Norepinephrine

Norepinephrine (INN) (abbreviated norepi or NE), also

called noradrenaline (BAN) (abbreviated NA, NAd,
or norad), or 4,5--trihydroxy phenethylamine is a
catecholamine with multiple roles including those as
a hormone and a neurotransmitter.[1] It is the hormone and neurotransmitter most responsible for vigilant
concentration in contrast to its most chemically similar hormone, dopamine, which is most responsible for
cognitive alertness.[2]

often limited to the increasing of blood pressure through

agonist activity on 1 and 2 receptors, and causing a
resultant increase in peripheral vascular resistance. At
high doses, and especially when it is combined with
other vasopressors, it can lead to limb ischemia and
limb death. Norepinephrine is used mainly to treat patients in vasodilatory shock states such as septic shock
and neurogenic shock, while showing fewer adverse sideeects compared to dopamine treatment.[8]

Medically it is used in those with severe hypotension. It

does this by increasing vascular tone (tension of vascular
smooth muscle) through -adrenergic receptor activation.

2 Physiological eects

Areas of the body that produce or are aected by norepinephrine are described as noradrenergic. The terms
noradrenaline (from the Latin) and norepinephrine (from
the Greek) are interchangeable, with noradrenaline being
the common name in most parts of the world. However
the U.S. National Library of Medicine[3] has promoted
norepinephrine as the favored name.

Norepinephrine is released when a host of physiological

changes are activated by a stressful event.
In the brain, this is caused in part by activation of an area
of the brain stem called the locus coeruleus (LC). This
nucleus is the origin of most norepinephrine pathways in
the brain. Noradrenergic neurons project bilaterally (send
signals to both sides of the brain) from the locus coeruleus
along distinct pathways to many locations, including the
cerebral cortex, limbic system, and the spinal cord, forming a neurotransmitter system.

One of the most important functions of norepinephrine

is its role as the neurotransmitter released from the
sympathetic neurons to aect the heart. An increase
in norepinephrine from the sympathetic nervous system
increases the rate of contractions in the heart.[4] As a
stress hormone, norepinephrine aects parts of the brain,
such as the amygdala, where attention and responses are
controlled.[5] Norepinephrine also underlies the ght-oright response, along with epinephrine, directly increasing heart rate, triggering the release of glucose from energy stores, and increasing blood ow to skeletal muscle.
It increases the brains oxygen supply.[6]

Norepinephrine is also released from postganglionic

neurons of the sympathetic nervous system, to transmit the ght-or-ight response in each tissue, respectively. The adrenal medulla can also contribute to such
post-ganglionic nerve cells, although they release norepinephrine into the blood.

2.1 Norepinephrine system

Norepinephrine is synthesized from dopamine by

dopamine -hydroxylase in the secretory granules of
the medullary chroman cells.[7] It is released from
the adrenal medulla into the blood as a hormone, and
is also a neurotransmitter in the central nervous system
and sympathetic nervous system, where it is released
from noradrenergic neurons in the locus coeruleus. The
actions of norepinephrine are carried out via the binding
to adrenergic receptors.

The noradrenergic neurons in the brain form a

neurotransmitter system, that, when activated, exerts eects on large areas of the brain. The eects are
manifested in alertness, arousal, and inuences on the
reward system.
The noradrenergic neurons originate both in the locus
coeruleus and the lateral tegmental eld. The axons of
the neurons in the locus coeruleus act on adrenergic receptors in:

Medical uses

Amygdala
Cingulate gyrus

Norepinephrine is used for hypotension as a vasopressor

medication for patients with critical hypotension. It is
given intravenously and acts on both 1 and 2 adrenergic receptors to cause vasoconstriction. Its eects are

Cingulum
Hippocampus
1

2 PHYSIOLOGICAL EFFECTS
Hypothalamus

has been shown to correlate with levels of drowsiness,

accurate task performance, and, when slightly more el Neocortex
evated, distractibility and erratic task performance. Furthermore, phasic activation of the LC is observed in re Spinal cord
sponse to both highly salient, unconditioned and taskrelevant stimuli. The phasic response occurs after stim Striatum
ulation and precedes a behavioral response in a time Thalamus
locked fashion.[19] As such, phasic activation of the LCNE system is proposed to enhance signal processing and
Some Brainstem nuclei
behavioral responses specically to task-relevant stimuli. Given the contrasting functional roles of LC tonic
Cerebellum
and phasic activity, it is plausible that projections from
this brain region are important for maintaining a balOn the other hand, axons of neurons of the lateral
ance between exploratory and goal-directed behaviors
tegmental eld act on adrenergic receptors in
that regulate probabilistic, environmental learning and
hypothalamus, for example.
corresponding decision making.
This structure explains some of the clinical uses of noreThe LC-NE system receives convergent input from
pinephrine, since a modication of this system aects
the orbitofrontal (OFC) and anterior cingulate cortices
large areas of the brain.
(ACC). The OFC has been associated with evaluation
of reward. For example, Tremblay et al. found that the
response magnitude of single-units in this region is var2.2 Role in cognition
ied with the hedonic value of a stimulus.[20] Additionally,
Cortical norepinephrine (NE) release during attention neurons in this region are activated by rewarding stimuli,
paradigms (patterns) can increase the alteration detec- but not by identication of the stimulus nor correspondtion rate (frequency at which an alteration was selected) ing response-preparation. Activation of the ACC appears
in multiple-cue probability learning during tasks involv- to reect some evaluation of cost-benet. Several studies
performance error,
ing giving predictive cues (such as auditory or visual), show ACC activation in response to [21][22][23]
[9]
negative
feedback,
or
monetary
loss.
Additionand thereby enhance subsequent learning. A. J. Yu et
[24]
ally,
ACC
responds
to
task
diculty.
Therefore,
ACC
al. developed a Bayesian framework to examine NE reactivation
may
serve
to
integrate
evaluations
of
task
diflease in instances of unexpected uncertainty, wherein a
culty
with
corresponding
outcome
information
to
gauge
drastic alteration in sensory information produces a large
disparity between top-down expectations and what actu- the benets of taking an action in regards to a particually occurs.[10] The model predicts that NE levels spike lar environmental stimulus. Conceivably, the functions
when the predictive context is switched, then subside. It of the ACC and OFC are directly related to decisionhas also been shown that lesions of the locus coeruleus making, and their projections to LC may modulate the
phasic release of NE in order to gain-modulate cortical
impair this attentional shift.[10]
responses to decision outcomes.
Similarly, several studies have implicated the LC-NE system in eliciting the P300, a cortical event-related po- LC-NE may play a signicant role in synchronizing cortential that responds to environmental stimuli with be- tical activity in response to a decision process. In comhaviorally relevant, motivational, or attention-grabbing putational modeling of decision, the most accurate and
properties.[11][12][13][14][15] The P300 may reect updat- ecient decision mechanisms are mathematically deing of prior knowledge regarding stimuli relevant for ac- ned random walk or drift-diusion processes that uticalculate the disparcurate and ecient decision making. Several studies lize single-layer neural networks to [25]
ity
in
evidence
between
two
options.
NE release gated
have searched for a P300 generator within the brain and
by
the
LC-NE
system
is
elicited
after
neurons
processing
have ultimately concluded that the potential must have a
sensory
information
have
presumably
reached
a decision
source that is distributed, synchronous and localized in
[26]
[16]
Thus,
the
phasic
burst
can
alter
activation
threshold.
This denition is ideally satised both funccortex.
in
all
cortical
processing
layers
in
a
temporally
depentionally and anatomically by the LC neuromodulatory sysdent
manner,
essentially
collapsing
the
vast
informationtem. Given its broad projection pattern and the correlation between NE release and increased sensory signal processing circuit to the outcome of a single-decision
transmission,[17] it seems likely that noradrenergic corti- layer. Brown et al. found that the addition of a phasic LC
mechanism was sucient to yield optimal performance
cal release is the neuronal mechanism of the P300.
from a single-layer decision network.[27]
Examination of the LCs tonic ring pattern has led to
speculation that it is important for the exploratory behavior essential for learning relations between sensory input, decision processing, motor output, and behavioral
feedback.[18] Tonic activation within the range of 05 Hz

3.5

2.3

Alzheimers Disease

Fasting

A study has shown that fasting leads to increased levels

of norepinephrine (NE) in the blood for up to 4 days of
fasting.[28]

2.4

Macronutrient intake

3
normetanephrine
steroid hormones
phenoxybenzamine

3.5 Alzheimers Disease

Glucose intake was found to signicantly increase plasma The norepinephrine from locus ceruleus cells in addiNE levels. In contrast, protein and fat intake was found tion to its neurotransmitter role locally diuses from
varicosities. As such, it provides an endogenous antito have no eect.[29]
inammatory agent in the microenvironment around the
neurons, glial cells, and blood vessels in the neocortex
and hippocampus.[32] Up to 70% of norepinephrine pro3 Drug interactions
jecting cells are lost in Alzheimers Disease. It has been
shown that norepinephrine stimulates mouse microglia to
Dierent medications aecting norepinephrine function suppress A-induced production of cytokines and their
have their targets at dierent points in the mechanism, phagocytosis of A, suggesting this loss might have a role
from synthesis to signal termination.
in causing this disease.[32]

3.1

Synthesis modulators

4 Chemistry

-Methyltyrosine is a substance that intervenes in norepinephrine synthesis by substituting tyrosine for tyrosine Norepinephrine is a catecholamine and a
hydroxylase, and blocking this enzyme.
phenethylamine.
The natural stereoisomer is L()-(R)-norepinephrine.
The prex nor- indicates
that norepinephrine is the next-lower homolog of
3.1.1 Vesicular transport modulators
epinephrine. The two structures dier only in that
epinephrine has a methyl group attached to its nitrogen,
This transportation can be inhibited by reserpine and
whereas the methyl group is replaced by a hydrogen
[30]
tetrabenazine.
atom in norepinephrine. The prex nor- is derived as an
abbreviation of the word normal, used to indicate a
demethylated compound.[33][34][35]
3.2 Release modulators

3.3

Receptor binding modulators

5 Mechanism

Examples include alpha blockers for the -receptors, and

beta blockers for the -receptors.
Norepinephrine is synthesized from tyrosine as a precursor, and packed into synaptic vesicles. It performs its action by being released into the synaptic cleft, where it acts
3.4 Termination modulators
on adrenergic receptors, followed by the signal termination, either by degradation of norepinephrine or by uptake
3.4.1 Uptake modulators
by surrounding cells.
Inhibitors[30] of uptake 1 include:
cocaine
tricyclic antidepressants
desipramine
phenoxybenzamine
amphetamine
reboxetine
Inhibitors[30] of uptake 2 include:

5.1 Biosynthesis
Norepinephrine is synthesized by a series of enzymatic
steps in the adrenal medulla and postganglionic neurons
of the sympathetic nervous system from the amino acid
tyrosine.

5.2 Vesicular transport

Between the decarboxylation and the nal -oxidation,
norepinephrine is transported into synaptic vesicles.

MECHANISM

For instance, there are inhibitory 2 adrenergic receptors

presynaptically that give negative feedback on release by
homotropic modulation.

5.4 Receptor binding

Main article: Adrenergic receptor
Norepinephrine performs its actions on the target cell by
binding to and activating adrenergic receptors. The target
cell expression of dierent types of receptors determines
the ultimate cellular eect, and thus norepinephrine has
dierent actions on dierent cell types.

5.5 Termination
Signal termination is a result of reuptake and degradation.
5.5.1 Uptake
Extracellular uptake of norepinephrine into the cytosol is
done either presynaptically (uptake 1) or by non-neuronal
cells in the vicinity (uptake 2). Furthermore, there
is a vesicular uptake mechanism from the cytosol into
synaptic vesicles.
5.5.2 Degradation
OH
OH

HO

NH2

Normetanephrine

Monoamine

CHO

Normetanephrine
aldehyde

HO

Aldehyde dehydrogenase

OH

OH

HO

OH

Biosynthesis of norepinephrine

Norepinephrine
OH

CHO

OH

3,4-dihydroxymandelic acid
OH

OH

HO

OH

HO

HO

Norepinephrine
aldehyde

Aldehyde reductase

HO

oxidase (MAO)

NH 2

vanillylmandelic
acid
COMT

Catechol-O-methyl transferase (COMT)

OH

OH

3-Methoxy-4-hydroxy
phenylglycol (MHPG)

HO

COMT
OH
HO

OH

HO

3,4-dihydroxyphenylglycol
This is accomplished by vesicular monoamine transporter (VMAT) in the lipid bilayer. This transporter
[39]
has equal anity for norepinephrine, epinephrine and Norepinephrine degradation. Enzymes are shown in boxes.
isoprenaline.[30]
In mammals, norepinephrine is rapidly degraded to various metabolites. The principal metabolites are:

5.3

Release

To perform its functions, norepinephrine must be released from synaptic vesicles. Many substances modulate
this release, some inhibiting it and some stimulating it.
An action potential reaches the presynaptic membrane,
which changes the membrane polarisation. Calcium ions
thus enter, resulting in vesicular fusion, releasing norepinephrine.

Normetanephrine (via the enzyme catechol-Omethyl transferase, COMT)

3,4-Dihydroxymandelic acid (via monoamine oxidase, MAO)
Vanillylmandelic
acid
(3-Methoxy-4hydroxymandelic acid), also referred to as
vanilmandelate or VMA (via MAO)

5
3-Methoxy-4-hydroxyphenylethylene
MHPG or MOPEG (via MAO)

glycol,

Epinephrine (via PNMT)[40]

In the periphery, VMA is the major metabolite of catecholamines, and is excreted unconjugated in the urine.
A minor metabolite (although the major one in the central nervous system) is MHPG, which is partly conjugated
to sulfate or glucuronide derivatives and excreted in the
urine.[41]

Nutritional sources

Philadelphia, Pennsylvania: Elsevier Inc. p. 122. ISBN

0-7216-0240-1.
[5] Tanaka M, Yoshida M, Emoto H, Ishii H (September
2000). Noradrenaline systems in the hypothalamus,
amygdala and locus coeruleus are involved in the provocation of anxiety: basic studies. Eur. J. Pharmacol. 405
(1-3): 397406. doi:10.1016/S0014-2999(00)00569-0.
PMID 11033344.
[6] The Hormone Foundation. The Endocrine System &
Types of Hormones.
[7] Introduction to Autonomic Pharmacology (PDF). Elsevier International. Link redirected to commercial site!
[8] De Backer, Daniel; et al. (4 March 2010). Comparison of Dopamine and Norepinephrine in the Treatment
of Shock. New England Journal of Medicine 362 (9):
11. doi:10.1056/nejmoa0907118.
[9] Devauges V, Sara SJ, Activation of the noradrenergic system facilitates an attentional shift in the rat. Behav. Brain
Res., 1990 Jun 18;39(1):1928.
[10] Yu, A. J.; Dayan, P. (2005). Uncertainty, neuromodulation, and attention. Neuron 46 (4): 68192.
doi:10.1016/j.neuron.2005.04.026. PMID 15944135.

Shown here is the chemical structure of L-tyrosine. The

biosynthesis of norepinephrine depends upon the presence of Ltyrosine, an amino acid building-block of many proteins in meat,
nuts, and eggs, for example.

[11] Johnson, R.; Jr (1993). On the neural generators

of the P300 component of the event-related potential.
Psychophysiology 30 (1): 9097. doi:10.1111/j.14698986.1993.tb03208.x. PMID 8416066.

The synthesis of norepinephrine depends on the presence [12] Pineda, J.A.; Foote, S.L.; Neville, H.J. (1989). Eects
of tyrosine, an amino acid found in proteins such as meat,
of Locus Coeruleus Lesions on Auditory Event-Related
nuts, and eggs. Dairy products such as cheese also conPotentials in Monkey. J. Neurosci 9 (1): 8193. PMID
2563282.
tain high amounts of tyrosine (the amino acid is named
for tyros, the Greek word for cheese). However, adult
humans readily synthesize tyrosine from phenylalanine, [13] Swick, D., Pineda, J. a, Schacher, S., & Foote, S. L.
(1994). Locus coeruleus neuronal activity in awake monan essential amino acid. Tyrosine is the precursor to
keys: relationship to auditory P300-like potentials and
dopamine, which in turn is a precursor to epinephrine and
spontaneous EEG. Experimental brain research. Exnorepinephrine.
perimentelle Hirnforschung. Exprimentation crbrale,
See also
Catecholaminergic polymorphic ventricular tachycardia
History of catecholamine research

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EXTERNAL LINKS

[31] Unless else specied in table, then ref is: Rang, H. P.

(2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4.Page 129
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(2010). Locus ceruleus controls Alzheimers disease
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Drugs. Anmol Publications. ISBN 81-261-1820-2.
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The Prex 'Nor' in
Chemical Nomenclature.
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Edinburgh: Churchill Livingstone. ISBN 0-443-071454. Page 167

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(2003). Pharmacology. Edinburgh: Churchill Livingstone. ISBN 0-443-07145-4. Page 167

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Humphrey P. Rang; Maureen M. Dale; Ritter, James
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Churchill Livingstone. ISBN 0-443-06911-5.

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[27] Brown, E. T., Gilzenrat, M. S., & Cohen, J. D. (2004).
The locus coeruleus, adaptive gain, and the optimization
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[28] Zauner, C., Schneeweiss, B., Kranz, A., Madl, C.,
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[39] Figure 11-4 in: Rod Flower; Humphrey P. Rang; Maureen M. Dale; Ritter, James M. (2007). Rang & Dales
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0-443-06911-5.
[40] Endokrynologia Kliniczna ISBN 83-200-0815-8, page
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8 External links
Mental Health: A report of surgeon general. Etiology of Anxiety Disorders
http://www.biopsychiatry.com/nordop.htm

Text and image sources, contributors, and licenses

9.1

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Norepinephrine Source: http://en.wikipedia.org/wiki/Norepinephrine?oldid=644447020 Contributors: AxelBoldt, Magnus Manske, Mav,

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9.2

Images

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