A phylogenetic tree showing how a number of monoamine receptors are related to each other.
As demonstrated by the wide existence of monoamine transmitters, an organism's ability to modify its behavior is advantageous to its survival. This system is found in various species such as nematodes, lobsters, desert locusts, hens, mice and zebra finches.
Disorders of monoamine neurotransmitters exist, part of a growing number of neurotransmitter disorders identified. Such disorders are responsible for biosynthesis degradation and difficulty in transporting neurotransmitters such as dopamine, norepinephrine, epinephrine, or serotonin. Monoamine neurotransmitter disorders mimic the symptoms of other more prevalent neurological disorders (e.g. cerebral palsy) and thus are frequently misdiagnosed.
^Mele, Tina; Čarman-Kržan, Marija; Jurič, Damijana Mojca (2010). "Regulatory role of monoamine neurotransmitters in astrocytic NT-3 synthesis". International Journal of Developmental Neuroscience28 (1): 13–9. doi:10.1016/j.ijdevneu.2009.10.003. PMID19854260.
^ abKurian, Manju A; Gissen, Paul; Smith, Martin; Heales, Simon JR; Clayton, Peter T (2011). "The monoamine neurotransmitter disorders: An expanding range of neurological syndromes". The Lancet Neurology10 (8): 721–33. doi:10.1016/S1474-4422(11)70141-7. PMID21777827.
^ abcdefgBroadley KJ (March 2010). "The vascular effects of trace amines and amphetamines". Pharmacol. Ther.125 (3): 363–375. doi:10.1016/j.pharmthera.2009.11.005. PMID19948186. "Trace amines are metabolized in the mammalian body via monoamine oxidase (MAO; EC 22.214.171.124) (Berry, 2004) (Fig. 2) ... It deaminates primary and secondary amines that are free in the neuronal cytoplasm but not those bound in storage vesicles of the sympathetic neurone ... Similarly, β-PEA would not be deaminated in the gut as it is a selective substrate for MAO-B which is not found in the gut ...
Brain levels of endogenous trace amines are several hundred-fold below those for the classical neurotransmitters noradrenaline, dopamine and serotonin but their rates of synthesis are equivalent to those of noradrenaline and dopamine and they have a very rapid turnover rate (Berry, 2004). Endogenous extracellular tissue levels of trace amines measured in the brain are in the low nanomolar range. These low concentrations arise because of their very short half-life ..."
^ abcdefLindemann L, Hoener MC (May 2005). "A renaissance in trace amines inspired by a novel GPCR family". Trends Pharmacol. Sci.26 (5): 274–281. doi:10.1016/j.tips.2005.03.007. PMID15860375. "In addition to the main metabolic pathway, TAs can also be converted by nonspecific N-methyltransferase (NMT)  and phenylethanolamine N-methyltransferase (PNMT)  to the corresponding secondary amines (e.g. synephrine , N-methylphenylethylamine and N-methyltyramine ), which display similar activities on TAAR1 (TA1) as their primary amine precursors...Both dopamine and 3-methoxytyramine, which do not undergo further N-methylation, are partial agonists of TAAR1 (TA1). ...
The dysregulation of TA levels has been linked to several diseases, which highlights the corresponding members of the TAAR family as potential targets for drug development. In this article, we focus on the relevance of TAs and their receptors to nervous system-related disorders, namely schizophrenia and depression; however, TAs have also been linked to other diseases such as migraine, attention deficit hyperactivity disorder, substance abuse and eating disorders [7,8,36]. Clinical studies report increased β-PEA plasma levels in patients suffering from acute schizophrenia  and elevated urinary excretion of β-PEA in paranoid schizophrenics , which supports a role of TAs in schizophrenia. As a result of these studies, β-PEA has been referred to as the body’s ‘endogenous amphetamine’ "
^Wainscott DB, Little SP, Yin T, Tu Y, Rocco VP, He JX, Nelson DL (January 2007). "Pharmacologic characterization of the cloned human trace amine-associated receptor1 (TAAR1) and evidence for species differences with the rat TAAR1". The Journal of Pharmacology and Experimental Therapeutics320 (1): 475–85. doi:10.1124/jpet.106.112532. PMID17038507.