View source for Neuron

{{Short description|Primary cell of the nervous system}}
{{About|the type of cell}}
{{Distinguish|Neutron}}
{{Infobox neuron
| name             = Neuron
| image            = Blausen 0657 MultipolarNeuron.png
| caption          = Anatomy of a [[multipolar neuron]]
| function         =
| neurotransmitter =
| morphology       =
| afferents        =
| efferents        =
}}

A '''neuron''' ([[American English]]), '''neurone''' ([[British English]]),<ref>Cambridge Dictionary, https://dictionary.cambridge.org/dictionary/english/neurone</ref> or '''nerve cell''', is an [[membrane potential#Cell excitability|excitable]] [[cell (biology)|cell]] that fires electric signals called [[action potentials]] across a [[neural network (biology)|neural network]] in the [[nervous system]]. They are located in the nervous system and help to receive and conduct impulses. Neurons communicate with other cells via [[synapse]]s, which are specialized connections that commonly use minute amounts of chemical [[neurotransmitter]]s to pass the electric signal from the presynaptic neuron to the target cell through the synaptic gap.

Neurons are the main components of [[nervous tissue]] in all [[Animalia|animals]] except [[sponge]]s and [[placozoans]]. [[Plant]]s and [[fungi]] do not have nerve cells. Molecular evidence suggests that the ability to generate electric signals first appeared in evolution some 700 to 800 million years ago, during the [[Tonian]] period. Predecessors of neurons were the [[peptidergic]] secretory cells. They eventually gained new gene modules which enabled cells to create post-synaptic scaffolds and [[ion channel]]s that generate fast electrical signals. The ability to generate electric signals was a key innovation in the evolution of the nervous system.<ref>{{Cite journal |last1=Najle |first1=Sebastián R. |last2=Grau-Bové |first2=Xavier |last3=Elek |first3=Anamaria |last4=Navarrete |first4=Cristina |last5=Cianferoni |first5=Damiano |last6=Chiva |first6=Cristina |last7=Cañas-Armenteros |first7=Didac |last8=Mallabiabarrena |first8=Arrate |last9=Kamm |first9=Kai |last10=Sabidó |first10=Eduard |last11=Gruber-Vodicka |first11=Harald |last12=Schierwater |first12=Bernd |last13=Serrano |first13=Luis |last14=Sebé-Pedrós |first14=Arnau |date=Oct 2023 |title=Stepwise emergence of the neuronal gene expression program in early animal evolution |doi-access=free |journal=Cell |language=en |volume=186 |issue=21 |pages=4676–4693.e29 |doi=10.1016/j.cell.2023.08.027 |pmc=10580291 |pmid=37729907 }}</ref>

Neurons are typically classified into three types based on their function. [[Sensory neuron]]s respond to [[Stimulus (physiology)|stimuli]] such as touch, sound, or light that affect the cells of the [[Sense|sensory organs]], and they send signals to the [[spinal cord]] and then to the sensorial area in the [[brain]]. [[Motor neuron]]s receive signals from the brain and spinal cord to control everything from [[muscle contraction]]s<ref>Zayia LC, Tadi P. [https://www.ncbi.nlm.nih.gov/books/NBK554616/ Neuroanatomy, Motor Neuron]. [Updated 2022 Jul 25]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-.</ref> to [[gland|glandular output]]. [[Interneuron]]s connect neurons to other neurons within the same region of the brain or spinal cord. When multiple neurons are functionally connected together, they form what is called a [[neural circuit]].

A neuron contains all the structures of other cells such as a [[Cell nucleus|nucleus]], [[mitochondria]], and [[Golgi bodies]] but has additional unique structures such as an [[axon]], and [[dendrite]]s.<ref name="Betts"/> The [[soma (biology)|soma]] or cell body, is a compact structure, and the axon and dendrites are filaments extruding from the soma. Dendrites typically branch profusely and extend a few hundred micrometers from the soma. The axon leaves the soma at a swelling called the [[axon hillock]] and travels for as far as 1 meter in humans or more in other species. It branches but usually maintains a constant diameter. At the farthest tip of the axon's branches are [[axon terminals]], where the neuron can transmit a signal across the [[synapse]] to another cell. Neurons may lack dendrites or have no axons. The term [[neurite]] is used to describe either a dendrite or an axon, particularly when the cell is [[Cellular differentiation|undifferentiated]].

Most neurons receive signals via the dendrites and soma and send out signals down the axon. At the majority of synapses, signals cross from the axon of one neuron to the dendrite of another. However, synapses can connect an axon to another axon or a dendrite to another dendrite. The signaling process is partly electrical and partly chemical. Neurons are electrically excitable, due to the maintenance of [[voltage]] gradients across their [[Cell membrane|membranes]]. If the voltage changes by a large enough amount over a short interval, the neuron generates an [[All-or-none law|all-or-nothing]] [[electrochemical]] pulse called an [[action potential]]. This potential travels rapidly along the axon and activates synaptic connections as it reaches them. Synaptic signals may be [[Excitatory postsynaptic potential|excitatory]] or [[Inhibitory postsynaptic potential|inhibitory]], increasing or reducing the net voltage that reaches the soma.

In most cases, neurons are generated by [[neural stem cell]]s during brain development and childhood. [[Neurogenesis]] largely ceases during adulthood in most areas of the brain.

{{toclimit|3}}

== Nervous system ==
Neurons are the primary components of the [[nervous system]], along with the [[glial cells]] that give them structural and metabolic support.<ref name="Moore3">{{Cite book|title = Clinically Oriented Anatomy|last1 = Moore|first1 = Keith|last2 = Dalley|first2 = Arthur|publisher = LWW|year = 2005|isbn = 0-7817-3639-0|edition = 5th|pages = [https://archive.org/details/clinicallyorient00moor_1/page/47 47]|quote = A bundle of nerve fibers (axons) connecting neighboring or distant nuclei of the CNS is a tract.|url-access = registration|url = https://archive.org/details/clinicallyorient00moor_1/page/47}}</ref> The nervous system is made up of the [[central nervous system]], which includes the [[brain]] and [[spinal cord]], and the [[peripheral nervous system]], which includes the [[autonomic nervous system|autonomic]], [[Enteric nervous system|enteric]] and [[somatic nervous system]]s.<ref>{{Cite web |title=What are the parts of the nervous system? |date=October 2018 |url=https://www.nichd.nih.gov/health/topics/neuro/conditioninfo/parts |access-date=2022-07-08 |language=en}}</ref> In vertebrates, the majority of neurons belong to the [[central nervous system]], but some reside in peripheral [[ganglion|ganglia]], and many sensory neurons are situated in sensory organs such as the [[retina]] and [[cochlea]].

Axons may bundle into [[nerve fascicle]]s that make up the [[nerve]]s in the peripheral nervous system (like strands of wire that make up a cable). In the [[central nervous system]] bundles of axons are called [[nerve tract]]s.

== Anatomy and histology ==
{{Multiple image
| total_width       = 300
| image1            = Complete neuron cell diagram en.svg
| caption1          = Diagram of a typical myelinated vertebrate motor neuron
| image2            = Anatomy of a Neuron with Synapse.png
| caption2          = Schematic of a single [[pyramidal neuron]], with a [[synapse]] from an incoming [[axon]] onto a [[dendritic spine]]
| direction         = vertical
}}
Neurons are highly specialized for the processing and transmission of cellular signals. Given the diversity of functions performed in different parts of the nervous system, there is a wide variety in their shape, size, and electrochemical properties. For instance, the soma of a neuron can vary from 4 to 100 [[Micrometre|micrometers]] in diameter.<ref>{{cite web |first = Melissa |last = Davies |title = The Neuron: size comparison |url = https://www.ualberta.ca/~neuro/OnlineIntro/NeuronExample.htm |work = Neuroscience: A journey through the brain |date = 2002-04-09 |access-date = 2009-06-20}}</ref>
* The '''[[Soma (biology)|soma]]''' is the body of the neuron. As it contains the [[cell nucleus|nucleus]], most [[protein biosynthesis|protein synthesis]] occurs here. The nucleus can range from 3 to 18 micrometers in diameter.<ref>{{cite web |first = Eric H. |last = Chudler | name-list-style = vanc |title = Brain Facts and Figures |url = http://faculty.washington.edu/chudler/facts.html |work = Neuroscience for Kids |access-date = 2009-06-20 }}</ref>
* The '''[[dendrites]]''' of a neuron are cellular extensions with many branches. This overall shape and structure are referred to metaphorically as a dendritic tree. The branches form fractal patterns that repeat at multiple size scales.<ref> J.H. Smith, C. Rowland, B. Harland, S. Moslehi, K. Schobert, R.M. Montgomery, W.J. Watterson, J. Dalrymple-Alford, R.P. Taylor, "How Neurons Exploit Fractal Geometry to Maximize Physical Connectivity", Scientific Reports, 11, 2332 (2021) </ref> This fractal tree is where the majority of input to the neuron occurs via the [[dendritic spine]].
* The '''[[axon]]''' is a finer, cable-like projection that can extend tens, hundreds, or even tens of thousands of times the diameter of the soma in length. The axon primarily carries [[nerve signal]]s away from the soma and carries some types of information back to it. Many neurons have only one axon, but this axon may—and usually will—undergo extensive branching, enabling communication with many target cells. The part of the axon where it emerges from the soma is called the '''[[axon hillock]]'''. Besides being an anatomical structure, the axon hillock also has the greatest density of [[voltage-dependent sodium channels]]. This makes it the most easily excited part of the neuron and the spike initiation zone for the axon. In electrophysiological terms, it has the most negative [[threshold potential]].
** While the axon and axon hillock are generally involved in information outflow, this region can also receive input from other neurons.
* The '''[[axon terminal]]''' is found at the end of the axon farthest from the soma and contains [[synapses]]. Synaptic boutons are specialized structures where [[neurotransmitter]] chemicals are released to communicate with target neurons. In addition to synaptic boutons at the axon terminal, a neuron may have [[en passant boutons]], which are located along the length of the axon.

The accepted view of the neuron attributes dedicated functions to its various anatomical components; however, dendrites and axons often act in ways contrary to their so-called main function.<ref>{{Cite web |date=2021-01-14 |title=16.7: Nervous System |url=https://bio.libretexts.org/Courses/Lumen_Learning/Book%3A_Fundamentals_of_Biology_I_(Lumen)/16%3A_Module_13%3A_Overview_of_Body_Systems/16.7%3A_Nervous_System |access-date=2022-02-28 |website=Biology LibreTexts |language=en}}</ref>

Axons and dendrites in the central nervous system are typically only about one micrometer thick, while some in the peripheral nervous system are much thicker. The soma is usually about 10–25 micrometers in diameter and often is not much larger than the cell nucleus it contains. The longest axon of a human [[motor neuron]] can be over a meter long, reaching from the base of the spine to the toes.

Sensory neurons can have axons that run from the toes to the [[posterior column]] of the spinal cord, over 1.5 meters in adults. [[Giraffe]]s have single axons several meters in length running along the entire length of their necks. Much of what is known about axonal function comes from studying the [[squid giant axon]], an ideal experimental preparation because of its relatively immense size (0.5–1 millimeter thick, several centimeters long).

Fully differentiated neurons are permanently [[G0 phase|postmitotic]]<ref>{{cite journal | vauthors = Herrup K, Yang Y | title = Cell cycle regulation in the postmitotic neuron: oxymoron or new biology? | journal = Nature Reviews. Neuroscience | volume = 8 | issue = 5 | pages = 368–78 | date = May 2007 | pmid = 17453017 | doi = 10.1038/nrn2124 | s2cid = 12908713 }}</ref> however, stem cells present in the adult brain may regenerate functional neurons throughout the life of an organism (see [[neurogenesis]]). [[Astrocyte]]s are star-shaped [[glial cell]]s that have been observed to turn into neurons by virtue of their stem cell-like characteristic of [[pluripotency]].<ref name="Talifu">{{cite journal |vauthors=Talifu Z, Liu JY, Pan YZ, Ke H, Zhang CJ, Xu X, Gao F, Yu Y, Du LJ, Li JJ |title=In vivo astrocyte-to-neuron reprogramming for central nervous system regeneration: a narrative review |journal=Neural Regen Res |volume=18 |issue=4 |pages=750–755 |date=April 2023 |pmid=36204831 |pmc=9700087 |doi=10.4103/1673-5374.353482 |doi-access=free |url=}}</ref>

===Membrane===
Like all animal cells, the [[Soma (biology)|cell body]] of every neuron is enclosed by a [[plasma membrane]], a bilayer of [[lipid]] molecules with many types of embedded protein structures.<ref>{{Cite journal |last=Giménez |first=C. |date=February 1998 |title=[Composition and structure of the neuronal membrane: molecular basis of its physiology and pathology] |journal=Revista de Neurologia |volume=26 |issue=150 |pages=232–239 |issn=0210-0010 |pmid=9563093}}</ref> A [[lipid bilayer]] is a powerful electrical [[Insulator (electricity)|insulator]], but in neurons, many of the protein structures embedded in the membrane are electrically active. These include [[ion channel]]s that permit electrically charged ions to flow across the membrane and ion pumps that chemically transport ions from one side of the membrane to the other. Most ion channels are [[Gating (electrophysiology)|gated]], permeable only to specific types of ions. Some ion channels are [[voltage-gated ion channel|voltage gated]], meaning that they can be switched between open and closed states by altering the voltage difference across the membrane. Others are chemically gated, meaning that they can be switched between open and closed states by interactions with chemicals that diffuse through the extracellular fluid. The [[ion]]s include [[sodium]], [[potassium]], [[chloride]], and [[calcium]]. The interactions between ion channels and [[Ion transporter|ion pump]]s produce a voltage difference across the membrane, typically a little less than 1/10 of a [[volt]] at baseline. This voltage has two functions: first, it provides a power source for an assortment of voltage-dependent protein machineries that are embedded in the membrane; second, it provides a basis for electrical signal transmission between different parts of the membrane.

===Histology and internal structure===
[[File:Gyrus Dentatus 40x.jpg|thumb|[[Golgi stain|Golgi-stained]] neurons in human [[hippocampal]] tissue]]
[[File:SUM 110913 Cort Neurons 2.5d in vitro 488 Phalloidin no perm 4 cmle-2.png|thumb|Actin filaments in a mouse cortical neuron in culture]]

Numerous microscopic clumps called [[Nissl body|Nissl bodies]] (or Nissl substance) are seen when nerve cell bodies are stained with a basophilic ("base-loving") dye. These structures consist of [[Endoplasmic reticulum#Rough endoplasmic reticulum|rough endoplasmic reticulum]] and associated [[ribosomal RNA]]. Named after German psychiatrist and neuropathologist [[Franz Nissl]] (1860–1919), they are involved in protein synthesis and their prominence can be explained by the fact that nerve cells are very metabolically active. Basophilic dyes such as [[aniline]] or (weakly) [[hematoxylin]]<ref>{{cite book|title=State Hospitals Bulletin|url={{google books |plainurl=y |id=Wp8CAAAAYAAJ|page=378}}|year=1897|publisher=State Commission in Lunacy.|page=378}}</ref> highlight negatively charged components, and so bind to the phosphate backbone of the ribosomal RNA.

The cell body of a neuron is supported by a complex mesh of structural proteins called [[neurofilament]]s, which together with [[neurotubule]]s (neuronal microtubules) are assembled into larger neurofibrils.<ref name="Webster">{{cite web |title=Medical Definition of Neurotubules |url=https://www.merriam-webster.com/medical/neurotubules |website=www.merriam-webster.com}}</ref> Some neurons also contain pigment granules, such as [[neuromelanin]] (a brownish-black pigment that is byproduct of synthesis of [[catecholamine]]s), and [[lipofuscin]] (a yellowish-brown pigment), both of which accumulate with age.<ref>{{cite journal | vauthors = Zecca L, Gallorini M, Schünemann V, Trautwein AX, Gerlach M, Riederer P, Vezzoni P, Tampellini D | title = Iron, neuromelanin and ferritin content in the substantia nigra of normal subjects at different ages: consequences for iron storage and neurodegenerative processes | journal = Journal of Neurochemistry | volume = 76 | issue = 6 | pages = 1766–73 | date = March 2001 | pmid = 11259494 | doi = 10.1046/j.1471-4159.2001.00186.x | s2cid = 31301135 }}</ref><ref>{{cite journal | vauthors = Herrero MT, Hirsch EC, Kastner A, Luquin MR, Javoy-Agid F, Gonzalo LM, Obeso JA, Agid Y | title = Neuromelanin accumulation with age in catecholaminergic neurons from Macaca fascicularis brainstem | journal = Developmental Neuroscience | volume = 15 | issue = 1 | pages = 37–48 | date = 1993 | pmid = 7505739 | doi = 10.1159/000111315 }}</ref><ref>{{cite journal | vauthors = Brunk UT, Terman A | title = Lipofuscin: mechanisms of age-related accumulation and influence on cell function | journal = Free Radical Biology & Medicine | volume = 33 | issue = 5 | pages = 611–9 | date = September 2002 | pmid = 12208347 | doi = 10.1016/s0891-5849(02)00959-0 }}</ref> Other structural proteins that are important for neuronal function are [[actin]] and the [[tubulin]] of [[microtubule]]s. [[Class III β-tubulin]] is found almost exclusively in neurons. Actin is predominately found at the tips of axons and dendrites during neuronal development. There the actin dynamics can be modulated via an interplay with microtubule.<ref>{{cite journal | vauthors = Zhao B, Meka DP, Schellenberg R, König T, Schwanke B, Kobler O, Windhorst S, Kreutz MR, Mikhaylova M, Calderon de Anda F | title = Microtubules Modulate F-actin Dynamics during Neuronal Polarization | journal = Scientific Reports | volume = 7 | issue = 1 | article-number = 9583 | date = August 2017 | pmid = 28851982 | pmc = 5575062 | doi = 10.1038/s41598-017-09832-8 | bibcode = 2017NatSR...7.9583Z }}</ref>

There are different internal structural characteristics between axons and dendrites. Typical axons seldom contain [[ribosomes]], except some in the initial segment. Dendrites contain granular endoplasmic reticulum or ribosomes, in diminishing amounts as the distance from the cell body increases.

==Classification==
[[File:GFPneuron.png|thumb|Image of pyramidal neurons in mouse [[cerebral cortex]] expressing [[green fluorescent protein]]. The red staining indicates [[GABA]]ergic interneurons.<ref>{{cite journal | vauthors = Lee WC, Huang H, Feng G, Sanes JR, Brown EN, So PT, Nedivi E | title = Dynamic remodeling of dendritic arbors in GABAergic interneurons of adult visual cortex | journal = PLOS Biology | volume = 4 | issue = 2 | article-number = e29 | date = February 2006 | pmid = 16366735 | pmc = 1318477 | doi = 10.1371/journal.pbio.0040029 |doi-access=free }}</ref>]]{{See also|List of distinct cell types in the adult human body#Nervous system}}
Neurons vary in shape and size and can be classified by their [[Morphology (biology)|morphology]] and function.<ref name="Al">{{cite book|last=Al|first=Martini, Frederic Et|title=Anatomy and Physiology' 2007 Ed.2007 Edition|year=2005 |url={{google books |plainurl=y |id=joJb82gVsLoC|page=288}}|publisher=Rex Bookstore, Inc.|isbn=978-971-23-4807-5|page=288}}</ref> The anatomist [[Camillo Golgi]] grouped neurons into two types; type I with long axons used to move signals over long distances and type II with short axons, which can often be confused with dendrites. Type I cells can be further classified by the location of the soma. The basic morphology of type I neurons, represented by spinal [[motor neurons]], consists of a cell body called the soma and a long thin axon covered by a [[myelin sheath]]. The dendritic tree wraps around the cell body and receives signals from other neurons. The end of the axon has branching [[axon terminal]]s that release neurotransmitters into a gap called the [[synaptic cleft]] between the terminals and the dendrites of the next neuron.{{citation needed|date=July 2022}}

===Structural classification===

====Polarity====
[[File:Structural_classification_of_neurons_by_polarity_hariadhi.svg|thumb|Different kinds of neurons]]
Most neurons can be anatomically characterized as:<ref name="Betts">{{CC-notice|cc=by4|url=https://openstax.org/books/anatomy-and-physiology/pages/12-2-nervous-tissue}} {{cite book|last1=Betts|first1=J Gordon|last2=Desaix|first2=Peter|last3=Johnson|first3=Eddie|last4=Johnson|first4=Jody E|last5=Korol|first5=Oksana|last6=Kruse|first6=Dean|last7=Poe|first7=Brandon|last8=Wise|first8=James|last9=Womble|first9=Mark D|last10=Young|first10=Kelly A|title=Anatomy & Physiology|location=Houston|publisher=OpenStax CNX|isbn=978-1-947172-04-3|date=June 8, 2023|at=12.2 Nervous tissue}}</ref>
* [[Unipolar neuron|Unipolar]]: single process. Unipolar cells are exclusively sensory neurons. Their dendrites receive sensory information, sometimes directly from the stimulus itself. The cell bodies of unipolar neurons are always found in ganglia. Sensory reception is a peripheral function, so the cell body is in the periphery, though closer to the CNS in a ganglion. The axon projects from the dendrite endings, past the cell body in a ganglion, and into the central nervous system.
* [[Bipolar cell|Bipolar]]: 1 axon and 1 dendrite. They are found mainly in the [[olfactory epithelium]], and as part of the retina.
* [[Multipolar neuron|Multipolar]]: 1 axon and 2 or more dendrites
** [[Golgi I]]: neurons with long-projecting axonal processes; examples are pyramidal cells, Purkinje cells, and anterior horn cells
** [[Golgi II]]: neurons whose axonal process projects locally; the best example is the granule cell
* [[Anaxonic neuron|Anaxonic]]: where the axon cannot be distinguished from the dendrite(s)
* [[Pseudounipolar cells|Pseudounipolar]]: 1 process which then serves as both an axon and a dendrite

====Other====
Some unique neuronal types can be identified according to their location in the nervous system and distinct shape. Some examples are:{{citation needed|date=July 2022}}
* [[Basket cell]]s, interneurons that form a dense plexus of terminals around the soma of target cells, found in the cortex and [[cerebellum]]
* [[Betz cell]]s, large motor neurons in [[primary motor cortex]]
* [[Lugaro cell]]s, interneurons of the cerebellum
* [[Medium spiny neuron]]s, most neurons in the [[corpus striatum]]
* [[Purkinje cell]]s, huge neurons in the cerebellum, a type of Golgi I multipolar neuron
* [[Pyramidal cell]]s, neurons with triangular soma, a type of Golgi I
* [[Rosehip neuron|Rosehip cells]], unique human inhibitory neurons that interconnect with Pyramidal cells
* [[Renshaw cell]]s, neurons with both ends linked to [[alpha motor neuron]]s
* [[Unipolar brush cell]]s, interneurons with unique dendrite ending in a brush-like tuft
* [[Granule cell]]s, a type of Golgi II neuron
* [[Anterior horn (spinal cord)|Anterior horn]] cells, [[motoneurons]] located in the spinal cord
* [[Spindle neuron|Spindle cells]], interneurons that connect widely separated areas of the brain

===Functional classification===

====Direction====
* [[Afferent neuron]]s convey information from tissues and organs into the central nervous system and are also called [[sensory neurons]].
* [[Efferent neuron]]s (motor neurons) transmit signals from the central nervous system to the effector cells.
* [[Interneuron]]s connect neurons within specific regions of the central nervous system.

Afferent and efferent also refer generally to neurons that, respectively, bring information to or send information from the brain.

====Action on other neurons====
A neuron affects other neurons by releasing a neurotransmitter that binds to [[receptor (biochemistry)|chemical receptor]]s. The effect on the postsynaptic neuron is determined by the type of receptor that is activated, not by the presynaptic neuron or by the neurotransmitter. Receptors are classified broadly as ''excitatory'' (causing an increase in firing rate), ''inhibitory'' (causing a decrease in firing rate), or ''modulatory'' (causing long-lasting effects not directly related to firing rate).{{citation needed|date=July 2022}}

The two most common (90%+) neurotransmitters in the brain, [[glutamate]] and [[GABA]], have largely consistent actions. Glutamate acts on several types of receptors and has effects that are excitatory at [[ionotropic receptor]]s and a modulatory effect at [[metabotropic receptor]]s. Similarly, GABA acts on several types of receptors, but all of them have inhibitory effects (in adult animals, at least). Because of this consistency, it is common for neuroscientists to refer to cells that release glutamate as "excitatory neurons", and cells that release GABA as "inhibitory neurons". Some other types of neurons have consistent effects, for example, "excitatory" motor neurons in the spinal cord that release [[acetylcholine]], and "inhibitory" [[spinal neuron]]s that release [[glycine]].{{citation needed|date=July 2022}}

The distinction between excitatory and inhibitory neurotransmitters is not absolute. Rather, it depends on the class of chemical receptors present on the postsynaptic neuron. In principle, a single neuron, releasing a single neurotransmitter, can have excitatory effects on some targets, inhibitory effects on others, and modulatory effects on others still. For example, [[photoreceptor cell]]s in the retina constantly release the neurotransmitter glutamate in the absence of light. So-called OFF [[retinal bipolar cells|bipolar cells]] are, like most neurons, excited by the released glutamate. However, neighboring target neurons called ON bipolar cells are instead inhibited by glutamate, because they lack typical [[ionotropic receptor|ionotropic]] [[glutamate receptors]] and instead express a class of inhibitory [[metabotropic receptor|metabotropic]] glutamate receptors.<ref>{{cite journal | vauthors = Gerber U | title = Metabotropic glutamate receptors in vertebrate retina | journal = Documenta Ophthalmologica. Advances in Ophthalmology | volume = 106 | issue = 1 | pages = 83–7 | date = January 2003 | pmid = 12675489 | doi = 10.1023/A:1022477203420 | s2cid = 22296630 }}</ref> When light is present, the photoreceptors cease releasing glutamate, which relieves the ON bipolar cells from inhibition, activating them; this simultaneously removes the excitation from the OFF bipolar cells, silencing them.{{citation needed|date=July 2022}}

It is possible to identify the type of inhibitory effect a presynaptic neuron will have on a postsynaptic neuron, based on the proteins the presynaptic neuron expresses. [[Parvalbumin]]-expressing neurons typically dampen the output signal of the postsynaptic neuron in the [[visual cortex]], whereas [[somatostatin]]-expressing neurons typically block dendritic inputs to the postsynaptic neuron.<ref name="pmid22878717">{{cite journal | vauthors = Wilson NR, Runyan CA, Wang FL, Sur M | title = Division and subtraction by distinct cortical inhibitory networks in vivo | journal = Nature | volume = 488 | issue = 7411 | pages = 343–8 | date = August 2012 | pmid = 22878717 | pmc = 3653570 | doi = 10.1038/nature11347 | bibcode = 2012Natur.488..343W | hdl = 1721.1/92709 }}</ref>

====Discharge patterns====
Neurons have intrinsic electroresponsive properties like intrinsic transmembrane voltage [[Neural oscillation|oscillatory]] patterns.<ref name="llinas2014">{{cite journal | vauthors = Llinás RR | title = Intrinsic electrical properties of mammalian neurons and CNS function: a historical perspective | journal = Frontiers in Cellular Neuroscience | volume = 8 | page = 320 | date = 2014-01-01 | pmid = 25408634 | pmc = 4219458 | doi = 10.3389/fncel.2014.00320 | doi-access = free }}</ref> So neurons can be classified according to their [[electrophysiology|electrophysiological]] characteristics:
* Tonic or regular spiking. Some neurons are typically constantly (tonically) active, typically firing at a constant frequency. Example: interneurons in [[striatum|neurostriatum]].
* Phasic or [[bursting]]. Neurons that fire in bursts are called phasic.
* Fast-spiking. Some neurons are notable for their high firing rates, for example, some types of cortical inhibitory interneurons, cells in [[globus pallidus]], [[retinal ganglion cells]].<ref>{{cite conference | title = Ion conductances related to shaping the repetitive firing in rat retinal ganglion cells | vauthors = Kolodin YO, Veselovskaia NN, Veselovsky NS, Fedulova SA | conference = Acta Physiologica Congress | url = http://www.blackwellpublishing.com/aphmeeting/abstract.asp?MeetingID=&id=61198 | access-date = 2009-06-20 | archive-url = https://web.archive.org/web/20121007164451/http://www.blackwellpublishing.com/aphmeeting/abstract.asp?MeetingID=&id=61198 | archive-date = 2012-10-07 }}</ref><ref>{{cite web|url=http://ykolodin.50webs.com/ |title=Ionic conductances underlying excitability in tonically firing retinal ganglion cells of adult rat |publisher=Ykolodin.50webs.com |date=2008-04-27 |access-date=2013-02-16}}</ref>

====Neurotransmitter====
[[File:Neurotransmitters.jpg|thumb|Synaptic vesicles containing neurotransmitters]]
{{Main|Neurotransmitter}}
[[Neurotransmitter]]s are chemical messengers passed from one neuron to another neuron or to a [[muscle cell]] or [[Gland|gland cell]].
* Cholinergic neurons – acetylcholine. [[Acetylcholine]] is released from presynaptic neurons into the synaptic cleft. It acts as a [[ligand]] for both ligand-gated ion channels and [[Metabotropic receptor|metabotropic]] (GPCRs) [[Muscarinic acetylcholine receptor|muscarinic receptors]]. [[Nicotinic receptors]] are pentameric ligand-gated ion channels composed of alpha and beta subunits that bind [[nicotine]]. Ligand binding opens the channel causing the influx of [[Sodium|Na<sup>+</sup>]] depolarization and increases the probability of presynaptic neurotransmitter release. Acetylcholine is synthesized from [[choline]] and [[acetyl coenzyme A]].
* Adrenergic neurons – noradrenaline. [[Noradrenaline]] (norepinephrine) is released from most [[postganglionic]] neurons in the [[sympathetic nervous system]] onto two sets of GPCRs: [[Adrenergic receptor|alpha adrenoceptor]]s and [[beta adrenoceptor]]s. Noradrenaline is one of the three common [[catecholamine]] neurotransmitters, and the most prevalent of them in the [[peripheral nervous system]]; as with other catecholamines, it is synthesized from [[tyrosine]].
* GABAergic neurons – [[gamma aminobutyric acid]]. GABA is one of two neuroinhibitors in the [[central nervous system]] (CNS), along with glycine. GABA has a homologous function to [[Acetylcholine|ACh]], gating anion channels that allow [[Chlorine|Cl<sup>−</sup>]] ions to enter the post synaptic neuron. Cl<sup>−</sup> causes hyperpolarization within the neuron, decreasing the probability of an action potential firing as the voltage becomes more negative (for an action potential to fire, a positive voltage threshold must be reached). GABA is synthesized from glutamate neurotransmitters by the enzyme [[glutamate decarboxylase]].
* Glutamatergic neurons – glutamate. [[Glutamate]] is one of two primary excitatory amino acid neurotransmitters, along with [[Aspartic acid|aspartate]]. Glutamate receptors are one of four categories, three of which are ligand-gated ion channels and one of which is a [[G protein|G-protein]] coupled receptor (often referred to as GPCR).

:#[[AMPA]] and [[Kainic acid|Kainate]] receptors function as [[Ion|cation]] channels permeable to Na<sup>+</sup> cation channels mediating fast excitatory synaptic transmission.
:#[[N-Methyl-D-aspartic acid|NMDA]] receptors are another cation channel that is more permeable to [[Calcium in biology|Ca<sup>2+</sup>]]. The function of NMDA receptors depends on glycine receptor binding as a co-[[agonist]] within the channel pore. NMDA receptors do not function without both ligands present.
:#Metabotropic receptors, GPCRs modulate synaptic transmission and postsynaptic excitability.
:: Glutamate can cause excitotoxicity when blood flow to the brain is interrupted, resulting in [[brain damage]]. When blood flow is suppressed, glutamate is released from presynaptic neurons, causing greater NMDA and AMPA receptor activation than normal outside of stress conditions, leading to elevated Ca<sup>2+</sup> and Na<sup>+</sup> entering the post synaptic neuron and cell damage. Glutamate is synthesized from the amino acid glutamine by the enzyme [[Glutamine oxoglutarate aminotransferase|glutamate synthase]].
* Dopaminergic neurons—[[dopamine]]. [[Dopamine]] is a neurotransmitter that acts on D1 type (D1 and D5) Gs-coupled receptors, which increase cAMP and PKA, and D2 type (D2, D3, and D4) receptors, which activate Gi-coupled receptors that decrease cAMP and PKA. Dopamine is connected to mood and behavior and modulates both pre- and post-synaptic neurotransmission. Loss of dopamine neurons in the [[substantia nigra]] has been linked to [[Parkinson's disease]]. Dopamine is synthesized from the amino acid [[tyrosine]]. Tyrosine is catalyzed into levodopa (or [[L-DOPA]]) by [[tyrosine hydroxylase]], and levodopa is then converted into dopamine by the aromatic amino acid [[Carboxy-lyases|decarboxylase]].
* Serotonergic neurons—[[serotonin]]. [[Serotonin]] (5-Hydroxytryptamine, 5-HT) can act as excitatory or inhibitory. Of its four 5-HT receptor classes, 3 are GPCR and 1 is a ligand-gated cation channel. Serotonin is synthesized from [[tryptophan]] by [[tryptophan hydroxylase]], and then further by decarboxylase. A lack of 5-HT at postsynaptic neurons has been linked to depression. Drugs that block the presynaptic [[serotonin transporter]] are used for treatment, such as [[Prozac]] and [[Zoloft]].
* Purinergic neurons—ATP. [[Adenosine triphosphate|ATP]] is a neurotransmitter acting at both ligand-gated ion channels ([[P2X]] receptors) and GPCRs ([[P2Y receptor|P2Y]]) receptors. ATP is, however, best known as a [[cotransmitter]]. Such [[purinergic signaling]] can also be mediated by other [[purine]]s like [[adenosine]], which particularly acts at P2Y receptors.
* Histaminergic neurons—[[histamine]]. [[Histamine]] is a [[monoamine neurotransmitter]] and [[neuromodulator]]. Histamine-producing neurons are found in the [[tuberomammillary nucleus]] of the [[hypothalamus]].<ref>{{cite journal | vauthors = Scammell TE, Jackson AC, Franks NP, Wisden W, Dauvilliers Y | title = Histamine: neural circuits and new medications | journal = Sleep | volume = 42 | issue = 1 | date = January 2019 | pmid = 30239935 | pmc = 6335869 | doi = 10.1093/sleep/zsy183 }}</ref> Histamine is involved in [[arousal]] and regulating sleep/wake behaviors.

====Multimodel classification====
Since 2012 there has been a push from the cellular and [[computational neuroscience]] community to come up with a universal classification of neurons that will apply to all neurons in the brain as well as across species. This is done by considering the three essential qualities of all neurons: electrophysiology, morphology, and the individual transcriptome of the cells. Besides being universal this classification has the advantage of being able to classify astrocytes as well. A method called [[patch-sequencing]] in which all three qualities can be measured at once is used extensively by the [[Allen Institute for Brain Science]].<ref>{{cite web |url=https://www.news-medical.net/news/20201203/Patch-seq-technique-helps-depict-the-variation-of-neural-cells-in-the-brain.aspx |title=Patch-seq technique helps depict the variation of neural cells in the brain |work=News-medical.net |date=3 December 2020 |access-date=26 August 2021 }}</ref> In 2023, a comprehensive cell atlas of the adult, and developing human brain at the transcriptional, epigenetic, and functional levels was created through an international collaboration of researchers using the most cutting-edge molecular biology approaches.<ref>{{Cite web
| last = Science AAAS
| title = BRAIN CELL CENSUS 
| url = https://www.science.org/collections/brain-cell-census 
| access-date = 2023-10-17
}}
</ref>

==Connectivity==
{{Main|Synapse|Chemical synapse}}
[[File:Chemical synapse schema cropped.jpg|thumb|right|350px|A signal propagating down an axon to the cell body and dendrites of the next cell]]
[[File:Neuro Muscular Junction.png|thumb|Chemical synapse|left]]
Neurons communicate with each other via [[synapses]], where either the [[axon terminal]] of one cell contacts another neuron's dendrite, soma, or, less commonly, axon. Neurons such as Purkinje cells in the cerebellum can have over 1000 dendritic branches, making connections with tens of thousands of other cells; other neurons, such as the magnocellular neurons of the [[supraoptic nucleus]], have only one or two dendrites, each of which receives thousands of synapses.

Synapses can be excitatory or inhibitory, either increasing or decreasing activity in the target neuron, respectively. Some neurons also communicate via electrical synapses, which are direct, electrically conductive [[gap junction|junctions]] between cells.<ref>{{cite book |last1=Macpherson |first1=Gordon |title=Black's Medical Dictionary |date=2002 |publisher=Scarecrow Press |location=Lanham, MD |isbn=0-8108-4984-4 |pages=431–434 |edition=40 }}</ref>

When an action potential reaches the axon terminal, it opens [[Voltage-dependent calcium channel|voltage-gated calcium channels]], allowing [[Calcium in biology|calcium ions]] to enter the terminal. Calcium causes [[synaptic vesicles]] filled with neurotransmitter molecules to fuse with the membrane, releasing their contents into the synaptic cleft. The neurotransmitters diffuse across the synaptic cleft and activate receptors on the postsynaptic neuron. High cytosolic calcium in the [[axon terminal]] triggers mitochondrial calcium uptake, which, in turn, activates mitochondrial [[energy metabolism]] to produce [[Adenosine triphosphate|ATP]] to support continuous neurotransmission.<ref name="pmid23746507">{{cite journal | vauthors = Ivannikov MV, Macleod GT | title = Mitochondrial free Ca²⁺ levels and their effects on energy metabolism in Drosophila motor nerve terminals | journal = Biophysical Journal | volume = 104 | issue = 11 | pages = 2353–61 | date = June 2013 | pmid = 23746507 | pmc = 3672877 | doi = 10.1016/j.bpj.2013.03.064 | bibcode = 2013BpJ...104.2353I }}</ref>

An [[autapse]] is a synapse in which a neuron's axon connects to its dendrites.

The [[human brain]] has some 8.6 x 10<sup>10</sup> (eighty six billion) neurons.<ref>{{ cite journal | vauthors = Herculano-Houzel S | title = The human brain in numbers: a linearly scaled-up primate brain | journal = Frontiers in Human Neuroscience | volume = 3 | page = 31 | date = November 2009 | pmid = 19915731 | doi = 10.3389/neuro.09.031.2009 | pmc = 2776484 | doi-access = free }}</ref><ref name="Allen2022">{{cite web |title=Why is the human brain so difficult to understand? We asked 4 neuroscientists. |url=https://alleninstitute.org/news/why-is-the-human-brain-so-difficult-to-understand-we-asked-4-neuroscientists/ |website=Allen Institute |access-date=17 October 2023}}</ref> Each neuron has on average 7,000 synaptic connections to other neurons. It has been estimated that the brain of a three-year-old child has about 10<sup>15</sup> synapses (1 quadrillion). [[Synaptic pruning|This number declines with age]], stabilizing by adulthood. Estimates vary for an adult, ranging from 10<sup>14</sup> to 5 x 10<sup>14</sup> synapses (100 to 500 trillion).<ref>{{cite journal | vauthors = Drachman DA | title = Do we have brain to spare? | journal = Neurology | volume = 64 | issue = 12 | pages = 2004–5 | date = June 2005 | pmid = 15985565 | doi = 10.1212/01.WNL.0000166914.38327.BB | s2cid = 38482114 }}</ref>

=== Nonelectrochemical signaling ===
Beyond electrical and chemical signaling, studies suggest neurons in healthy human brains can also communicate through:
* force generated by the enlargement of dendritic spines<ref>{{cite journal |last1=Ucar |first1=Hasan |last2=Watanabe |first2=Satoshi |last3=Noguchi |first3=Jun |last4=Morimoto |first4=Yuichi |last5=Iino |first5=Yusuke |last6=Yagishita |first6=Sho |last7=Takahashi |first7=Noriko |last8=Kasai |first8=Haruo |title=Mechanical actions of dendritic-spine enlargement on presynaptic exocytosis |journal=Nature |date=December 2021 |volume=600 |issue=7890 |pages=686–689 |doi=10.1038/s41586-021-04125-7 |pmid=34819666 |bibcode=2021Natur.600..686U |s2cid=244648506 |language=en |issn=1476-4687}}<br />Lay summary:<br />{{cite news |title=Forceful synapses reveal mechanical interactions in the brain |url=https://www.nature.com/articles/d41586-021-03516-0 |access-date=21 February 2022 |journal=Nature |date=24 November 2021 |language=en |doi=10.1038/d41586-021-03516-0}}</ref>
* the transfer of [[protein]]s – transneuronally transported proteins (TNTPs)<!--e.g. between [[Retinal ganglion cell|RGC]] and [[Excitatory synapse|excitatory]] [[lateral geniculate nucleus|LGN]] neurons--><ref>{{cite news |title=Researchers discover new type of cellular communication in the brain |url=https://medicalxpress.com/news/2022-01-cellular-brain.html |access-date=12 February 2022 |work=The Scripps Research Institute |language=en}}</ref><ref>{{cite journal |last1=Schiapparelli |first1=Lucio M. |last2=Sharma |first2=Pranav |last3=He |first3=Hai-Yan |last4=Li |first4=Jianli |last5=Shah |first5=Sahil H. |last6=McClatchy |first6=Daniel B. |last7=Ma |first7=Yuanhui |last8=Liu |first8=Han-Hsuan |last9=Goldberg |first9=Jeffrey L. |last10=Yates |first10=John R. |last11=Cline |first11=Hollis T. |title=Proteomic screen reveals diverse protein transport between connected neurons in the visual system |journal=Cell Reports |date=25 January 2022 |volume=38 |issue=4 |article-number=110287 |doi=10.1016/j.celrep.2021.110287 |pmid=35081342 |pmc=8906846 |language=English |issn=2211-1247}}</ref>

They can also get modulated by input from the environment and [[hormone]]s released from other parts of the organism,<ref>{{cite book |last1=Levitan |first1=Irwin B. |last2=Kaczmarek |first2=Leonard K. |title=The Neuron |chapter=Electrical Signaling in Neurons |year=2015 |pages=41–62 |doi=10.1093/med/9780199773893.003.0003 |publisher=Oxford University Press |isbn=978-0-19-977389-3 }}</ref> which could be influenced more or less directly by neurons. This also applies to [[neurotrophin]]s such as [[BDNF]]. The [[gut microbiome]] is also connected with the brain.<ref>{{cite journal |last1=O'Leary |first1=Olivia F. |last2=Ogbonnaya |first2=Ebere S. |last3=Felice |first3=Daniela |last4=Levone |first4=Brunno R. |last5=C. Conroy |first5=Lorraine |last6=Fitzgerald |first6=Patrick |last7=Bravo |first7=Javier A. |last8=Forsythe |first8=Paul |last9=Bienenstock |first9=John |last10=Dinan |first10=Timothy G. |last11=Cryan |first11=John F. |title=The vagus nerve modulates BDNF expression and neurogenesis in the hippocampus |journal=European Neuropsychopharmacology |date=1 February 2018 |volume=28 |issue=2 |pages=307–316 |doi=10.1016/j.euroneuro.2017.12.004 |pmid=29426666 |s2cid=46819013 |language=en |issn=0924-977X|doi-access=free }}</ref>
Neurons also communicate with [[microglia]], the brain's main immune cells via specialized contact sites, called "somatic junctions". These connections enable microglia to constantly monitor and regulate neuronal functions, and exert neuroprotection when needed.<ref name="Science">{{cite journal |vauthors=Cserép C, Pósfai B, Lénárt N, Fekete R, László ZI, Lele Z |date=January 2020 |title=Microglia monitor and protect neuronal function through specialized somatic purinergic junctions |url= https://epub.ub.uni-muenchen.de/76442/|journal=Science |volume=367 |issue=6477 |pages=528–537 |doi=10.1126/science.aax6752 |pmid=31831638|bibcode=2020Sci...367..528C |s2cid=209343260 }}</ref>

==Mechanisms for propagating action potentials==
{{Main|Action potential}}
In 1937 [[John Zachary Young]] suggested that the [[squid giant axon]] could be used to study neuronal electrical properties.<ref>{{cite web |first = Eric H. |last = Chudler | name-list-style = vanc |title = Milestones in Neuroscience Research |url = http://faculty.washington.edu/chudler/hist.html |work = Neuroscience for Kids |access-date = 2009-06-20}}</ref> It is larger than but similar to human neurons, making it easier to study. By inserting electrodes into the squid giant axons, accurate measurements were made of the [[membrane potential]].

The cell membrane of the axon and soma contain voltage-gated ion channels that allow the neuron to generate and propagate an electrical signal (an action potential). Some neurons also generate [[subthreshold membrane potential oscillations]]. These signals are generated and propagated by charge-carrying [[ions]] including sodium (Na<sup>+</sup>), potassium (K<sup>+</sup>), chloride (Cl<sup>−</sup>), and [[Calcium signaling|calcium (Ca<sup>2+</sup>)]].

Several stimuli can activate a neuron leading to electrical activity, including [[Mechanoreceptor|pressure]], stretch, chemical transmitters, and changes in the electric potential across the cell membrane.<ref>{{cite web|first1=Joe |last1=Patlak |first2=Ray |last2=Gibbons | name-list-style = vanc |title=Electrical Activity of Nerves |url=http://physioweb.med.uvm.edu/cardiacep/EP/nervecells.htm |work=Action Potentials in Nerve Cells |date=2000-11-01 |access-date=2009-06-20 |archive-url=https://web.archive.org/web/20090827220335/http://physioweb.med.uvm.edu/cardiacep/EP/nervecells.htm |archive-date=August 27, 2009 }}</ref> Stimuli cause specific ion-channels within the cell membrane to open, leading to a flow of ions through the cell membrane, changing the membrane potential. Neurons must maintain the specific electrical properties that define their neuron type.<ref name="Harris-Warrick">{{cite journal |last1=Harris-Warrick |first1=RM |title=Neuromodulation and flexibility in Central Pattern Generator networks. |journal=Current Opinion in Neurobiology |date=October 2011 |volume=21 |issue=5 |pages=685–92 |doi=10.1016/j.conb.2011.05.011 |pmid=21646013|pmc=3171584 }}</ref>

Thin neurons and axons require less [[metabolism|metabolic]] expense to produce and carry action potentials, but thicker axons convey impulses more rapidly. To minimize metabolic expense while maintaining rapid conduction, many neurons have insulating sheaths of [[myelin]] around their axons. The sheaths are formed by [[glia]]l cells: [[oligodendrocyte]]s in the central nervous system and [[Schwann cell]]s in the peripheral nervous system. The sheath enables action potentials to travel [[saltatory conduction|faster]] than in unmyelinated axons of the same diameter, whilst using less energy. The myelin sheath in peripheral nerves normally runs along the axon in sections about 1&nbsp;mm long, punctuated by unsheathed [[node of Ranvier|nodes of Ranvier]], which contain a high density of voltage-gated ion channels. [[Multiple sclerosis]] is a neurological disorder that results from the demyelination of axons in the central nervous system.

Some neurons do not generate action potentials but instead generate a [[graded potential|graded electrical signal]], which in turn causes graded neurotransmitter release. Such [[non-spiking neurons]] tend to be sensory neurons or interneurons, because they cannot carry signals long distances.

==Neural coding==
[[Neural coding]] is concerned with how sensory and other information is represented in the brain by neurons. The main goal of studying neural coding is to characterize the relationship between the [[Stimulus (physiology)|stimulus]] and the individual or [[Neural ensemble|ensemble]] neuronal responses and the relationships among the electrical activities of the neurons within the ensemble.<ref name="Brown">{{cite journal | vauthors = Brown EN, Kass RE, Mitra PP | title = Multiple neural spike train data analysis: state-of-the-art and future challenges | journal = Nature Neuroscience | volume = 7 | issue = 5 | pages = 456–61 | date = May 2004 | pmid = 15114358 | doi = 10.1038/nn1228 | s2cid = 562815 }}</ref> It is thought that neurons can encode both [[Digital data|digital]] and [[analog signal|analog]] information.<ref>{{cite book | vauthors = Thorpe SJ |chapter=Spike arrival times: A highly efficient coding scheme for neural networks |chapter-url= http://pop.cerco.ups-tlse.fr/fr_vers/documents/thorpe_sj_90_91.pdf |pages= 91–94 |title=Parallel processing in neural systems and computers| veditors = Eckmiller R, Hartmann G, Hauske G |date=1990|publisher=North-Holland|isbn=978-0-444-88390-2 |url={{google books |plainurl=y |id=boBqAAAAMAAJ}}|language=en|archive-url=https://web.archive.org/web/20120215151304/http://pop.cerco.ups-tlse.fr/fr_vers/documents/thorpe_sj_90_91.pdf|archive-date=2012-02-15}}</ref>

==All-or-none principle==
[[File:All-or-none law en.svg|thumb|318x318px|As long as the stimulus reaches the threshold, the full response will be given. A larger stimulus does not result in a larger response, and vice versa.<ref name="Kalat, James W-2016">{{Cite book |last=Kalat, James W |title=Biological psychology |publisher=Cengage Learning |year=2016 |isbn=978-1-305-10540-9 |edition=12 |location=Australia |oclc=898154491}}</ref>{{Rp|31}}]]
{{Main|All-or-none law}}
The conduction of nerve impulses is an example of an [[All-or-none law|all-or-none]] response. In other words, if a neuron responds at all, then it must respond completely. Greater intensity of stimulation, like brighter image/louder sound, does not produce a stronger signal but can increase firing frequency.<ref name="Kalat, James W-2016" />{{Rp|31}} Receptors respond in different ways to stimuli. Slowly adapting or [[tonic (physiology)|tonic receptors]] respond to a steady stimulus and produce a steady rate of firing. Tonic receptors most often respond to increased stimulus intensity by increasing their firing frequency, usually as a power function of stimulus plotted against impulses per second. This can be likened to an intrinsic property of light where greater intensity of a specific frequency (color) requires more photons, as the photons cannot become "stronger" for a specific frequency.

Other receptor types include quickly adapting or phasic receptors, where firing decreases or stops with a steady stimulus; examples include [[Human skin|skin]] which, when touched causes neurons to fire, but if the object maintains even pressure, the neurons stop firing. The neurons of the skin and muscles that are responsive to pressure and vibration have filtering accessory structures that aid their function.

The [[pacinian corpuscle]] is one such structure. It has concentric layers like an onion, which form around the axon terminal. When pressure is applied and the corpuscle is deformed, mechanical stimulus is transferred to the axon, which fires. If the pressure is steady, the stimulus ends; thus, these neurons typically respond with a transient depolarization during the initial deformation and again when the pressure is removed, which causes the corpuscle to change shape again. Other types of adaptation are important in extending the function of several other neurons.<ref>{{cite book | last1 = Eckert | first1 = Roger | last2 = Randall | first2 = David | name-list-style = vanc | title = Animal physiology: mechanisms and adaptations | year = 1983 | publisher = W.H. Freeman | location = San Francisco | isbn = 978-0-7167-1423-1 | page = [https://archive.org/details/animalphysiology0000ecke/page/239 239] | url = https://archive.org/details/animalphysiology0000ecke/page/239 }}</ref>

Although neurons have long been assumed to always give a stereotyped maximal response or none at all, there is a body of research that argues that this is only partially correct, and that while it is true that Neurons either fire an Action Potential or do not, the amplitude and duration of the Action Potentials that a Neuron fires can vary greatly, allowing the Neuron to encode information in at least the strength of the Action Potential. Additionally, the analog information carried in the Action Potential has been shown to be able to survive and travel distances originally not thought to be possible. This has been proposed to be a highly effective way to encode information compared to the usual rate and temporal coding theories commonly seen in the literature, with the ability to transfer around 4 times more information than current wisdom would suggest.<ref>{{cite web |last1=Juusola |first1=Mikko |last2=Robinson |first2=Hugh P. C. |last3=de Polavieja |first3=Gonzalo G. |title=Coding with spike shapes and graded potentials in cortical networks |url=https://www.researchgate.net/publication/6575241_Coding_with_spike_shapes_and_graded_potentials_in_cortical_networks |website=BioEssays: News and Reviews in Molecular, Cellular and Developmental Biology |pages=178–187 |doi=10.1002/bies.20532 |date=February 2007}}</ref><ref>{{cite journal |title=Myelination Increases the Spatial Extent of Analog Modulation of Synaptic Transmission: A Modeling Study |url=https://www.researchgate.net/publication/339655307|journal=Frontiers in Cellular Neuroscience}}</ref><ref>{{cite journal |title=Past and Future of Analog-Digital Modulation of Synaptic Transmission |year=2019 |pmc=6492051 |last1=Zbili |first1=M. |last2=Debanne |first2=D. |journal=Frontiers in Cellular Neuroscience |volume=13 |page=160 |doi=10.3389/fncel.2019.00160 |pmid=31105529 |doi-access=free }}</ref><ref>{{cite journal |title=Neural Coding: Analog Signalling in Axons | journal=Current Biology | date=8 August 2006 | volume=16 | issue=15 | pages=R585–R588 | doi=10.1016/j.cub.2006.07.007 | last1=Clark | first1=Beverley | last2=Häusser | first2=Michael | pmid=16890514 | s2cid=8295969 | doi-access=free }}</ref><ref>{{cite journal |title=Analog transmission of action potential fine structure in spiral ganglion axons |year=2021 |doi=10.1152/jn.00237.2021 |last1=Liu |first1=Wenke |last2=Liu |first2=Qing |last3=Crozier |first3=Robert A. |last4=Davis |first4=Robin L. |journal=Journal of Neurophysiology |volume=126 |issue=3 |pages=888–905 |pmid=34346782 |pmc=8461829 }}</ref>

==Etymology and spelling==

The German anatomist [[Heinrich Wilhelm Gottfried von Waldeyer-Hartz|Heinrich Wilhelm Waldeyer]] introduced the term ''neuron'' in 1891,<ref name="finger"/> based on the [[Greek language|ancient Greek]] νεῦρον ''neuron'' 'sinew, cord, nerve'.<ref name="oed">''[[Oxford English Dictionary]]'', 3rd edition, 2003, ''s.v.''</ref> 

The word was adopted in French with the spelling ''neurone''. That spelling was also used by many writers in English,<ref name="Mehta">{{cite journal | vauthors = Mehta AR, Mehta PR, Anderson SP, MacKinnon BL, Compston A | title = Grey Matter Etymology and the neuron(e) | journal = Brain | volume = 143 | issue = 1 | pages = 374–379 | date = January 2020 | pmid = 31844876 | pmc = 6935745 | doi = 10.1093/brain/awz367 | url = }}</ref> but has now become rare in American usage and uncommon in British usage.<ref name="ngram">{{cite web |title=Google Books Ngram Viewer |url=https://books.google.com/ngrams/graph?content=neuron%2Cneurone&year_start=1900&year_end=2008&case_insensitive=on&corpus=15&smoothing=3&direct_url=t4%3B%2Cneuron%3B%2Cc0%3B%2Cs0%3B%3Bneuron%3B%2Cc0%3B%3BNeuron%3B%2Cc0%3B%3BNEURON%3B%2Cc0%3B.t4%3B%2Cneurone%3B%2Cc0%3B%2Cs0%3B%3Bneurone%3B%2Cc0%3B%3BNeurone%3B%2Cc0%3B%3BNEURONE%3B%2Cc0 |website=books.google.com |access-date=19 December 2020 |language=en}}</ref><ref name="oed"/>

Some previous works used ''nerve cell'' (''cellule nervose''), as adopted in [[Camillo Golgi]]'s 1873 paper on the discovery of the silver staining technique used to visualize nervous tissue under light microscopy.<ref>Golgi, C. (1873). Sulla struttura della sostanza grigia del cervello (Comunicazione preventiva). ''Gaz. Med. Ital. Lomb.'' 33, 244–246. [https://books.google.com.br/books?id=cydbAAAAcAAJ].</ref>

==History==
{{Further|History of neuroscience}}
[[File:Golgi Hippocampus.jpg|left|thumb|Drawing by Camillo Golgi of a [[hippocampus]] stained using the [[silver nitrate]] method]]
[[File:Purkinje cell by Cajal.png|thumb|Drawing of a Purkinje cell in the [[cerebellar cortex]] done by [[Santiago Ramón y Cajal]], demonstrating the ability of Golgi's staining method to reveal fine detail]]

The neuron's place as the primary functional unit of the nervous system was first recognized in the late 19th century through the work of the Spanish anatomist [[Santiago Ramón y Cajal]].<ref name="López-Muñoz">{{cite journal | vauthors = López-Muñoz F, Boya J, Alamo C | title = Neuron theory, the cornerstone of neuroscience, on the centenary of the Nobel Prize award to Santiago Ramón y Cajal | journal = Brain Research Bulletin | volume = 70 | issue = 4–6 | pages = 391–405 | date = October 2006 | pmid = 17027775 | doi = 10.1016/j.brainresbull.2006.07.010 | s2cid = 11273256 }}</ref>

To make the structure of individual neurons visible, Ramón y Cajal improved a [[Golgi's method|silver staining process]] that had been developed by [[Camillo Golgi]].<ref name="López-Muñoz" /> The improved process involves a technique called "double impregnation" and is still in use.

In 1888 Ramón y Cajal published a paper about the bird cerebellum. In this paper, he stated that he could not find evidence for [[anastomosis]] between axons and dendrites and called each nervous element "an autonomous canton."<ref name="López-Muñoz" /><ref name="finger">{{Cite book|title=Origins of neuroscience: a history of explorations into brain function|last=Finger|first=Stanley|publisher=Oxford University Press|year=1994|url=https://books.google.com/books?id=BdRqAAAAMAAJ&pg=PA47|isbn=978-0-19-514694-3|oclc=27151391|page=47 |quote=Ramon y Cajal's first paper on the Golgi stain was on the bird cerebellum, and it appeared in the ''Revista''<nowiki> in 1888. He acknowledged that he found the nerve fibers to be very intricate, but stated that he could find no evidence for either axons or dendrites undergoing anastomosis and forming nets. He called each nervous element 'an autonomous canton.'</nowiki>}}</ref> This became known as the [[neuron doctrine]], one of the central tenets of modern [[neuroscience]].<ref name="López-Muñoz" />

In 1891, the German anatomist [[Heinrich Wilhelm Gottfried von Waldeyer-Hartz|Heinrich Wilhelm Waldeyer]] wrote a highly influential review of the neuron doctrine in which he introduced the term ''neuron'' to describe the anatomical and physiological unit of the nervous system.<ref>{{Cite book|title=Origins of neuroscience: a history of explorations into brain function|last=Finger|first=Stanley|publisher=Oxford University Press|year=1994|url=https://books.google.com/books?id=BdRqAAAAMAAJ&pg=PA47|isbn=978-0-19-514694-3|oclc=27151391|page=47 |quote=... a man who would write a highly influential review of the evidence in favor of the neuron doctrine two years later. In his paper, Waldeyer (1891), ... , wrote that nerve cells terminate freely with end arborizations and that the 'neuron' is the anatomical and physiological unit of the nervous system. The word 'neuron' was born this way.}}</ref><ref>{{cite web|url=http://www.whonamedit.com/doctor.cfm/1846.html|title=Whonamedit - dictionary of medical eponyms|website=www.whonamedit.com|quote=Today, Wilhelm von Waldeyer-Hartz is remembered as the founder of the neurone theory, coining the term "neurone" to describe the cellular function unit of the nervous system and enunciating and clarifying that concept in 1891.}}</ref>

The silver impregnation stains are a useful method for [[Neuroanatomy|neuroanatomical]] investigations because, for reasons unknown, it stains only a small percentage of cells in a tissue, exposing the complete micro structure of individual neurons without much overlap from other cells.<ref name="Grant">{{cite journal | vauthors = Grant G | title = How the 1906 Nobel Prize in Physiology or Medicine was shared between Golgi and Cajal | journal = Brain Research Reviews | volume = 55 | issue = 2 | pages = 490–8 | date = October 2007 | pmid = 17306375 | doi = 10.1016/j.brainresrev.2006.11.004 | s2cid = 24331507 }}</ref>

===Neuron doctrine===
[[File:PurkinjeCell.jpg|thumb|Drawing of neurons in the pigeon [[cerebellum]], by Spanish neuroscientist [[Santiago Ramón y Cajal]] in 1899. (A) denotes [[Purkinje cell]]s and (B) denotes [[granule cells]], both of which are multipolar.]]
The neuron doctrine is the now fundamental idea that neurons are the basic structural and functional units of the nervous system. The theory was put forward by Santiago Ramón y Cajal in the late 19th century. It held that neurons are discrete cells (not connected in a meshwork), acting as metabolically distinct units.

Later discoveries yielded refinements to the doctrine. For example, [[Neuroglia|glial cells]], which are non-neuronal, play an essential role in information processing.<ref>{{cite journal | vauthors = Witcher MR, Kirov SA, Harris KM | title = Plasticity of perisynaptic astroglia during synaptogenesis in the mature rat hippocampus | journal = Glia | volume = 55 | issue = 1 | pages = 13–23 | date = January 2007 | pmid = 17001633 | doi = 10.1002/glia.20415 | citeseerx = 10.1.1.598.7002 | s2cid = 10664003 }}</ref> Also, electrical synapses are more common than previously thought,<ref>{{cite journal | vauthors = Connors BW, Long MA | title = Electrical synapses in the mammalian brain | journal = Annual Review of Neuroscience | volume = 27 | issue = 1 | pages = 393–418 | year = 2004 | pmid = 15217338 | doi = 10.1146/annurev.neuro.26.041002.131128 | url = https://zenodo.org/record/894386 }}</ref> comprising direct, cytoplasmic connections between neurons; In fact, neurons can form even tighter couplings: the squid giant axon arises from the fusion of multiple axons.<ref>{{cite journal | vauthors = Guillery RW | title = Observations of synaptic structures: origins of the neuron doctrine and its current status | journal = Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences | volume = 360 | issue = 1458 | pages = 1281–307 | date = June 2005 | pmid = 16147523 | pmc = 1569502 | doi = 10.1098/rstb.2003.1459 }}</ref>

Ramón y Cajal also postulated the Law of Dynamic Polarization, which states that a neuron receives signals at its dendrites and cell body and transmits them, as action potentials, along the axon in one direction: away from the cell body.<ref name="sabb">{{cite journal | vauthors = Sabbatini RM | date = April–July 2003 | url = http://www.cerebromente.org.br/n17/history/neurons3_i.htm | title = Neurons and Synapses: The History of Its Discovery | journal = Brain & Mind Magazine | page = 17 }}</ref> The Law of Dynamic Polarization has important exceptions; dendrites can serve as synaptic output sites of neurons<ref>{{cite journal | vauthors = Djurisic M, Antic S, Chen WR, Zecevic D | title = Voltage imaging from dendrites of mitral cells: EPSP attenuation and spike trigger zones | journal = The Journal of Neuroscience | volume = 24 | issue = 30 | pages = 6703–14 | date = July 2004 | pmid = 15282273 | pmc = 6729725 | doi = 10.1523/JNEUROSCI.0307-04.2004 | hdl = 1912/2958 }}
</ref> and axons can receive synaptic inputs.<ref>{{cite journal | vauthors = Cochilla AJ, Alford S | title = Glutamate receptor-mediated synaptic excitation in axons of the lamprey | journal = The Journal of Physiology | volume = 499 | issue = Pt 2 | pages = 443–57 | date = March 1997 | pmid = 9080373 | pmc = 1159318 | doi = 10.1113/jphysiol.1997.sp021940 }}</ref>

===Compartmental modelling of neurons===
Although neurons are often described as "fundamental units" of the brain, they perform internal computations. Neurons integrate input within dendrites, and this complexity is lost in models that assume neurons to be a fundamental unit. Dendritic branches can be modeled as spatial compartments, whose activity is related to passive membrane properties, but may also be different depending on input from synapses. [[Compartmental modelling of dendrites]] is especially helpful for understanding the behavior of neurons that are too small to record with electrodes, as is the case for ''Drosophila melanogaster''.<ref>{{cite journal | vauthors = Gouwens NW, Wilson RI | title = Signal propagation in Drosophila central neurons | journal = Journal of Neuroscience | volume = 29 | issue = 19 | pages = 6239–6249 | year = 2009 | pmid = 19439602 | pmc = 2709801 | doi = 10.1523/jneurosci.0764-09.2009 | doi-access = free }}</ref>

==Neurons in the brain==
The number of neurons in the brain varies dramatically from species to species.<ref name="nerve net">{{cite journal | vauthors = Williams RW, Herrup K | title = The control of neuron number | journal = Annual Review of Neuroscience | volume = 11 | issue = 1 | pages = 423–53 | year = 1988 | pmid = 3284447 | doi = 10.1146/annurev.ne.11.030188.002231 }}</ref> In a human, there are an estimated 10–20 billion neurons in the [[cerebral cortex]]<!--<ref name="pmid27187682" />--> and 55–70 billion neurons in the [[cerebellum]].<ref name="pmid27187682">{{cite journal | vauthors = von Bartheld CS, Bahney J, Herculano-Houzel S | title = The search for true numbers of neurons and glial cells in the human brain: A review of 150 years of cell counting | journal = The Journal of Comparative Neurology | volume = 524 | issue = 18 | pages = 3865–3895 | date = December 2016 | pmid = 27187682 | pmc = 5063692 | doi = 10.1002/cne.24040 }}</ref> By contrast, the [[nematode]] worm ''[[Caenorhabditis elegans]]'' has just 302 neurons, making it an ideal [[model organism]] as scientists have been able to map all of its neurons. The fruit fly ''[[Drosophila melanogaster]]'', a common subject in biological experiments, has around 100,000 neurons and exhibits many complex behaviors. Many properties of neurons, from the type of neurotransmitters used to ion channel composition, are maintained across species, allowing scientists to study processes occurring in more complex organisms in much simpler experimental systems.

==Neurological disorders==
{{Main|Neurological disorders}}
{{More citations needed|date=May 2018}}
[[Charcot–Marie–Tooth disease]] (CMT) is a heterogeneous inherited disorder of nerves ([[neuropathy]]) that is characterized by loss of muscle tissue and touch sensation, predominantly in the feet and legs extending to the hands and arms in advanced stages. Presently incurable, this disease is one of the most common inherited [[neurological disorder]]s, affecting 36 in 100,000 people.<ref name=Krajewski>{{cite journal | vauthors = Krajewski KM, Lewis RA, Fuerst DR, Turansky C, Hinderer SR, Garbern J, Kamholz J, Shy ME | title = Neurological dysfunction and axonal degeneration in Charcot-Marie-Tooth disease type 1A | journal = Brain | volume = 123 | issue = 7 | pages = 1516–27 | date = July 2000 | pmid = 10869062 | doi = 10.1093/brain/123.7.1516 | doi-access =  }}</ref>

[[Alzheimer's disease]] (AD), also known simply as ''Alzheimer's'', is a [[neurodegenerative disease]] characterized by progressive [[cognitive]] deterioration, together with declining activities of daily living and [[neuropsychiatric]] symptoms or behavioral changes.<ref name="nihstages">{{cite web|title=About Alzheimer's Disease: Symptoms|url=http://www.nia.nih.gov/alzheimers/topics/symptoms|publisher=National Institute on Aging|access-date=28 December 2011|archive-url=https://web.archive.org/web/20120115201854/http://www.nia.nih.gov/alzheimers/topics/symptoms|archive-date=15 January 2012|df=dmy-all}}</ref> The most striking early symptom is loss of short-term memory ([[amnesia]]), which usually manifests as minor forgetfulness that becomes steadily more pronounced with illness progression, with relative preservation of older memories. As the disorder progresses, cognitive (intellectual) impairment extends to the domains of language ([[aphasia]]), skilled movements ([[apraxia]]), and recognition ([[agnosia]]), and functions such as decision-making and planning become impaired.<ref name="BMJ2009">{{cite journal | vauthors = Burns A, Iliffe S | title = Alzheimer's disease | journal = BMJ | volume = 338 | pages = b158 | date = February 2009 | pmid = 19196745 | doi = 10.1136/bmj.b158 | s2cid = 8570146 }}</ref><ref name=NEJM2010>{{cite journal | vauthors = Querfurth HW, LaFerla FM | title = Alzheimer's disease | journal = The New England Journal of Medicine | volume = 362 | issue = 4 | pages = 329–44 | date = January 2010 | pmid = 20107219 | doi = 10.1056/NEJMra0909142 | s2cid = 205115756 }}</ref>

[[Parkinson's disease]] (PD), also known as ''Parkinson's'', is a degenerative disorder of the central nervous system that often impairs motor skills and speech.<ref name=NIH2016>{{cite web|title=Parkinson's Disease Information Page|url=https://www.ninds.nih.gov/health-information/disorders/parkinsons-disease|website=NINDS|access-date=18 July 2016|date=30 June 2016|url-status=live|archive-url=https://web.archive.org/web/20170104201403/http://www.ninds.nih.gov/Disorders/All-Disorders/Parkinsons-Disease-Information-Page|archive-date=4 January 2017|df=dmy-all}}</ref> Parkinson's disease belongs to a group of conditions called [[movement disorders]].<ref>{{cite web | title = Movement Disorders| url = http://www.neuromodulation.com/movement-disorders | work = The International Neuromodulation Society }}</ref> It is characterized by muscle rigidity, [[tremor]], a slowing of physical movement ([[bradykinesia]]), and in extreme cases, a loss of physical movement ([[akinesia]]). The primary symptoms are the results of decreased stimulation of the [[motor cortex]] by the [[basal ganglia]], normally caused by the insufficient formation and action of dopamine, which is produced in the [[dopaminergic neurons]] of the brain. Secondary symptoms may include high-level [[cognitive dysfunction]] and subtle language problems. PD is both chronic and progressive.

[[Myasthenia gravis]] is a [[neuromuscular disease]] leading to fluctuating [[muscle weakness]] and fatigability during simple activities. Weakness is typically caused by circulating [[antibodies]] that block [[acetylcholine receptors]] at the postsynaptic neuromuscular junction, inhibiting the stimulative effect of the neurotransmitter acetylcholine. Myasthenia is treated with [[immunosuppressants]], [[cholinesterase]] inhibitors and, in selected cases, [[thymectomy]].

===Demyelination===
{{Further|Demyelinating disease}}
[[File:Guillain-barré syndrome - Nerve Damage.gif|thumb|[[Guillain–Barré syndrome]] – demyelination]]
[[Demyelination]] is a process characterized by the gradual loss of the myelin sheath enveloping nerve fibers. When myelin deteriorates, signal conduction along nerves can be significantly impaired or lost, and the nerve eventually withers. Demyelination may affect both central and peripheral nervous systems, contributing to various neurological disorders such as [[multiple sclerosis]], [[Guillain–Barré syndrome|Guillain-Barré syndrome]], and [[chronic inflammatory demyelinating polyneuropathy]]. Although demyelination is often caused by an [[Autoimmunity|autoimmune]] reaction, it may also be caused by viral infections, metabolic disorders, trauma, and some medications.

===Axonal degeneration===
Although most injury responses include a calcium influx signaling to promote resealing of severed parts, axonal injuries initially lead to acute [[axonal degeneration]], which is the rapid separation of the proximal and distal ends, occurring within 30 minutes of injury.<ref name="NM">{{cite journal | vauthors = Kerschensteiner M, Schwab ME, Lichtman JW, Misgeld T | s2cid = 25287010 | title = In vivo imaging of axonal degeneration and regeneration in the injured spinal cord | journal = Nature Medicine | volume = 11 | issue = 5 | pages = 572–7 | date = May 2005 | pmid = 15821747 | doi = 10.1038/nm1229 }}</ref> Degeneration follows with swelling of the [[axolemma]], and eventually leads to bead-like formation. Granular disintegration of the axonal [[cytoskeleton]] and inner [[organelle]]s occurs after axolemma degradation. Early changes include accumulation of [[mitochondria]] in the paranodal regions at the site of injury. The endoplasmic reticulum degrades and mitochondria swell up and eventually disintegrate. The disintegration is dependent on [[ubiquitin]] and [[calpain]] [[proteases]] (caused by the influx of calcium ions), suggesting that axonal degeneration is an active process that produces complete fragmentation. The process takes about roughly 24 hours in the PNS and longer in the CNS. The signaling pathways leading to axolemma degeneration are unknown.

==Development==
{{Main|Neurogenesis}}
Neurons develop through the process of [[neurogenesis]], in which [[neural stem cell]]s divide to produce [[Cellular differentiation|differentiated neurons]]. Once fully differentiated they are no longer capable of undergoing [[mitosis]]. Neurogenesis primarily occurs during [[embryonic development]].

Neurons initially develop from the [[neural tube]] in the embryo. The neural tube has three layers – a [[ventricular zone]], an [[Development of the cerebral cortex|intermediate zone]], and a marginal zone. The ventricular zone surrounds the tube's central canal and becomes the [[ependyma]]. Dividing cells of the ventricular zone form the intermediate zone which stretches to the outermost layer of the neural tube called the pial layer. The [[gray matter]] of the brain is derived from the intermediate zone. The extensions of the neurons in the intermediate zone make up the marginal zone when [[myelinated]] becomes the brain's [[white matter]].<ref name="Caire">{{cite journal |last1=Caire |first1=Michael J. |last2=Reddy |first2=Vamsi |last3=Varacallo |first3=Matthew |title=Physiology, Synapse |url=https://www.ncbi.nlm.nih.gov/books/NBK526047/ |website=StatPearls |publisher=StatPearls Publishing |access-date=10 July 2024 |date=2024|pmid=30252303 }}</ref>

Differentiation of the neurons is ordered by their size. Large [[motor neuron]]s are first. Smaller sensory neurons together with [[glial cell]] differentiate at [[birth]].<ref name="Caire"/>

[[Adult neurogenesis]] can occur and studies of the age of human neurons suggest that this process occurs only for a minority of cells and that the vast majority of neurons in the [[neocortex]] form before birth and persist without replacement. The extent to which adult neurogenesis exists in humans, and its contribution to cognition are controversial, with conflicting reports published in 2018.<ref>{{cite journal | vauthors = Kempermann G, Gage FH, Aigner L, Song H, Curtis MA, Thuret S, Kuhn HG, Jessberger S, Frankland PW, Cameron HA, Gould E, Hen R, Abrous DN, Toni N, Schinder AF, Zhao X, Lucassen PJ, Frisén J | title = Human Adult Neurogenesis: Evidence and Remaining Questions | journal = Cell Stem Cell | volume = 23 | issue = 1 | pages = 25–30 | date = July 2018 | pmid = 29681514 | pmc = 6035081 | doi = 10.1016/j.stem.2018.04.004 }}</ref>

The body contains a variety of stem cell types that can differentiate into neurons. Researchers found a way to transform human skin cells into nerve cells using [[transdifferentiation]], in which "cells are forced to adopt new identities".<ref name=twsX33>{{Cite journal |doi=10.1038/news.2011.328 | last = Callaway | first = Ewen |title= How to make a human neuron | journal = Nature |quote= By transforming cells from human skin into working nerve cells, researchers may have come up with a model for nervous-system diseases and perhaps even regenerative therapies based on cell transplants. The achievement, reported online today in ''Nature'', is the latest in a fast-moving field called transdifferentiation, in which cells are forced to adopt new identities. In the past year, researchers have converted connective tissue cells found in the skin into heart cells, blood cells, and liver cells.
 |date= 26 May 2011 }}</ref>

During [[neurogenesis]] in the mammalian brain, progenitor and stem cells progress from proliferative divisions to differentiative divisions. This progression leads to the neurons and glia that populate cortical layers. [[Epigenetics|Epigenetic]] modifications play a key role in regulating [[gene expression]] in differentiating [[neural stem cells]], and are critical for cell fate determination in the developing and adult mammalian brain. Epigenetic modifications include [[DNA methylation|DNA cytosine methylation]] to form [[5-methylcytosine]] and [[DNA demethylation|5-methylcytosine demethylation]].<ref name=Wang2016>{{cite journal | vauthors = Wang Z, Tang B, He Y, Jin P | title = DNA methylation dynamics in neurogenesis | journal = Epigenomics | volume = 8 | issue = 3 | pages = 401–14 | date = March 2016 | pmid = 26950681 | pmc = 4864063 | doi = 10.2217/epi.15.119 }}</ref>  [[DNA methylation|DNA cytosine methylation]] is catalyzed by [[DNA methyltransferase|DNA methyltransferases (DNMTs)]]. Methylcytosine demethylation is catalyzed in several stages by [[TET enzymes]] that carry out oxidative reactions (e.g. [[5-methylcytosine]] to [[5-hydroxymethylcytosine]]) and enzymes of the DNA [[base excision repair]] (BER) pathway.<ref name=Wang2016/>

At different stages of mammalian nervous system development, two DNA repair processes are employed in the repair of DNA double-strand breaks. These pathways are [[homologous recombination]]al repair used in proliferating neural precursor cells, and [[non-homologous end joining]] used mainly at later developmental stages<ref>{{cite journal | vauthors = Orii KE, Lee Y, Kondo N, McKinnon PJ | title = Selective utilization of nonhomologous end-joining and homologous recombination DNA repair pathways during nervous system development | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 103 | issue = 26 | pages = 10017–22 | date = June 2006 | pmid = 16777961 | pmc = 1502498 | doi = 10.1073/pnas.0602436103 | bibcode = 2006PNAS..10310017O | doi-access = free }}</ref>

Intercellular communication between developing neurons and [[microglia]] is also indispensable for proper neurogenesis and brain development.<ref>{{cite journal |last1=Cserép |first1=Csaba |last2=Schwarcz |first2=Anett D. |last3=Pósfai |first3=Balázs |last4=László |first4=Zsófia I. |last5=Kellermayer |first5=Anna |last6=Környei |first6=Zsuzsanna |last7=Kisfali |first7=Máté |last8=Nyerges |first8=Miklós |last9=Lele |first9=Zsolt |last10=Katona |first10=István |title=Microglial control of neuronal development via somatic purinergic junctions |journal=Cell Reports |date=September 2022 |volume=40 |issue=12 |article-number=111369 |doi=10.1016/j.celrep.2022.111369|pmid=36130488 |pmc=9513806 |s2cid=252416407 }}</ref>

== Nerve regeneration ==
{{Main|Neuroregeneration}}
Peripheral axons can regrow if they are severed,<ref name="Yiu_2006">{{cite journal | vauthors = Yiu G, He Z | title = Glial inhibition of CNS axon regeneration | journal = Nature Reviews. Neuroscience | volume = 7 | issue = 8 | pages = 617–27 | date = August 2006 | pmid = 16858390 | pmc = 2693386 | doi = 10.1038/nrn1956 }}</ref> but one neuron cannot be functionally replaced by one of another type ([[Llinás' law]]).<ref name="llinas2014"/>

== See also ==
{{Div col|colwidth=20em}}
* [[Artificial neuron]]
* [[Bidirectional cell]]
* [[Biological neuron model]]
* [[Cellular neuroscience]]
* [[Compartmental neuron models]]
* [[Connectome]]
* [[Dogiel cell]]
* [[Growth cone]]
* [[List of animals by number of neurons]]
* [[List of neuroscience databases]]
* [[Neuronal galvanotropism]]
* [[Neuroplasticity]]
* [[Red neuron]]
* [[Sholl analysis]]
{{Div col end}}

== References ==

{{Reflist}}

== Further reading ==
{{refbegin}}
* {{cite journal | vauthors = Bullock TH, Bennett MV, Johnston D, Josephson R, Marder E, Fields RD | title = Neuroscience. The neuron doctrine, redux | journal = Science | volume = 310 | issue = 5749 | pages = 791–3 | date = November 2005 | pmid = 16272104 | doi = 10.1126/science.1114394 | s2cid = 170670241 }}
* {{Cite book | vauthors = Kandel ER, Schwartz JH, Jessell TM |year=2000 |title=[[Principles of Neural Science]] |edition=4th |publisher=McGraw-Hill |location=New York |isbn=0-8385-7701-6 }}
* {{Cite book | vauthors = Peters A, Palay SL, Webster HS |year=1991 |title=The Fine Structure of the Nervous System |edition=3rd |location=New York |publisher=Oxford University Press |isbn=0-19-506571-9 }}
* {{Cite book | vauthors = Ramón y Cajal S |year=1933 |title=Histology |edition=10th |publisher=Wood |location=Baltimore }}
* {{Cite book | vauthors = Roberts A, Bush BM |year=1981 |title=Neurones without Impulses |publisher=Cambridge University Press |location=Cambridge |isbn=0-521-29935-7 }}
* {{Cite book |title=Clinical Neuroanatomy | vauthors = Snell RS |date=2010 |publisher=Lippincott Williams & Wilkins |isbn=978-0-7817-9427-5 |language=en |url=https://books.google.com/books?id=ABPmvroyrD0C }}
{{refend}}

== External links ==
{{sister project links|d=Q43054|n=no|b=Human_Anatomy/The_Neuron|v=no|voy=no|wikt=neuron|m=no|mw=no|s=no|species=no}}
* [https://web.archive.org/web/20130425202653/http://ibro.info/ IBRO (International Brain Research Organization)]. Fostering neuroscience research especially in less well-funded countries.
* [http://NeuronBank.org NeuronBank] {{Webarchive|url=https://web.archive.org/web/20210413061850/http://neuronbank.org/ |date=2021-04-13 }} an online neuromics tool for cataloging neuronal types and synaptic connectivity.
* [https://web.archive.org/web/20190621124504/http://brainmaps.org/ High Resolution Neuroanatomical Images of Primate and Non-Primate Brains].
* The [[v:Topic:Neuroscience|Department of Neuroscience]] at [[v:|Wikiversity]], which presently offers two courses: [[v:Fundamentals of Neuroscience|Fundamentals of Neuroscience]] and [[v:Comparative Neuroscience|Comparative Neuroscience]].
* [https://www.neuinfo.org/mynif/search.php?q=Neuron&t=data&s=cover&b=0&r=20 NIF Search&nbsp;– Neuron] {{Webarchive|url=https://web.archive.org/web/20150122215813/https://www.neuinfo.org/mynif/search.php?q=Neuron&t=data&s=cover&b=0&r=20 |date=2015-01-22 }} via the [[Neuroscience Information Framework]]
* [https://web.archive.org/web/20110813070057/http://ccdb.ucsd.edu/sand/main?event=showMPByType&typeid=0&start=1&pl=y Cell Centered Database&nbsp;– Neuron]
* [http://neurolex.org/wiki/Category:Neuron Complete list of neuron types] according to the Petilla convention, at [[NeuroLex]].
* [http://NeuroMorpho.org NeuroMorpho.Org] an online database of digital reconstructions of neuronal morphology.
* [https://web.archive.org/web/20111008142032/http://www.immunoportal.com/modules.php?name=gallery2&g2_view=keyalbum.KeywordAlbum&g2_keyword=Neuron Immunohistochemistry Image Gallery: Neuron]
* [https://www.khanacademy.org/science/biology/human-biology/neuron-nervous-system/v/anatomy-of-a-neuron Khan Academy: Anatomy of a neuron]
* [http://www.histology-world.com/photoalbum/thumbnails.php?album=96 Neuron images]

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[[Category:Neurons| ]]
[[Category:Medical terminology]]