The pharmacology of antidepressants is not entirely clear. The earliest and probably most widely accepted scientific theory of antidepressant action is the monoamine hypothesis (which can be traced back to the 1950s), which states that depression is due to an imbalance (most often a deficiency) of the monoamine neurotransmitters (namely serotonin, norepinephrine and dopamine).[1] It was originally proposed based on the observation that certain hydrazine anti-tuberculosis agents produce antidepressant effects, which was later linked to their inhibitory effects on monoamine oxidase, the enzyme that catalyses the breakdown of the monoamine neurotransmitters.[1] All currently marketed antidepressants have the monoamine hypothesis as their theoretical basis, with the possible exception of agomelatine which acts on a dual melatonergic-serotonergic pathway.[1] Despite the success of the monoamine hypothesis it has a number of limitations: for one, all monoaminergic antidepressants have a delayed onset of action of at least a week; and secondly, there are a sizeable portion (>40%) of depressed patients that do not adequately respond to monoaminergic antidepressants.[2][3] Further evidence to the contrary of the monoamine hypothesis are the recent findings that a single intravenous infusion with ketamine, an antagonist of the NMDA receptor — a type of glutamate receptor — produces rapid (within 2 hours), robust and sustained (lasting for up to a fortnight) antidepressant effects.[3] Monoamine precursor depletion also fails to alter mood.[4][5][6] To overcome these flaws with the monoamine hypothesis a number of alternative hypotheses have been proposed, including the glutamate, neurogenic, epigenetic, cortisol hypersecretion and inflammatory hypotheses.[2][3][7][8]
Another hypothesis that has been proposed which would explain the delay is the hypothesis that monoamines don't directly influence mood, but influence emotional perception biases.[9]
^ abcBrunton LL, Chabner B, Knollmann BC, eds. (2011). Goodman & Gilman's The Pharmacological Basis of Therapeutics (12th ed.). New York: McGraw-Hill. ISBN 978-0-07-162442-8.
^ abMaes M, Yirmyia R, Noraberg J, Brene S, Hibbeln J, Perini G, et al. (March 2009). "The inflammatory & neurodegenerative (I&ND) hypothesis of depression: leads for future research and new drug developments in depression". Metabolic Brain Disease. 24 (1): 27–53. doi:10.1007/s11011-008-9118-1. hdl:11577/2380064. PMID 19085093. S2CID 4564675.
^ abcSanacora G, Treccani G, Popoli M (January 2012). "Towards a glutamate hypothesis of depression: an emerging frontier of neuropsychopharmacology for mood disorders". Neuropharmacology. 62 (1): 63–77. doi:10.1016/j.neuropharm.2011.07.036. PMC 3205453. PMID 21827775.
^Oldman AD, Walsh AE, Salkovskis P, Laver DA, Cowen PJ (January 1994). "Effect of acute tryptophan depletion on mood and appetite in healthy female volunteers". Journal of Psychopharmacology. 8 (1): 8–13. doi:10.1177/026988119400800102. PMID 22298474. S2CID 25812087.
^Leyton M, Young SN, Blier P, Ellenbogen MA, Palmour RM, Ghadirian AM, Benkelfat C (April 1997). "The effect of tryptophan depletion on mood in medication-free, former patients with major affective disorder". Neuropsychopharmacology. 16 (4): 294–297. doi:10.1016/s0893-133x(96)00262-x. PMID 9094147.
^Hughes JH, Dunne F, Young AH (November 2000). "Effects of acute tryptophan depletion on mood and suicidal ideation in bipolar patients symptomatically stable on lithium". The British Journal of Psychiatry. 177 (5): 447–451. doi:10.1192/bjp.177.5.447. PMID 11059999.
^Menke A, Klengel T, Binder EB (2012). "Epigenetics, depression and antidepressant treatment". Current Pharmaceutical Design. 18 (36): 5879–5889. doi:10.2174/138161212803523590. PMID 22681167.
^Vialou V, Feng J, Robison AJ, Nestler EJ (January 2013). "Epigenetic mechanisms of depression and antidepressant action". Annual Review of Pharmacology and Toxicology. 53 (1): 59–87. doi:10.1146/annurev-pharmtox-010611-134540. PMC 3711377. PMID 23020296.
^Outhred T, Hawkshead BE, Wager TD, Das P, Malhi GS, Kemp AH (September 2013). "Acute neural effects of selective serotonin reuptake inhibitors versus noradrenaline reuptake inhibitors on emotion processing: Implications for differential treatment efficacy". Neuroscience and Biobehavioral Reviews. 37 (8): 1786–1800. doi:10.1016/j.neubiorev.2013.07.010. PMID 23886514. S2CID 15469440.
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