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.
Synapses form the circuits in which the neurons of the central nervous system interconnect. 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 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".
At a prototypical synapse, such as a dendritic spine, 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 is sometimes called 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 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.
Note: There also exists a less elaborate form of junction called an electrical synapse.
Signalling 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: 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, at which point the vesicles fuse with the membrane and release their contents to the outside. 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 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, which in turn is a function of the type of receptors and neurotransmitter employed at the synapse.
Synaptic strength is the amount of current, or, more strictly, the change in transmembrane potential of the synapse. It is subject to biological regulation. The variability of synaptic strength is often referred to as synaptic plasticity.
One regulatory trigger of synaptic strength involves the simple coincidence sensory stimuli and action potentials in the synaptically linked cells.
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 connects or "synapses" to 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. 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 so are thought to figure similarly in neural circuits.
Detailed properties and regulation
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 EPSP. 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 apparently tunes 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 drugs known as selective serotonin re-uptake inhibitors or SSRIs affect certain synapses by inhibiting the re-uptake of the neurotransmitter serotonin.
One important excitatory neurotransmitter, acetylcholine, does not undergo reuptake, but instead is removed from the synapse by the action of the enzyme acetylcholinesterase.
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