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


Yuen, Eunice Y.; Wei, Jing; Liu, Wenhua;

Zhong, Ping; Li, Xiangning et al. (2012)

Repeated Stress Causes Cognitive

Impairment by Suppressing Glutamate

Receptor Expression and Function in

Prefrontal Cortex


vol. 73 (5) p. 962-977

Gamma-aminobutyric acid


Gamma-aminobutyric acid (GABA)

functions as an inhibitory neurotransmit-

ter in the central nervous system (CNS).

GABA acts in opposition to glutamate,

the primary excitatory neurotransmitter.

Studies demonstrate decreased GABA

levels in animal models of depression,

and clinical studies report low plasma

and cerebro-spinal fluid GABA levels in

mood disorder patients. Very recent ev-

idence indicates that GABA-mediated

signals may contribute to synchronized

neural network oscillations in the brain

that facilitate cognition and information

processing. Disruption of GABA trans-

mission at synapses may perturb the

neural oscillations and may contribute

to symptoms of schizophrenia.

GABA and dopamine “crosstalk” is

modulated by glutamate and creates a

complex interaction between these neu-

rotransmitters and their effects. GABA

may, through GABA receptor activity,

induce norepinephrine activity in the

brain (animal studies), even as GABA

may be affected by the activity of ad-

renergic receptors. GABA may modu-

late serotonin signaling in certain areas

of the brain, and GABA may respond

to signals from 5-HT serotonin recep-

tors. Disruptions in GABA signaling

during development affects nerve cell

migration, maturation and differenti-

ation; GABA signaling is mostly excit-

atory during early development. Altered

GABA signaling has been associated

with neurodevelopmental disorders

such as autism, Fragile X, Down’s syn-

drome, schizophrenia, Tourette’s syn-

drome and neurofibromatosis. Adult

neuron generation and post-develop-

ment neural plasticity is also regulated

by GABA signaling. Astroglia possesses

GABA receptors; they may be sensitive

to, and release, GABA.

GABA is found throughout the gas-

trointestinal tract (GIT), where it may

both serve as a neurotransmitter and

mediate endocrine responses. Myenteric

neurons in the gut regulate motili-

ty; 5-8% of myenteric neurons contain

GABA. GABA-B receptors contribute

to the regulation of gastric emptying,

stomach pH and gut motility. GABA

transporters are found in cells of the

enteric (GIT) nervous system that in-

nervate the small intestine (duodenum,

ileum) and the large intestine. In vitro

and animal studies indicate that GABA

signaling may also affect intestinal flu-

id levels, electrolyte levels, serotonin

release and nitric oxide signaling in the


The GABA signaling system is affect-

ed by ethanol (alcohol) and ingestion

has been associated with some of the

symptoms associated with drinking such

as poor coordination sedation, loss of in-

hibition, and withdrawal.



GABA levels have been

associated with neurological disorders

such as Huntington’s chorea, Parkinson’s

and Alzheimer’s disease. GABA defi-

ciency may also play a role in psychiat-

ric disorders such as anxiety, depression,

chronic pain, panic, or mania. Studies

indicate that plasma GABA levels are

lower in 40% of depressed, manic or eu-