Editing Psychopharmacology (section)

===Antidepressants===
[[Antidepressant]]s reduce symptoms of mood disorders primarily through the regulation of [[norepinephrine]] and [[serotonin]] (particularly the [[5-HT receptor]]s). After chronic use, neurons adapt to the change in biochemistry, resulting in a change in pre- and postsynaptic receptor density and second messenger function.<ref name=Psychopharm /> The Monoamine Theory of Depression and Anxiety, which states that the disruption of the activity of nitrogen containing neurotransmitters (i.e. serotonin, norepinephrine, and dopamine) is strongly correlated with the presence of depressive symptoms.<ref>{{Cite book | vauthors = Wagner H |date=2014-02-25 |title=The Psychobiology of Human Motivation |url=http://dx.doi.org/10.4324/9781315812328 |doi=10.4324/9781315812328|isbn=9781317798200 |s2cid=141555822 }}</ref> Despite its longstanding prominence in pharmaceutical advertising, the myth that low serotonin levels cause depression is not supported by scientific evidence.<ref>{{cite book | vauthors=((Whitaker, R.)), ((Cosgrove, L.)) | date=23 April 2015 | title=Psychiatry Under the Influence: Institutional Corruption, Social Injury, and Prescriptions for Reform | publisher=Palgrave Macmillan US | url=https://play.google.com/store/books/details?id=QYwEogEACAAJ | isbn=9781137506924}}</ref><ref>{{cite journal | vauthors=((Moncrieff, J.)), ((Cooper, R. E.)), ((Stockmann, T.)), ((Amendola, S.)), ((Hengartner, M. P.)), ((Horowitz, M. A.)) | journal=Molecular Psychiatry | title=The serotonin theory of depression: a systematic umbrella review of the evidence | pages=3243–3256 | publisher=Nature Publishing Group | date=20 July 2022 | volume=28 | issue=8 | issn=1359-4184 | doi=10.1038/s41380-022-01661-0 | pmid=35854107 | s2cid=250646781 | doi-access=free | pmc=10618090 }}</ref><ref>{{Citation | vauthors=((Ghaemi, N.)), ((M., P. H.)) | year=2022 | title=Has the Serotonin Hypothesis Been Debunked? | url=https://www.psychologytoday.com/us/blog/mood-swings/202210/has-the-serotonin-hypothesis-been-debunked | access-date=2 May 2023}}</ref>

[[Monoamine oxidase inhibitor]]s (MAOIs) are the oldest class of antidepressants. They inhibit [[monoamine oxidase]], the enzyme that metabolizes the monoamine neurotransmitters in the presynaptic terminals that are not contained in protective synaptic vesicles. The inhibition of the enzyme increases the amount of neurotransmitter available for release. It increases norepinephrine, dopamine, and 5-HT, thus increasing the action of the transmitters at their receptors. MAOIs have been somewhat disfavored because of their reputation for more serious side effects.<ref name=Psychopharm />

[[Tricyclic antidepressant]]s (TCAs) work through binding to the presynaptic transporter proteins and blocking the reuptake of norepinephrine or 5-HT into the presynaptic terminal, prolonging the duration of transmitter action at the synapse.

[[Selective serotonin reuptake inhibitor]]s (SSRIs) selectively block the reuptake of serotonin (5-HT) through their inhibiting effects on the sodium/potassium [[Adenosine triphosphate|ATP]]-dependent serotonin transporter in presynaptic neurons. This increases the availability of 5-HT in the synaptic cleft.<ref name="Clinical">{{cite book|title=Manual of Clinical Psychopharmacology| vauthors = Schatzberg AF, Cole JO, DeBattista C |publisher=American Psychiatric Publishing|year=2010|isbn=978-1-58562-377-8|edition=Seventh|location=Washington, D.C.|lccn=2010006867}}</ref> The main parameters to consider in choosing an antidepressant are side effects and safety. Most SSRIs are available generically and are relatively inexpensive. Older antidepressants such as TCAs and MAOIs usually require more visits and monitoring, which may offset the low expense of the drugs. SSRIs are relatively safe in overdoses and better tolerated than TCAs and MAOIs for most patients.<ref name=Clinical />