Editing Mood stabilizer (section)

==Pharmacodynamics==
As mentioned above, "mood stabilizers" do not have a unified mechanism of action; the term simply describes how these drugs can be used.

The precise mechanism of action of lithium is still unknown, and it is suspected that it acts at various points of the neuron between the nucleus and the synapse. Lithium is known to inhibit the enzyme [[Glycogen synthase kinase-3 beta|GSK-3B]]. This improves the functioning of the [[circadian clock]]—which is thought to be often malfunctioning in people with bipolar disorder—and positively modulates gene transcription of [[brain-derived neurotrophic factor]] (BDNF). The resulting increase in neural plasticity may be central to lithium's therapeutic effects. How lithium works in the human body is not completely understood, but its benefits are most likely related to its effects on electrolytes such as potassium, sodium, calcium and magnesium.<ref>Raber, Jack H. "Lithium carbonate." The Gale Encyclopedia of Mental Disorders, edited by Madeline Harris and Ellen Thackerey, vol. 1, Gale, 2003, pp. 571-573. Gale eBooks, link.gale.com/apps/doc/CX3405700220/GVRL?u=tamp44898&sid=GVRL&xid=9ef84e18. Accessed 20 Jan. 2021.</ref> Lithium is, broadly speaking, neuroprotective.<ref name=Quiroz>{{cite journal | vauthors = Quiroz JA, Machado-Vieira R, Zarate CA, Manji HK | title = Novel insights into lithium's mechanism of action: neurotrophic and neuroprotective effects | journal = Neuropsychobiology | volume = 62 | issue = 1 | pages = 50–60 | date = 2010 | pmid = 20453535 | doi = 10.1159/000314310 | pmc = 2889681 }}</ref>

The classical theory of valporate's action involves affecting [[GABA]] levels and blocking [[voltage-gated sodium channel]]s (which would affect the brain's [[Glutamate (neurotransmitter)|glutamate system]]).<ref name=Gh2013>{{cite journal | vauthors = Ghodke-Puranik Y, Thorn CF, Lamba JK, Leeder JS, Song W, Birnbaum AK, Altman RB, Klein TE | title = Valproic acid pathway: pharmacokinetics and pharmacodynamics | journal = Pharmacogenetics and Genomics | volume = 23 | issue = 4 | pages = 236–241 | date = April 2013 | pmid = 23407051 | pmc = 3696515 | doi = 10.1097/FPC.0b013e32835ea0b2 }}</ref> It has since been found to have many other cellular effects, such as inhibiting [[histone deacetylase]]s and increasing [[Lymphoid enhancer-binding factor 1|LEF1]].<ref>{{cite journal | vauthors = Santos R, Linker SB, Stern S, Mendes AP, Shokhirev MN, Erikson G, Randolph-Moore L, Racha V, Kim Y, Kelsoe JR, Bang AG, Alda M, Marchetto MC, Gage FH | title = Deficient LEF1 expression is associated with lithium resistance and hyperexcitability in neurons derived from bipolar disorder patients | journal = Molecular Psychiatry | volume = 26 | issue = 6 | pages = 2440–2456 | date = June 2021 | pmid = 33398088 | pmc = 9129103 | doi = 10.1038/s41380-020-00981-3 }}</ref> It is also neuroprotective.<ref name=Quiroz/>

[[Carbamazepine]] is mainly a [[sodium channel blocker]], though it too has other activities.<ref>{{cite journal | vauthors = Rogawski MA, Löscher W, Rho JM | title = Mechanisms of Action of Antiseizure Drugs and the Ketogenic Diet | journal = Cold Spring Harbor Perspectives in Medicine | volume = 6 | issue = 5 | pages = a022780 | date = May 2016 | pmid = 26801895 | pmc = 4852797 | doi = 10.1101/cshperspect.a022780 }}</ref> [[Lamotrigine]] is a similar case.<ref>{{Cite web|url=https://www.accessdata.fda.gov/drugsatfda_docs/label/2006/020241s10s21s25s26s27,020764s3s14s18s19s20lbl.pdf|title=Prescribing Information for LAMICTAL (lamotrigine)|website=FDA|access-date=12 January 2020|archive-date=12 January 2020|archive-url=https://web.archive.org/web/20200112201226/https://www.accessdata.fda.gov/drugsatfda_docs/label/2006/020241s10s21s25s26s27,020764s3s14s18s19s20lbl.pdf|url-status=dead}}</ref>

{{see also|Atypical antipsychotic#Pharmacodynamics}}

One possible downstream target of several mood stabilizers such as lithium, valproate, and carbamazepine is the [[Arachidonic acid#Biosynthesis and cascade in humans|arachidonic acid cascade]].<ref name=pmid18347600>{{cite journal |vauthors=Rao JS, Lee HJ, Rapoport SI, Bazinet RP |title=Mode of action of mood stabilizers: is the arachidonic acid cascade a common target? |journal=[[Mol. Psychiatry]] |volume=13 |issue=6 |pages=585–96 |date=June 2008 |pmid=18347600 |doi=10.1038/mp.2008.31|s2cid=21273538 |doi-access= }}</ref>