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

iors. Chronic administration of anti-de-

pressant medications may decrease the

expression of GABA-A receptors in

the brain (animal studies). GABA-A


Are directly affected by ethanol,

which functions as a receptor agonist

Function by allowing chloride influx

through cell membranes into nerve

cells (action potential)

May be in the synapse or


Receptor subtypes





each subtype and its subunits may

bind to different types of molecules

– in addition to GABA, many bind

to sedative drugs (barbiturates),

anxiolytics (benzo-diazepines),

anesthetics and ethanol

-adrenergic receptor signaling

(norepinephrine, epinephrine)

signaling may affect GABA receptor

function through second messenger

signaling (increased phosphorylation

of GABA receptors) and enhance

GABA-A receptor activity

Metabolites of progesterone,

testosterone, and stress hormone

deoxycorticosterone may act as

GABA-A receptor agonists (in vitro


Dehydroepiandrosterone sulfate

(DHEA-S), pregnenolone sulfate

(and similar 3-betahydroxy-

pregnane steroids) may antagonize

GABA-A receptors (in vitro studies)

May be modulated by zinc; in

vitro studies have shown that zinc

antagonizes GABA neuron functions

Activation of GABA-A receptors in

the pancreas decreases insulin and

glucagon excretion (in vitro)

GABA-B receptors

Abnormal regulation of GABA-B re-

ceptor activity may contribute to mood

disorders, visceral pain perception and

affect digestive functions.

Altered activity has been associated

with several neuropsychiatric


Found on excitatory and inhibitory

neurons; contribute to the function

of multi-neuron “circuits”

Inhibit multiple glutamate vesicle

releases from pre-synaptic terminals

(decrease synaptic glutamate


Two metabotropic isoforms act

to regulate potassium influx into

neurons by second-messenger

signaling (action potential)

Inhibit calcium permeability of

NMDA receptors to inhibit calcium-

dependent signaling ins post-

synaptic neurons (action potential)

Valproate, lithium and

carbamazepine may upregulate

GABA-B receptors (animal studies)

Activation of GABA-B receptors in

the pancreas increases insulin release

(in vitro)

Contribute to spinal and vagal

afferent (from periphery to CNS)

signaling and may affect visceral

pain (nociception) perception by

decreasing afferent signaling and

enhancing anti-nociceptive signaling

Are abundant in the gastrointestinal

(GI) and may contribute to gastric

emptying, gastric pH, gut motility,

intestinal fluid levels, electrolyte

levels, serotonin release and nitric

oxide signaling in the gut.