Editing Nervous system (section)

===Neurons and synapses===
[[File:Chemical synapse schema cropped.jpg|thumb|350px|Major elements in synaptic transmission. An electrochemical wave called an [[action potential]] travels along the [[axon]] of a [[neuron]]. When the wave reaches a [[synapse]], it provokes release of a small amount of [[neurotransmitter]] molecules, which bind to chemical receptor molecules in the membrane of the target cell.]]

Most neurons send signals via their [[axon]]s, although some types are capable of dendrite-to-dendrite communication. (In fact, the types of neurons called [[amacrine cell]]s have no axons, and communicate only via their dendrites.) Neural signals propagate along an axon in the form of electrochemical waves called [[action potential]]s, which produce cell-to-cell signals at points where [[axon terminal]]s make [[synapse|synaptic]] contact with other cells.<ref name=KandelCh9/>

Synapses may be electrical or chemical. [[Electrical synapse]]s make direct electrical connections between neurons,<ref name=Hormuzdi/> but [[chemical synapse]]s are much more common, and much more diverse in function.<ref name=KandelCh10/> At a chemical synapse, the cell that sends signals is called presynaptic, and the cell that receives signals is called postsynaptic. Both the presynaptic and postsynaptic areas are full of molecular machinery that carries out the signalling process. The presynaptic area contains large numbers of tiny spherical vessels called [[synaptic vesicle]]s, packed with [[neurotransmitter]] chemicals.<ref name=KandelCh9/> When the presynaptic terminal is electrically stimulated, an array of molecules embedded in the membrane are activated, and cause the contents of the vesicles to be released into the narrow space between the presynaptic and postsynaptic membranes, called the [[synaptic cleft]]. The neurotransmitter then binds to [[neurotransmitter receptor|receptors]] embedded in the postsynaptic membrane, causing them to enter an activated state.<ref name=KandelCh10/> Depending on the type of receptor, the resulting effect on the postsynaptic cell may be excitatory, inhibitory, or modulatory in more complex ways. For example, release of the neurotransmitter [[acetylcholine]] at a synaptic contact between a [[motor neuron]] and a [[muscle cell]] induces rapid contraction of the muscle cell.<ref name=KandelCh11/> The entire synaptic transmission process takes only a fraction of a millisecond, although the effects on the postsynaptic cell may last much longer (even indefinitely, in cases where the synaptic signal leads to the formation of a [[memory trace]]).<ref name=KandelCh4/>

{{Synapse map}}

There are literally hundreds of different types of synapses. In fact, there are over a hundred known neurotransmitters, and many of them have multiple types of receptors.<ref name=KandelCh15/> Many synapses use more than one neurotransmitter—a common arrangement is for a synapse to use one fast-acting small-molecule neurotransmitter such as [[glutamic acid|glutamate]] or [[gamma-Aminobutyric acid|GABA]], along with one or more [[peptide]] neurotransmitters that play slower-acting modulatory roles. Molecular neuroscientists generally divide receptors into two broad groups: [[ligand-gated ion channel|chemically gated ion channels]] and [[second messenger system]]s. When a chemically gated ion channel is activated, it forms a passage that allows specific types of ions to flow across the membrane. Depending on the type of ion, the effect on the target cell may be excitatory or inhibitory. When a second messenger system is activated, it starts a cascade of molecular interactions inside the target cell, which may ultimately produce a wide variety of complex effects, such as increasing or decreasing the sensitivity of the cell to stimuli, or even altering [[gene transcription]].

According to a rule called [[Dale's principle]], which has only a few known exceptions, a neuron releases the same neurotransmitters at all of its synapses.<ref name=Strata/> This does not mean, though, that a neuron exerts the same effect on all of its targets, because the effect of a synapse depends not on the neurotransmitter, but on the receptors that it activates.<ref name=KandelCh10/> Because different targets can (and frequently do) use different types of receptors, it is possible for a neuron to have excitatory effects on one set of target cells, inhibitory effects on others, and complex modulatory effects on others still. Nevertheless, it happens that the two most widely used neurotransmitters, [[glutamic acid|glutamate]] and [[gamma-Aminobutyric acid|GABA]], each have largely consistent effects. Glutamate has several widely occurring types of receptors, but all of them are excitatory or modulatory. Similarly, GABA has several widely occurring receptor types, but all of them are inhibitory.<ref>There are a number of exceptional situations in which GABA has been found to have excitatory effects, mainly during early development. For a review see {{Cite journal |vauthors=Marty A, Llano I |title=Excitatory effects of GABA in established brain networks |journal=Trends Neurosci. |volume=28 |issue=6 |pages=284–289 |date=June 2005 |pmid=15927683 |doi=10.1016/j.tins.2005.04.003 |s2cid=40022079}}</ref> Because of this consistency, glutamatergic cells are frequently referred to as "excitatory neurons", and GABAergic cells as "inhibitory neurons". Strictly speaking, this is an abuse of terminology—it is the receptors that are excitatory and inhibitory, not the neurons—but it is commonly seen even in scholarly publications.

One very important subset of synapses are capable of forming [[memory trace]]s by means of long-lasting activity-dependent changes in synaptic strength.<ref name=Paradiso>{{Cite book |vauthors=Paradiso MA, Bear MF, Connors BW |title=Neuroscience: Exploring the Brain |publisher=Lippincott Williams & Wilkins |year=2007 |page=[https://archive.org/details/neuroscienceexpl00mark/page/718 718] |isbn=978-0-7817-6003-4 |url=https://archive.org/details/neuroscienceexpl00mark/page/718}}</ref> The best-known form of neural memory is a process called [[long-term potentiation]] (abbreviated LTP), which operates at synapses that use the neurotransmitter [[glutamic acid|glutamate]] acting on a special type of receptor known as the [[NMDA receptor]].<ref name=Cooke>{{Cite journal |vauthors=Cooke SF, Bliss TV |title=Plasticity in the human central nervous system |journal=Brain |volume=129 |issue=Pt 7 |pages=1659–1673 |year=2006 |pmid=16672292 |doi=10.1093/brain/awl082 |doi-access=free}}</ref> The NMDA receptor has an "associative" property: if the two cells involved in the synapse are both activated at approximately the same time, a channel opens that permits calcium to flow into the target cell.<ref name=Bliss>{{Cite journal |vauthors=Bliss TV, Collingridge GL |title=A synaptic model of memory: long-term potentiation in the hippocampus |journal=Nature |volume=361 |issue=6407 |pages=31–39 |date=January 1993 |pmid=8421494 |doi=10.1038/361031a0 |bibcode=1993Natur.361...31B |s2cid=4326182}}</ref> The calcium entry initiates a second messenger cascade that ultimately leads to an increase in the number of glutamate receptors in the target cell, thereby increasing the effective strength of the synapse. This change in strength can last for weeks or longer. Since the discovery of LTP in 1973, many other types of synaptic memory traces have been found, involving increases or decreases in synaptic strength that are induced by varying conditions, and last for variable periods of time.<ref name=Cooke/> The [[reward system]], that reinforces desired behaviour for example, depends on a variant form of LTP that is conditioned on an extra input coming from a reward-signalling pathway that uses [[dopamine]] as neurotransmitter.<ref name=Kauer>{{Cite journal |vauthors=Kauer JA, Malenka RC |title=Synaptic plasticity and addiction |journal=Nat. Rev. Neurosci. |volume=8 |issue=11 |pages=844–858 |date=November 2007 |pmid=17948030 |doi=10.1038/nrn2234 |s2cid=38811195 |doi-access=free}}</ref> All these forms of synaptic modifiability, taken collectively, give rise to [[neural plasticity]], that is, to a capability for the nervous system to adapt itself to variations in the environment.