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


Glycine transporters as novel therapeutic

targets in schizophrenia, alcohol depen-

dence and pain

Nature Publishing Group, a division of

Macmillan Publishers Limited. All Rights


vol. 12 (11) p. 866-885

Legendre, P. (2001)

The glycinergic inhibitory synapse

Cellular and Molecular Life Sciences

vol. 58

(5) p. 760-793

Paul, Steven M. (2002)

GABA and Glycine

Neuropsychopharmacology: The Fifth

Generation of Progress Editors:

Lippincott, Williams, & Wilkins,

Philadelphia, Pennsylvania, 2002

Satoru Yoshikawa, Tomohiko Oguchi (2012)

Glycine transporter type 2 (GlyT2) inhibitor

ameliorates bladder overactivity and no-

ciceptive behavior in rats.

European urology

vol. 62 (4) p. 704 - 12

Winkelmann, Aline; Maggio, Nicola; Eller,

Joanna; Caliskan, Gürsel; Semtner,

Marcus et al. (2014)

Changes in neural network homeostasis trig-

ger neuropsychiatric symptoms.

The Journal of clinical investigation

vol. 124

(2) p. 696-711

Yang, Charles R.; Svensson, Kjell A. (2008)

Allosteric modulation of NMDA recep-

tor via elevation of brain glycine and

d-serine: The therapeutic potentials for


Pharmacology & Therapeutics

vol. 120 (3) p.



Histamine is derived from the es-

sential amino acid histidine. Histamine

mediates numerous biologic reactions

by binding with its receptors in the

brain and in the body. Histamine is one

of the most important neurotransmit-

ters to stimulate and maintain arousal

in the central nervous system (CNS).

Histamine-acetylcholine signaling in-

teractions contribute to wakefulness

(arousal), attention, circadian rhythms,

appetite control, learning, memory and

emotion. Histamine may also bind to

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

tors. Histamine may affect the secretion

of posterior and anterior pituitary hor-

mones, including the release of prolac-

tin. Histamine may also contribute to

the stress-related release of adrenocorti-

cotropic hormone (ACTH).

In the peripheral nervous system,

histamine signaling affects smooth mus-

cle tone, digestion, gut motility and

immune responses. Histamine is a me-

diator of allergic Type I hypersensitivi-

ty reactions. Histamine released during

allergic reactions may result in itching,

flushing, hives, vomiting, syncope (faint-

ing), anaphylaxis or shock.



histamine levels in the

CNS may result from nicotinic acetyl-

choline receptor and serotonin signal-

ing. Sedatives such as ethanol, tetrahy-

drocannabinol (THC), barbiturates and

benzodiazepines may also decrease his-

tamine levels. Low levels of CNS hista-

mine may also contribute to Tourette’s

syndrome, narcolepsy and other hyper-

somnia (sleep) disorders. Alterations in

CNS histamine levels may contribute

to age-related neurodegenerative dis-

eases such as Parkinson’s disease and

Alzheimer’s disease. Current research

indicates that increases or decreases in

CNS histamine levels may occur locally

in specific brain areas during neurode-

generative diseases.

Low levels of the precursor essential

amino acid histidine may occur from

poor diet or digestive disorders. Two