Editing Carbamazepine (section)

=== Mechanism of action ===
Carbamazepine is a [[sodium channel blocker]].<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>  It binds preferentially to [[Voltage gated sodium channels|voltage-gated sodium channels]] in their inactive conformation, which prevents repetitive and sustained firing of an [[action potential]].  Carbamazepine has effects on serotonin systems but the relevance to its antiseizure effects is uncertain. There is evidence that it is a [[serotonin releasing agent]] and possibly even a [[serotonin reuptake inhibitor]].<ref>{{cite journal | vauthors = Dailey JW, Reith ME, Steidley KR, Milbrandt JC, Jobe PC | title = Carbamazepine-induced release of serotonin from rat hippocampus in vitro | journal = Epilepsia | volume = 39 | issue = 10 | pages = 1054–63 | date = October 1998 | pmid = 9776325 | doi = 10.1111/j.1528-1157.1998.tb01290.x | s2cid = 20382623 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Dailey JW, Reith ME, Yan QS, Li MY, Jobe PC | title = Carbamazepine increases extracellular serotonin concentration: lack of antagonism by tetrodotoxin or zero Ca2+ | journal = European Journal of Pharmacology | volume = 328 | issue = 2–3 | pages = 153–62 | date = June 1997 | pmid = 9218697 | doi = 10.1016/s0014-2999(97)83041-5 }}</ref><ref>{{cite journal | vauthors = Kawata Y, Okada M, Murakami T, Kamata A, Zhu G, Kaneko S | title = Pharmacological discrimination between effects of carbamazepine on hippocampal basal, Ca(2+)- and K(+)-evoked serotonin release | journal = British Journal of Pharmacology | volume = 133 | issue = 4 | pages = 557–67 | date = June 2001 | pmid = 11399673 | pmc = 1572811 | doi = 10.1038/sj.bjp.0704104 }}</ref> It has been suggested that carbamazepine can also block [[voltage-gated calcium channel]]s, which will reduce neurotransmitter release.<ref>{{cite journal | vauthors = Gambeta E, Chichorro JG, Zamponi GW | title = Trigeminal Neuralgia: an overview from pathophysiology to pharmacological treatments | journal = Molecular Pain |date = January 2020 | volume = 16 | pmid = 31908187|  doi = 10.1177/1744806920901890 | pmc = 6985973 }}</ref>