The Monoamine Theory Of Depression

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Monoamine Theory of Depression

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Monoamine Theory of Depression

Monoamines play important roles in the physiology of humans. In the case of

depression pathophysiology, the important monoamines are serotonin, dopamine and

norepinephrine. The monoamine theory, the most relevant regarding depression

pharmacology, postulates that a deficiency of the three amines in the central nervous system

(CNS) contributes to the pathology in depression (Hasler, 2010). The Origins of the theory

are in studies that indicated that medications that target to increase the levels of the

monamine transmitters in the synaptic clefts have been effective in neutralizing depressive

mood symptoms.

In support of the theory, the 5-HT (serotonin) system has been shown to regulate

depression. Alterations to the 5-HT1A receptor leading to reduced binding contribute to

depression according to a meta-analytic study carried out by Ling et al. (2016). Activation of

the same receptor during the postnatal period has also been reported to result to increased

probability for adulthood depression, but vice versa for anxiety, in mouse models (Ishikawa

& Shiga, 2017). Further, polymorphisms in the 5-HT gene promoter region were identified in

the development of overgeneral autobiographical memory, which is a symptom in depression

(Sumner et al. 2014). Noteworthy in the support of the monoamine theory is also a study that

was carried out on persons predisposed to depression. In the study, the depletion of

tryptophan (necessary for serotonin production) led to the development of depressive

symptoms (Neumeister, 2004).

Besides serotonin, norepinephrine has also been implicated in depression. Hasler

reports on depressed patients as presenting with various abnormalities in the noradrenergic

system, from metabolism to transportation (2010). Further, post-mortem results from brains

of suicide patients point to abnormalities related to decreased levels of norepinephrine in the

CNS (Hasler, 2010). Dopamine levels have also been reported to be lower than normal in

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depressed patients, with systems that ensure dopamine re-uptake and increased neuro-

transmission being effective anti-depressants (Albert , 2012; Hasler, 2010).

However, Philip and Browning advocate against the use of simple clinical

biochemistry studies’ results in arguing for the role of monoamines in depression, since the

results of such studies have been unreliable (2015). The absence of sustained elevated levels

of the monoamines, after anti-depressants administration even though the medications

continue to be effective (Delgado, 2000), makes the theory questionable. Further, such

medications are effective for some patients and not others, while drugs devoid of any

monoaminergic activity have been effective against depression (Albert et al., 2012; Delgado,

2000). Delgado, further, points to inconsistencies whereby depleting monoamines from

systems of un-medicated healthy study participants does not affect their mood in any

significant ways, and does not show a worsening of un-medicated disordered cases (2000).

Important is also the fact that it is difficult to have a direct quantification of the monoamines,

hence, evidence is limited.

Even though such inconsistencies have discredited the monoamine theory, Philip and

Browning, reports that the theory, like many others around individual monoamines, have

played a big role in advancing knowledge in the pathophysiology of depression. The

monoamines also have an indirect role in depression pathophysiology and pharmacology.

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References

Albert, P. R., Benkelfat, C., & Descarries, L. (2012). The neurobiology of depression

revisiting the serotonin hypothesis. I. Cellular and molecular

mechanisms. Philosophical Transactions of the Royal Society B: Biological

Sciences, 367(1601), 2378–2381. http://doi.org/10.1098/rstb.2012.0190

Cowen, P. J., & Browning, M. (2015). What has serotonin to do with depression? World

Psychiatry, 14(2), 158–160. http://doi.org/10.1002/wps.20229

Delgado, P. L. (2000). Depression: The Case for a Monoamine Deficiency. Journal of

Clinical Psychiatry, 617-11.

Hasler, G. (2010). Pathophysiology of Depression: Do We Have Any Solid Evidence of

Interest to Clinicians? World Psychiatry, 9(3), 155–161.

Ishikawa, C., & Shiga, T. (2017). The postnatal 5-HT1A receptor regulates adult anxiety and

depression differently via multiple molecules. Progress in Neuropsychopharmacology

&Biological Psychiatry, 7866-74. doi:10.1016/j.pnpbp.2017.04.014

Ling, W., Chanjuan, Z., Dan, Z., Xinfa, W., Liang, F., Jiaju, Z., & ... Peng, X. (2016).

Serotonin-1A receptor alterations in depression: a meta-analysis of molecular imaging

studies. BMC Psychiatry, 161-9. doi:10.1186/s12888-016-1025-0

Neumeister, A., Nugent, A. C., Waldeck, T., Geraci, M., Schwarz, M., Bonne, O., & ...

Drevets, W. C. (2004). Neural and behavioral responses to tryptophan depletion in

unmedicated patients with remitted major depressive disorder and controls. Archives

of General Psychiatry, (8), 765.

Sumner, J. A., Vrshek-Schallhorn, S., Mineka, S., Zinbarg, R. E., Craske, M. G., Redei, E. E.,

& ... Adam, E. K. (2014). Effects of the serotonin transporter polymorphism and

history of major depression on overgeneral autobiographical memory. Cognition &

Emotion, 28(5), 947-958. doi:10.1080/02699931.2013.865596

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The Monoamine theory of depression

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