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Functional Assessment of Urinary Neuro-biogenic Amines—A COMPREHENSIVE GUIDE 

111

Tyramine

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-

rine.

In vitro

and

in vivo

studies indicate

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

amphetamines.

Effects:

Decreased

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.

Excess

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

Syndrome.

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,