Functional Assessment of Urinary Neuro-biogenic Amines—A COMPREHENSIVE GUIDE
Tyramine is a trace amine derived
from the essential amino acid phenylal-
anine. Trace amines are not considered
neurotransmitters, they are believed to
act as neuromodulators. The interaction
of trace amines, and their receptors, in
the brain may play a role in psychiat-
ric and neurological disease processes.
Experimental evidence suggests that
dysregulation of trace amines may al-
ter the levels of dopamine, norepineph-
rine or serotonin, and thereby contrib-
ute to neuropsychiatric disorders such
as attention deficit hyperactivity disor-
der (ADHD), schizophrenia, depres-
sion and neurodegenerative diseases.
Tyramine may potentiate neuron re-
sponses to dopamine and norepineph-
that tyramine and phenylethylamine
(PEA) may enhance neuron response
to norepinephrine and dopamine signal-
ing and may decrease post-synaptic re-
sponses to GABA-B receptor signaling.
As a neuromodulator, evidence indicates
that tyramine may also alter neuron re-
sponsiveness to monoamine neurotrans-
mitters such as histamine and serotonin.
Tyramine has been shown to inhibit the
responses of gamma-aminobutyric acid
(GABA) receptors in vitro and both in
vitro and in vivo studies indicate that ty-
ramine may inhibit prolactin secretion.
Trace amines may also alter neuron ac-
tive transport mechanisms and vesicle
dynamics. Clinically, trace amines are
generally considered sympathomimetic
(they mimic the action of sympathet-
ic nerve stimulation), they may affect
vasoconstriction and blood pressure.
In large, supra-physiologic doses, the
effects of trace amines are similar to
levels of tyramine or de-
ficient trace amine functions may con-
tribute to some depressive disorders.
Altered aromatic L-amino acid decar-
boxylase (AADC) activity may alter
trace amine levels which may affect do-
pamine signaling. Activation of mono-
amine neurotransmitter receptors (via
receptor agonists or electrical stimula-
tion) decreases AADC activity and trace
amine levels. Loss of D-neurons con-
taining AADC has been associated with
some forms of schizophrenia. Reserpine
may deplete CNS levels of trace amines.
tyramine and increased
AADC activity have been associat-
ed with some forms of schizophrenia,
and may resemble the effects of am-
phetamines: increased alertness, irrita-
bility, euphoria, insomnia, tachycardia,
tremor, decreased appetite and chang-
es in blood pressure. Nausea, vomiting,
shortness of breath, sweating, increased
body temperature, and headache have
also been reported. Excess tryamine in
the kidney may increase urine output.
Increased AADC activity may increase
trace amine levels without affecting the
levels of monoamine neurotransmitters.
Decreased monoamine neurotransmit-
ter receptor activation (receptor an-
tagonists, neurotransmitter depletion)
may result in an increase in AADC ac-
tivity and increased trace amine levels.
Elevated plasma and urinary tyramine
levels have been reported in Reye’s
Elevated tyramine levels do not
seem to correlate with migraine or clus-
ter headaches in research, but elevated
levels of the tyramine metabolite octo-
pamine have been associated with mi-
graine and cluster headaches. Tyramine
and other sympathomimetic amines,