000 to 5,000 trillion).

   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". Chemical synapses are not
   the only type of biological synapse: electrical and immunological
   synapses exist as well. Without a qualifier, however, "synapse" by
   itself most commonly refers to a chemical synapse.

Anatomy

   At a prototypical chemical synapse, such as those found at dendritic
   spines, a mushroom-shaped bud projects from each of two cells and the
   caps of these buds press flat against one another. At this interface,
   the membranes of the two cells flank each other across a slender gap,
   the narrowness of which enables signalling molecules known as
   neurotransmitters to pass rapidly from one cell to the other by
   diffusion. This gap, which is about 20 nm wide, is known as the
   synaptic cleft.

   Such synapses are asymmetric both in structure and in how they operate.
   Only the so-called pre-synaptic neuron secretes the neurotransmitter,
   which binds to receptors facing into the synapse from the post-synaptic
   cell. The pre-synaptic nerve terminal (also called the synaptic button
   or bouton) generally buds from the tip of an axon, while the
   post-synaptic target surface typically appears on a dendrite, a cell
   body, or another part of a cell. The parts of synapses where
   neurotransmitter is released are called the active zones. At active
   zones the membranes of the two adjacent cells are held in close contact
   by cell adhesion proteins. Immediately behind the post-synaptic
   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 which
   modulate the activity of the receptors. The postsynaptic cell need not
   be a neuron, and can also be gland or muscle cells.

Signaling across chemical synapses

   The release of neurotransmitter is triggered by the arrival of a nerve
   impulse (or action potential) and occurs through an unusually rapid
   process of cellular secretion, also known as exocytosis: Within the
   pre-synaptic nerve terminal, vesicles containing neurotransmitter sit
   "docked" and ready at the synaptic membrane. 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 in the presynaptic terminal
   known as SNAREs. The membrane added by this fusion is later retrieved
   by endocytosis and recycled for the formation of fresh
   neurotransmitter-filled vesicles. Receptors on the opposite side of the
   synaptic gap bind neurotransmitter molecules and respond by opening
   nearby ion channels in the post-synaptic cell membrane, causing ions to
   rush in or out and changing the local transmembrane potential of the
   cell. The resulting change in voltage is called a postsynaptic
   potential. In general, the result is excitatory, in the case of
   depolarizing currents, or inhibitory in the case of hyperpolarizing
   currents. Whether a synapse is excitatory or inhibitory depends on what
   type(s) of ion channel conduct the post-synaptic current display(s),
   which in turn is a function of the type of receptors and
   neurotransmitter employed at the synapse.

Modulation of synaptic transmission

   Following fusion of the synaptic vesicles and release of transmitter
   molecules into the synaptic cleft, the neurotransmitter is rapidly
   cleared from the space for recycling by specialized membrane proteins
   in the pre-synaptic or post-synaptic membrane. This " re-uptake"
   prevents " desensitization" of the post-synaptic receptors and ensures
   that succeeding action potentials will elicit the same size
   post-synaptic potential ("PSP"). The necessity of re-uptake and the
   phenomenon of desensitization in receptors and ion channels 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. The size, number and replenishment rate of vesicles also are
   subject to regulation, as are many other elements of synaptic
   transmission. For example, a class of drugs known as selective
   serotonin re-uptake inhibitors or SSRIs affect certain synapses by
   inhibiting the re-uptake of the neurotransmitter serotonin. In
   contrast, one important excitatory neurotransmitter, acetylcholine,
   does not undergo re-uptake, but instead is removed from the synapse by
   the action of the enzyme acetylcholinesterase.

Integration of synaptic inputs

   Generally, if an excitatory synapse is strong, an action potential in
   the pre-synaptic neuron will trigger another in the post-synaptic 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 action potentials fire simultaneously in several neurons that
   weakly synapse on a single cell, they may initiate an impulse in that
   cell even though the synapses are weak. This process is known as
   summation. On the other hand, a pre-synaptic neuron releasing an
   inhibitory neurotransmitter such as GABA can cause inhibitory
   postsynaptic potential in the post-synaptic 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 input of many others, each of which may have a different degree of
   influence, depending on the strength of its 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. Complex input/output relationships form
   the basis of transistor-based computations in computers, and are
   thought to figure similarly in neural circuits.

Synaptic strength

   The strength of a synapse is defined by the change in transmembrane
   potential resulting from activation of the postsynaptic
   neurotransmitter receptors. This change in voltage is known as a
   post-synaptic potential, and is a direct result of ionic currents
   flowing through the post-synaptic receptor-channels. Changes in
   synaptic strength can be short-term and without permanent structural
   changes in the neurons themselves, lasting seconds to minutes - or
   long-term ( long-term potentiation, or LTP), in which repeated or
   continuous synaptic activation can result in second messenger molecules
   initiating protein synthesis in the neuron's nucleus, resulting in
   alteration of the structure of the synapse itself. Learning and memory
   are believed to result from long-term changes in synaptic strength, via
   a mechanism known as synaptic plasticity.

Relationship to electrical synapses

   An electrical synapse is a mechanical and 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 (Kandel et al., 2000,
   p. 179), a much shorter distance than the 20 to 40 nm distance that
   separates cells at chemical synapses (Hormuzdi et al., 2004). 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 and more reliable than
   chemical synapses. Electrical synapses are found throughout the nervous
   system, yet are less common than chemical synapses.

   Retrieved from " http://en.wikipedia.org/wiki/Chemical_synapse"
   This reference article is mainly selected from the English Wikipedia
   with only minor checks and changes (see www.wikipedia.org for details
   of authors and sources) and is available under the GNU Free
   Documentation License. See also our Disclaimer.
