Neuron

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This article is about cells in the nervous system. For other uses, see Neuron (disambiguation).
"rain cells" redirects here. For other uses, see !lial cell.
Neuron: nerve cell
"ra#ing by $antiago %am&n y 'a(al of neurons in the
pigeon cerebellum. ()) "enotes *urkin(e cells, an
e+ample of a multipolar neuron. () "enotes granule
cells, #hich are also multipolar.
NeuroLex ID sao1417703748
) neuron (,n( -r n , NYEWR -on or ,n -r n , NEWR -on. also kno#n as a neurone or nerve cell) is an
electrically e+citable cell that processes and transmits information through electrical and chemical signals.
These signals bet#een neurons occur via synapses, speciali/ed connections #ith other cells. Neurons can
connect to each other to form neural net#orks. Neurons are the core components of the nervous system, #hich
includes the brain, spinal cord and the ganglia of the peripheral nervous system (*N$) #hich comprises the
central nervous system ('N$). $peciali/ed types of neurons include0 sensory neurons #hich respond to touch,
sound, light and all other stimuli affecting the cells of the sensory organs that then send signals to the spinal
cord and brain, motor neurons that receive signals from the brain and spinal cord to cause muscle contractions
and affect glandular outputs, and interneurons #hich connect neurons to other neurons #ithin the same region
of the brain or spinal cord in neural net#orks.
) typical neuron possesses a cell body (soma), dendrites, and an a+on. The term neurite is used to describe
either a dendrite or an a+on, particularly in its undifferentiated stage. "endrites are thin structures that arise
from the cell body, often e+tending for hundreds of micrometres and branching multiple times, giving rise to a
comple+ "dendritic tree". )n a+on is a special cellular e+tension that arises from the cell body at a site called
the a+on hillock and travels for a distance, as far as 1 meter in humans or even more in other species. The cell
body of a neuron fre2uently gives rise to multiple dendrites, but never to more than one a+on, although the a+on
may branch hundreds of times before it terminates. )t the ma(ority of synapses, signals are sent from the a+on
of one neuron to a dendrite of another. There are, ho#ever, many e+ceptions to these rules0 neurons that lack
dendrites, neurons that have no a+on, synapses that connect an a+on to another a+on or a dendrite to another
dendrite, etc.
)ll neurons are electrically e+citable, maintaining voltage gradients across their membranes by means of
metabolically driven ion pumps, #hich combine #ith ion channels embedded in the membrane to generate
intracellular3versus3e+tracellular concentration differences of ions such as sodium, potassium, chloride, and
calcium. 'hanges in the cross3membrane voltage can alter the function of voltage3dependent ion channels. 4f
the voltage changes by a large enough amount, an all3or3none electrochemical pulse called an action potential is
generated, #hich travels rapidly along the cell5s a+on, and activates synaptic connections #ith other cells #hen
it arrives.
Neurons do not undergo cell division. 4n most cases, neurons are generated by special types of stem cells. )
type of glial cell, called astrocytes (named for being some#hat star3shaped), have also been observed to turn
into neurons by virtue of the stem cell characteristic pluripotency. 4n humans, neurogenesis largely ceases
during adulthood6but in t#o brain areas, the hippocampus and olfactory bulb, there is strong evidence for
generation of substantial numbers of ne# neurons.
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Contents
1 :vervie#
9 )natomy and histology
o 9.1 ;istology and internal structure
< 'lassification
o <.1 $tructural classification
<.1.1 *olarity
<.1.9 :ther
o <.9 Functional classification
<.9.1 "irection
<.9.9 )ction on other neurons
<.9.< "ischarge patterns
<.9.= 'lassification by neurotransmitter production
= 'onnectivity
> ?echanisms for propagating action potentials
@ Neural coding
A )ll3or3none principle
B ;istory
o B.1 The neuron doctrine
C Neurons in the brain
1D Neurological disorders
o 1D.1 "emyelination
o 1D.9 )+onal degeneration
11 Nerve regeneration
19 $ee also
1< %eferences
1= Further reading
1> E+ternal links
Overview
$tructure of a typical neuron
Neuron (peripheral nervous system)
"endrite
$oma
)+on
Nucleus
Node of
%anvier
)+on terminal
$ch#ann cell
?yelin sheath
)natomy of a multipolar neuron
) neuron is a speciali/ed type of cell found in the bodies of all eumeto/oans. :nly sponges and a fe# other
simpler animals lack neurons. The features that define a neuron are electrical e+citability and the presence of
synapses, #hich are comple+ membrane (unctions that transmit signals to other cells. The body5s neurons, plus
the glial cells that give them structural and metabolic support, together constitute the nervous system. 4n
vertebrates, the ma(ority of neurons belong to the central nervous system, but some reside in peripheral ganglia,
and many sensory neurons are situated in sensory organs such as the retina and cochlea.
)lthough neurons are very diverse and there are e+ceptions to nearly every rule, it is convenient to begin #ith a
schematic description of the structure and function of a "typical" neuron. ) typical neuron is divided into three
parts0 the soma or cell body, dendrites, and a+on. The soma is usually compact. the a+on and dendrites are
filaments that e+trude from it. "endrites typically branch profusely, getting thinner #ith each branching, and
e+tending their farthest branches a fe# hundred micrometers from the soma. The a+on leaves the soma at a
s#elling called the a+on hillock, and can e+tend for great distances, giving rise to hundreds of branches. Fnlike
dendrites, an a+on usually maintains the same diameter as it e+tends. The soma may give rise to numerous
dendrites, but never to more than one a+on. $ynaptic signals from other neurons are received by the soma and
dendrites. signals to other neurons are transmitted by the a+on. ) typical synapse, then, is a contact bet#een the
a+on of one neuron and a dendrite or soma of another. $ynaptic signals may be e+citatory or inhibitory. 4f the
net e+citation received by a neuron over a short period of time is large enough, the neuron generates a brief
pulse called an action potential, #hich originates at the soma and propagates rapidly along the a+on, activating
synapses onto other neurons as it goes. This is called saltatory conduction.
?any neurons fit the foregoing schema in every respect, but there are also e+ceptions to most parts of it. There
are no neurons that lack a soma, but there are neurons that lack dendrites, and others that lack an a+on.
Furthermore, in addition to the typical a+odendritic and a+osomatic synapses, there are a+oa+onic (a+on3to3
a+on) and dendrodendritic (dendrite3to3dendrite) synapses.
The key to neural function is the synaptic signaling process, #hich is partly electrical and partly chemical. The
electrical aspect depends on properties of the neuron5s membrane. Gike all animal cells, the cell body of every
neuron is enclosed by a plasma membrane, a bilayer of lipid molecules #ith many types of protein structures
embedded in it. ) lipid bilayer is a po#erful electrical insulator, but in neurons, many of the protein structures
embedded in the membrane are electrically active. These include ion channels that permit electrically charged
ions to flo# across the membrane, and ion pumps that actively transport ions from one side of the membrane to
the other. ?ost ion channels are permeable only to specific types of ions. $ome ion channels are voltage gated,
meaning that they can be s#itched bet#een open and closed states by altering the voltage difference across the
membrane. :thers are chemically gated, meaning that they can be s#itched bet#een open and closed states by
interactions #ith chemicals that diffuse through the e+tracellular fluid. The interactions bet#een ion channels
and ion pumps produce a voltage difference across the membrane, typically a bit less than 1,1D of a volt at
baseline. This voltage has t#o functions0 first, it provides a po#er source for an assortment of voltage3
dependent protein machinery that is embedded in the membrane. second, it provides a basis for electrical signal
transmission bet#een different parts of the membrane.
Neurons communicate by chemical and electrical synapses in a process kno#n as neurotransmission also called
synaptic transmission. The fundamental process that triggers the release of neurotransmitters is the action
potential, a propagating electrical signal that is generated by e+ploiting the electrically e+citable membrane of
the neuron. This is also kno#n as a #ave of depolari/ation.
Anatomy and histology
"iagram of a typical myelinated vertebrate motor neuron
Neurons are highly speciali/ed for the processing and transmission of cellular signals. !iven their diversity of
functions performed in different parts of the nervous system, there is, as e+pected, a #ide variety in their shape,
si/e, and electrochemical properties. For instance, the soma of a neuron can vary from = to 1DD micrometers in
diameter.
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The soma is the body of the neuron. )s it contains the nucleus, most protein synthesis occurs here. The
nucleus can range from < to 1B micrometers in diameter.
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The dendrites of a neuron are cellular e+tensions #ith many branches. This overall shape and structure
is referred to metaphorically as a dendritic tree. This is #here the ma(ority of input to the neuron occurs
via the dendritic spine.
The a+on is a finer, cable3like pro(ection that can e+tend tens, hundreds, or even tens of thousands of
times the diameter of the soma in length. The a+on carries nerve signals a#ay from the soma (and also
carries some types of information back to it). ?any neurons have only one a+on, but this a+on may6
and usually #ill6undergo e+tensive branching, enabling communication #ith many target cells. The
part of the a+on #here it emerges from the soma is called the a+on hillock. esides being an anatomical
structure, the a+on hillock is also the part of the neuron that has the greatest density of voltage3
dependent sodium channels. This makes it the most easily e+cited part of the neuron and the spike
initiation /one for the a+on0 in electrophysiological terms it has the most negative action potential
threshold. While the a+on and a+on hillock are generally involved in information outflo#, this region
can also receive input from other neurons.
The a+on terminal contains synapses, speciali/ed structures #here neurotransmitter chemicals are
released to communicate #ith target neurons.
)lthough the canonical vie# of the neuron attributes dedicated functions to its various anatomical components,
dendrites and a+ons often act in #ays contrary to their so3called main function.
)+ons and dendrites in the central nervous system are typically only about one micrometer thick, #hile some in
the peripheral nervous system are much thicker. The soma is usually about 1DH9> micrometers in diameter and
often is not much larger than the cell nucleus it contains. The longest a+on of a human motoneuron can be over
a meter long, reaching from the base of the spine to the toes. $ensory neurons have a+ons that run from the toes
to the dorsal columns, over 1.> meters in adults. !iraffes have single a+ons several meters in length running
along the entire length of their necks. ?uch of #hat is kno#n about a+onal function comes from studying the
s2uid giant a+on, an ideal e+perimental preparation because of its relatively immense si/e (D.>H1 millimeters
thick, several centimeters long).
Fully differentiated neurons are permanently postmitotic.
7>8
ho#ever, recent research sho#s that additional
neurons throughout the brain can originate from neural stem cells found throughout the brain but in particularly
high concentrations in the subventricular /one and subgranular /one through the process of neurogenesis.
7@8
Histology and internal structure
!olgi3stained neurons in human hippocampal tissue
Nerve cell bodies stained #ith basophilic dyes sho# numerous microscopic clumps of Nissl substance (named
after !erman psychiatrist and neuropathologist Fran/ Nissl, 1B@DH1C1C), #hich consists of rough endoplasmic
reticulum and associated ribosomal %N). The prominence of the Nissl substance can be e+plained by the fact
that nerve cells are metabolically very active, and hence are involved in large amounts of protein synthesis.
The cell body of a neuron is supported by a comple+ mesh of structural proteins called neurofilaments, #hich
are assembled into larger neurofibrils. $ome neurons also contain pigment granules, such as neuromelanin (a
bro#nish3black pigment, byproduct of synthesis of catecholamines) and lipofuscin (yello#ish3bro#n pigment
that accumulates #ith age).
There are different internal structural characteristics bet#een a+ons and dendrites. Typical a+ons almost never
contain ribosomes, e+cept some in the initial segment. "endrites contain granular endoplasmic reticulum or
ribosomes, #ith diminishing amounts #ith distance from the cell body.
Classiication
4mage of pyramidal neurons in mouse cerebral corte+ e+pressing green fluorescent protein. The red staining
indicates !))ergic interneurons.
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$?4<93stained pyramidal neurons in cerebral corte+
Neurons e+ist in a number of different shapes and si/es and can be classified by their morphology and function.
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The anatomist 'amillo !olgi grouped neurons into t#o types. type 4 #ith long a+ons used to move signals
over long distances and type 44 #ith short a+ons, #hich can often be confused #ith dendrites. Type 4 cells can
be further divided by #here the cell body or soma is located. The basic morphology of type 4 neurons,
represented by spinal motor neurons, consists of a cell body called the soma and a long thin a+on covered by
the myelin sheath. )round the cell body is a branching dendritic tree that receives signals from other neurons.
The end of the a+on has branching terminals (a+on terminal) that release neurotransmitters into a gap called the
synaptic cleft bet#een the terminals and the dendrites of the ne+t neuron.
!tructural classiication
"olarity
"ifferent kinds of neurons0
1 Fnipolar neuron
9 ipolar neuron
< ?ultipolar neuron
= *seudounipolar neuron
?ost neurons can be anatomically characteri/ed as0
Fnipolar or pseudounipolar0 dendrite and a+on emerging from same process.
ipolar0 a+on and single dendrite on opposite ends of the soma.
?ultipolar0 t#o or more dendrites, separate from the a+on0
o !olgi 40 neurons #ith long3pro(ecting a+onal processes. e+amples are pyramidal cells, *urkin(e
cells, and anterior horn cells.
o !olgi 440 neurons #hose a+onal process pro(ects locally. the best e+ample is the granule cell.
)na+onic0 #here a+on cannot be distinguished from dendrites.
Other
Furthermore, some uni2ue neuronal types can be identified according to their location in the nervous system
and distinct shape. $ome e+amples are0
asket cells, interneurons that form a dense ple+us of terminals around the soma of target cells, found in
the corte+ and cerebellum.
et/ cells, large motor neurons.
Gugaro cells, interneurons of the cerebellum.
?edium spiny neurons, most neurons in the corpus striatum.
*urkin(e cells, huge neurons in the cerebellum, a type of !olgi 4 multipolar neuron.
*yramidal cells, neurons #ith triangular soma, a type of !olgi 4.
%ensha# cells, neurons #ith both ends linked to alpha motor neurons.
Fnipolar brush cells, interneurons #ith uni2ue dendrite ending in a brush3like tuft.
!ranule cells, a type of !olgi 44 neuron.
)nterior horn cells, motoneurons located in the spinal cord.
$pindle cells, interneurons that connect #idely separated areas of the brain
#unctional classiication
Direction
)fferent neurons convey information from tissues and organs into the central nervous system and are
sometimes also called sensory neurons.
Efferent neurons transmit signals from the central nervous system to the effector cells and are
sometimes called motor neurons.
4nterneurons connect neurons #ithin specific regions of the central nervous system.
)fferent and efferent also refer generally to neurons that, respectively, bring information to or send information
from the brain region.
Action on other neurons
) neuron affects other neurons by releasing a neurotransmitter that binds to chemical receptors. The effect upon
the postsynaptic neuron is determined not by the presynaptic neuron or by the neurotransmitter, but by the type
of receptor that is activated. ) neurotransmitter can be thought of as a key, and a receptor as a lock0 the same
type of key can here be used to open many different types of locks. %eceptors can be classified broadly as
excitatory (causing an increase in firing rate), inhibitory (causing a decrease in firing rate), or modulatory
(causing long3lasting effects not directly related to firing rate).
The t#o most common neurotransmitters in the brain, glutamate and !)), have actions that are largely
consistent. !lutamate acts on several different types of receptors, and have effects that are e+citatory at
ionotropic receptors and a modulatory effect at metabotropic receptors. $imilarly !)) acts on several
different types of receptors, but all of them have effects (in adult animals, at least) that are inhibitory. ecause
of this consistency, it is common for neuroscientists to simplify the terminology by referring to cells that release
glutamate as "e+citatory neurons", and cells that release !)) as "inhibitory neurons". $ince over CDI of the
neurons in the brain release either glutamate or !)), these labels encompass the great ma(ority of neurons.
There are also other types of neurons that have consistent effects on their targets, for e+ample "e+citatory"
motor neurons in the spinal cord that release acetylcholine, and "inhibitory" spinal neurons that release glycine.
The distinction bet#een e+citatory and inhibitory neurotransmitters is not absolute, ho#ever. %ather, it depends
on the class of chemical receptors present on the postsynaptic neuron. 4n principle, a single neuron, releasing a
single neurotransmitter, can have e+citatory effects on some targets, inhibitory effects on others, and
modulatory effects on others still. For e+ample, photoreceptor cells in the retina constantly release the
neurotransmitter glutamate in the absence of light. $o3called :FF bipolar cells are, like most neurons, e+cited
by the released glutamate. ;o#ever, neighboring target neurons called :N bipolar cells are instead inhibited by
glutamate, because they lack the typical ionotropic glutamate receptors and instead e+press a class of inhibitory
metabotropic glutamate receptors.
7C8
When light is present, the photoreceptors cease releasing glutamate, #hich
relieves the :N bipolar cells from inhibition, activating them. this simultaneously removes the e+citation from
the :FF bipolar cells, silencing them.
4t is possible to identify the type of inhibitory effect a presynaptic neuron #ill have on a postsynaptic neuron,
based on the proteins the presynaptic neuron e+presses. *arvalbumin3e+pressing neurons typically dampen the
output signal of the postsynaptic neuron in the visual corte+, #hereas somatostatin3e+pressing neurons typically
block dendritic inputs to the postsynaptic neuron.
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Discharge patterns
Neurons can be classified according to their electrophysiological characteristics0
$onic or regular spi%ing. $ome neurons are typically constantly (or tonically) active. E+ample0
interneurons in neurostriatum.
"hasic or &ursting. Neurons that fire in bursts are called phasic.
#ast spi%ing. $ome neurons are notable for their high firing rates, for e+ample some types of cortical
inhibitory interneurons, cells in globus pallidus, retinal ganglion cells.
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Classiication &y neurotransmitter production
'holinergic neurons6acetylcholine. )cetylcholine is released from presynaptic neurons into the
synaptic cleft. 4t acts as a ligand for both ligand3gated ion channels and metabotropic (!*'%s)
muscarinic receptors. Nicotinic receptors, are pentameric ligand3gated ion channels composed of alpha
and beta subunits that bind nicotine. Gigand binding opens the channel causing influ+ of Na
J

depolari/ation and increases the probability of presynaptic neurotransmitter release.
!))ergic neurons6gamma aminobutyric acid. !)) is one of t#o neuroinhibitors in the 'N$, the
other being !lycine. !)) has a homologous function to )'h, gating anion channels that allo# 'l
K

ions to enter the post synaptic neuron. 'l
K
causes hyperpolari/ation #ithin the neuron, decreasing the
probability of an action potential firing as the voltage becomes more negative (recall that for an action
potential to fire, a positive voltage threshold must be reached).
!lutamatergic neurons6glutamate. !lutamate is one of t#o primary e+citatory amino acids, the other
being )spartate. !lutamate receptors are one of four categories, three of #hich are ligand3gated ion
channels and one of #hich is a !3protein coupled receptor (often referred to as !*'%).
1. )?*) and Lainate receptors both function as cation channels permeable to Na
J
cation channels
mediating fast e+citatory synaptic transmission
9. N?") receptors are another cation channel that is more permeable to 'a
9J
. The function of
N?") receptors is dependant on !lycine receptor binding as a co3agonist #ithin the channel
pore. N?") receptors do not function #ithout both ligands present.
<. ?etabotropic receptors, !*'%s modulate synaptic transmission and postsynaptic e+citability.
!lutamate can cause e+citoto+icity #hen blood flo# to the brain is interrupted, resulting in brain
damage. When blood flo# is suppressed, glutamate is released from presynaptic neurons causing
N?") and )?*) receptor activation more so than #ould normally be the case outside of stress
conditions, leading to elevated 'a
9J
and Na
J
entering the post synaptic neuron and cell damage.
"opaminergic neurons6dopamine. "opamine is a neurotransmitter that acts on "1 type ("1 and ">)
!s coupled receptors, #hich increase c)?* and *L), and "9 type ("9, "<, and "=) receptors, #hich
activate !i3coupled receptors that decrease c)?* and *L). "opamine is connected to mood and
behavior, and modulates both pre and post synaptic neurotransmission. Goss of dopamine neurons in the
substantia nigra has been linked to *arkinson5s disease.
$erotonergic neurons6serotonin. $erotonin (>3;ydro+ytryptamine, >3;T) can act as e+citatory or
inhibitory. :f the four >3;T receptor classes, < are !*'% and 1 is ligand gated cation channel.
$erotonin is synthesi/ed from tryptophan by tryptophan hydro+ylase, and then further by aromatic acid
decarbo+ylase. ) lack of >3;T at postsynaptic neurons has been linked to depression. "rugs that block
the presynaptic serotonin transporter are used for treatment, such as *ro/ac and Moloft.
Connectivity
?ain articles0 $ynapse and 'hemical synapse
Neurons communicate #ith one another via synapses, #here the a+on terminal or en passant boutons (terminals
located along the length of the a+on) of one cell impinges upon another neuron5s dendrite, soma or, less
commonly, a+on. Neurons such as *urkin(e cells in the cerebellum can have over 1DDD dendritic branches,
making connections #ith tens of thousands of other cells. other neurons, such as the magnocellular neurons of
the supraoptic nucleus, have only one or t#o dendrites, each of #hich receives thousands of synapses. $ynapses
can be e+citatory or inhibitory and either increase or decrease activity in the target neuron. $ome neurons also
communicate via electrical synapses, #hich are direct, electrically conductive (unctions bet#een cells.
7citation needed8
4n a chemical synapse, the process of synaptic transmission is as follo#s0 #hen an action potential reaches the
a+on terminal, it opens voltage3gated calcium channels, allo#ing calcium ions to enter the terminal. 'alcium
causes synaptic vesicles filled #ith neurotransmitter molecules to fuse #ith the membrane, releasing their
contents into the synaptic cleft. The neurotransmitters diffuse across the synaptic cleft and activate receptors on
the postsynaptic neuron. ;igh cytosolic calcium in the a+on terminal also triggers mitochondrial calcium
uptake, #hich, in turn, activates mitochondrial energy metabolism to produce )T* to support continuous
neurotransmission.
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The human brain has a huge number of synapses. Each of the 1D
11
(one hundred billion) neurons has on average
A,DDD synaptic connections to other neurons. 4t has been estimated that the brain of a three3year3old child has
about 1D
1>
synapses (1 2uadrillion). This number declines #ith age, stabili/ing by adulthood. Estimates vary for
an adult, ranging from 1D
1=
to > + 1D
1=
synapses (1DD to >DD trillion).
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'echanisms or propagating action potentials
) signal propagating do#n an a+on to the cell body and dendrites of the ne+t cell
4n 1C<A, Nohn Machary Ooung suggested that the s2uid giant a+on could be used to study neuronal electrical
properties.
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eing larger than but similar in nature to human neurons, s2uid cells #ere easier to study. y
inserting electrodes into the giant s2uid a+ons, accurate measurements #ere made of the membrane potential.
The cell membrane of the a+on and soma contain voltage3gated ion channels that allo# the neuron to generate
and propagate an electrical signal (an action potential). These signals are generated and propagated by charge3
carrying ions including sodium (Na
J
), potassium (L
J
), chloride ('l
K
), and calcium ('a
9J
).
There are several stimuli that can activate a neuron leading to electrical activity, including pressure, stretch,
chemical transmitters, and changes of the electric potential across the cell membrane.
71@8
$timuli cause specific
ion3channels #ithin the cell membrane to open, leading to a flo# of ions through the cell membrane, changing
the membrane potential.
Thin neurons and a+ons re2uire less metabolic e+pense to produce and carry action potentials, but thicker a+ons
convey impulses more rapidly. To minimi/e metabolic e+pense #hile maintaining rapid conduction, many
neurons have insulating sheaths of myelin around their a+ons. The sheaths are formed by glial cells0
oligodendrocytes in the central nervous system and $ch#ann cells in the peripheral nervous system. The sheath
enables action potentials to travel faster than in unmyelinated a+ons of the same diameter, #hilst using less
energy. The myelin sheath in peripheral nerves normally runs along the a+on in sections about 1 mm long,
punctuated by unsheathed nodes of %anvier, #hich contain a high density of voltage3gated ion channels.
?ultiple sclerosis is a neurological disorder that results from demyelination of a+ons in the central nervous
system.
$ome neurons do not generate action potentials, but instead generate a graded electrical signal, #hich in turn
causes graded neurotransmitter release. $uch nonspiking neurons tend to be sensory neurons or interneurons,
because they cannot carry signals long distances.
Neural coding
Neural coding is concerned #ith ho# sensory and other information is represented in the brain by neurons. The
main goal of studying neural coding is to characteri/e the relationship bet#een the stimulus and the individual
or ensemble neuronal responses, and the relationships amongst the electrical activities of the neurons #ithin the
ensemble.
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4t is thought that neurons can encode both digital and analog information.
71B8
All(or(none principle
The conduction of nerve impulses is an e+ample of an all3or3none response. 4n other #ords, if a neuron
responds at all, then it must respond completely. !reater intensity of stimulation does not produce a stronger
signal but can produce a higher fre2uency of firing. There are different types of receptor response to stimulus,
slo#ly adapting or tonic receptors respond to steady stimulus and produce a steady rate of firing. These tonic
receptors most often respond to increased intensity of stimulus by increasing their firing fre2uency, usually as a
po#er function of stimulus plotted against impulses per second. This can be likened to an intrinsic property of
light #here to get greater intensity of a specific fre2uency (color) there have to be more photons, as the photons
can5t become "stronger" for a specific fre2uency.
There are a number of other receptor types that are called 2uickly adapting or phasic receptors, #here firing
decreases or stops #ith steady stimulus. e+amples include0 skin #hen touched by an ob(ect causes the neurons
to fire, but if the ob(ect maintains even pressure against the skin, 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. 4t has concentric layers like an onion, #hich form around the a+on
terminal. When pressure is applied and the corpuscle is deformed, mechanical stimulus is transferred to the
a+on, #hich fires. 4f the pressure is steady, there is no more stimulus. thus, typically these neurons respond #ith
a transient depolari/ation during the initial deformation and again #hen the pressure is removed, #hich causes
the corpuscle to change shape again. :ther types of adaptation are important in e+tending the function of a
number of other neurons.
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History
Further information0 ;istory of neuroscience
"ra#ing by 'amillo !olgi of a hippocampus stained using the silver nitrate method
"ra#ing of a *urkin(e cell in the cerebellar corte+ done by $antiago %am&n y 'a(al, demonstrating the ability
of !olgi5s staining method to reveal fine detail
The term neuron #as coined by the !erman anatomist ;einrich Wilhelm Waldeyer. The neuron5s place as the
primary functional unit of the nervous system #as first recogni/ed in the early 9Dth century through the #ork of
the $panish anatomist $antiago %am&n y 'a(al.
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%am&n y 'a(al proposed that neurons #ere discrete cells that
communicated #ith each other via speciali/ed (unctions, or spaces, bet#een cells.
79D8
This became kno#n as the
neuron doctrine, one of the central tenets of modern neuroscience.
79D8
To observe the structure of individual
neurons, %am&n y 'a(al improved a silver staining process kno#n as !olgi5s method, #hich had been
developed by his rival, 'amillo !olgi.
79D8
'a(al5s improvement, #hich involved a techni2ue he called "double
impregnation", is still in use. The silver impregnation stains are an e+tremely useful method for
neuroanatomical investigations because, for reasons unkno#n, it stains a very small percentage of cells in a
tissue, so one is able to see the complete micro structure of individual neurons #ithout much overlap from other
cells in the densely packed brain.
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$he neuron doctrine
The neuron doctrine is the no# fundamental idea that neurons are the basic structural and functional units of the
nervous system. The theory #as put for#ard by $antiago %am&n y 'a(al in the late 1Cth century. 4t held that
neurons are discrete cells (not connected in a mesh#ork), acting as metabolically distinct units.
Gater discoveries yielded a fe# refinements to the simplest form of the doctrine. For e+ample, glial cells, #hich
are not considered neurons, play an essential role in information processing.
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)lso, electrical synapses are
more common than previously thought,
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meaning that there are direct, cytoplasmic connections bet#een
neurons. 4n fact, there are e+amples of neurons forming even tighter coupling0 the s2uid giant a+on arises from
the fusion of multiple a+ons.
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%am&n y 'a(al also postulated the Ga# of "ynamic *olari/ation, #hich states that a neuron receives signals at
its dendrites and cell body and transmits them, as action potentials, along the a+on in one direction0 a#ay from
the cell body.
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The Ga# of "ynamic *olari/ation has important e+ceptions. dendrites can serve as synaptic
output sites of neurons
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and a+ons can receive synaptic inputs.
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Neurons in the &rain
The number of neurons in the brain varies dramatically from species to species.
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:ne estimate (published in
1CBB) puts the human brain at about 1DD billion (1D
11
) neurons and 1DD trillion (1D
1=
) synapses.
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) lo#er
estimate (published in 9DDC) is B@ billion neurons, of #hich 1@.< billion are in the cerebral corte+, and @C
billion in the cerebellum.
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y contrast, the nematode #orm Caenorhabditis elegans has (ust <D9 neurons,
making it an ideal e+perimental sub(ect as scientists have been able to map all of the organism5s neurons. The
fruit fly Drosophila melanogaster, a common sub(ect in biological e+periments, has around 1DD,DDD neurons
and e+hibits many comple+ behaviors. ?any properties of neurons, from the type of neurotransmitters used to
ion channel composition, are maintained across species, allo#ing scientists to study processes occurring in
more comple+ organisms in much simpler e+perimental systems.
Neurological disorders
?ain article0 Neurology
Charcot)'arie)$ooth disease ('?T), also kno#n as hereditary motor and sensory neuropathy (;?$N),
hereditary sensorimotor neuropathy and peroneal muscular atrophy, is a heterogeneous inherited disorder of
nerves (neuropathy) that is characteri/ed by loss of muscle tissue and touch sensation, predominantly in the feet
and legs but also in the hands and arms in the advanced stages of disease. *resently incurable, this disease is
one of the most common inherited neurological disorders, #ith <A in 1DD,DDD affected.
Al*heimer+s disease ()"), also kno#n simply as Alzheimers, is a neurodegenerative disease characteri/ed by
progressive cognitive deterioration together #ith declining activities of daily living and neuropsychiatric
symptoms or behavioral changes. The most striking early symptom is loss of short3term memory (amnesia),
#hich usually manifests as minor forgetfulness that becomes steadily more pronounced #ith illness
progression, #ith relative preservation of older memories. )s the disorder progresses, cognitive (intellectual)
impairment e+tends to the domains of language (aphasia), skilled movements (apra+ia), and recognition
(agnosia), and functions such as decision3making and planning become impaired.
"ar%inson+s disease (*"), also kno#n as !ar"inson disease, is a degenerative disorder of the central nervous
system that often impairs the sufferer5s motor skills and speech. *arkinson5s disease belongs to a group of
conditions called movement disorders. 4t is characteri/ed by muscle rigidity, tremor, a slo#ing of physical
movement (bradykinesia), and in e+treme cases, a loss of physical movement (akinesia). The primary
symptoms are the results of decreased stimulation of the motor corte+ by the basal ganglia, normally caused by
the insufficient formation and action of dopamine, #hich is produced in the dopaminergic neurons of the brain.
$econdary symptoms may include high level cognitive dysfunction and subtle language problems. *" is both
chronic and progressive.
'yasthenia gravis is a neuromuscular disease leading to fluctuating muscle #eakness and fatigability during
simple activities. Weakness is typically caused by circulating antibodies that block acetylcholine receptors at
the post3synaptic neuromuscular (unction, inhibiting the stimulative effect of the neurotransmitter acetylcholine.
?yasthenia is treated #ith immunosuppressants, cholinesterase inhibitors and, in selected cases, thymectomy.
Demyelination
"emyelination is the act of demyelinating, or the loss of the myelin sheath insulating the nerves. When myelin
degrades, conduction of signals along the nerve can be impaired or lost, and the nerve eventually #ithers. This
leads to certain neurodegenerative disorders like multiple sclerosis and chronic inflammatory demyelinating
polyneuropathy.
Axonal degeneration
)lthough most in(ury responses include a calcium influ+ signaling to promote resealing of severed parts, a+onal
in(uries initially lead to acute a+onal degeneration, #hich is rapid separation of the pro+imal and distal ends
#ithin <D minutes of in(ury. "egeneration follo#s #ith s#elling of the a+olemma, and eventually leads to bead
like formation. !ranular disintegration of the a+onal cytoskeleton and inner organelles occurs after a+olemma
degradation. Early changes include accumulation of mitochondria in the paranodal regions at the site of in(ury.
Endoplasmic reticulum degrades and mitochondria s#ell up and eventually disintegrate. The disintegration is
dependent on ubi2uitin and calpain proteases (caused by influ+ of calcium ion), suggesting that a+onal
degeneration is an active process. Thus the a+on undergoes complete fragmentation. The process takes about
roughly 9= hrs in the *N$, and longer in the 'N$. The signaling path#ays leading to a+olemma degeneration
are currently unkno#n.
Nerve regeneration
?ain article0 Neuroregeneration
4t has been demonstrated that neurogenesis can sometimes occur in the adult vertebrate brain, a finding that led
to controversy in 1CCC.
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;o#ever, more recent studies of the age of human neurons suggest that this process
occurs only for a minority of cells, and the over#helming ma(ority of neurons comprising the neocorte+ #ere
formed before birth and persist #ithout replacement.
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4t is often possible for peripheral a+ons to regro# if they are severed. %ecent studies have also sho#n that the
body contains a variety of stem cell types that have the capacity to differentiate into neurons. ) report in #ature
suggested that researchers had found a #ay to transform human skin cells into #orking nerve cells using a
process called transdifferentiation in #hich "cells are forced to adopt ne# identities".
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