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

97

Bulletin of Clinical Psychopharmacology

vol.

21 (1) p. 73-79

Tang, Ya-Li; Wang, Shih-Wei; Lin, Shyh-Mirn

(2008)

Both inorganic and organic selenium sup-

plements can decrease brain monoamine

oxidase B enzyme activity in adult rats.

The British journal of nutrition

vol. 100 (3)

p. 660-5

Yu, Ai-Ming; Granvil, Camille P.; Haining,

Robert L.; Krausz, Kristopher W.;

Corchero, Javier et al. (2003)

The Relative Contribution of Monoamine

Oxidase and Cytochrome P450 Isozymes

to the Metabolic Deamination of the

Trace Amine Tryptamine.

J. Pharmacol. Exp. Ther.

vol. 304 (2) p.

539-546

Zucchi, R; Chiellini, G; Scanlan, T S; Grandy,

D K (2006)

Trace amine-associated receptors and their

ligands.

British journal of pharmacology

vol. 149 (8)

p. 967-78

Glutamate

Glutamate is a non-essential ami-

no acid that may be synthesized in the

body or obtained from the diet. It acts as

an excitatory neurotransmitter for meta-

bolic and oncogenic (tumor causing) sig-

naling pathways. In the central nervous

system (CNS), glutamate is recognized

as the primary excitatory neurotrans-

mitter; the glutamate signaling system

is involved in fast synaptic transmission

between neurons. Glutamate signaling

affects neuron maturation, plasticity

and higher cognitive functions (mood,

memory, behavior). In the periphery,

glutamate receptors are found in the

gastrointestinal mucosal cells. Animal

studies indicate that free glutamate in

the gut lumen activates the vagus nerve

and stimulates the brain. Glutamate sig-

naling via taste and gut receptors may

affect physiologic functions such as di-

gestion, thermoregulation and ener-

gy production. Evidence indicates that

glutamate excitatory signaling seems

uniquely dependent on coordinated ac-

tivity between CNS astroglia support

cells and neurons.

Effects:

Decreased

glutamate signaling con-

tributes to apoptosis (self-destruction)

of immature neurons. Decreased glu-

tamate signaling has been associated

with depressive disorders and psycho-

sis. Research continues into associations

between glutamate signaling and cog-

nitive disorders. Disturbances in gluta-

mine metabolism, glutamate synthesis,

or amino acid digestion and absorption

may affect glutamate levels. Studies us-

ing magnetic resonance spectroscopy

indicate that astroglia amino acid me-

tabolism may decrease with chronic

stress. Decreased function or blockage of

N-methyl-D-aspartate (NMDA) recep-

tors may contribute to psychotic symp-

toms. Reduced glutamate signaling has

been associated with elevations in dopa-

mine that may contribute to symptoms

of schizophrenia.

Excess

activation of glutamate re-

ceptors is associated with either neuron

necrosis (death) or apoptosis (self-de-

struction). Excess activation of iono-

tropic receptors may contribute to neu-

ron degeneration. Glutamate “spillover”

from the synaptic cleft both reduces

the input specificity of neural signaling

and activates extra-synaptic receptors.

Excess glutamate signaling, and its ef-

fects, has been termed “excitotoxicity”,

and is considered a contributing fac-

tor in the neurodegeneration seen in

Huntington’s disease, Alzheimer’s dis-

ease, amyotrophic lateral sclerosis (ALS)