Editing Phenytoin (section)

===Mechanism of action===
[[File:Phenytoin sodium mechanism of action.png|thumb|The mechanism of action of phenytoin sodium. Sodium channels are: 1) Closed 2) Open 3) Inactive (phenytoin effect)]]
Phenytoin is believed to protect against seizures by causing voltage-dependent block of [[voltage gated sodium channel]]s.<ref>{{cite journal | vauthors = Rogawski MA, Löscher W | title = The neurobiology of antiepileptic drugs | journal = Nature Reviews. Neuroscience | volume = 5 | issue = 7 | pages = 553–564 | date = July 2004 | pmid = 15208697 | doi = 10.1038/nrn1430 | s2cid = 2201038 | url = https://zenodo.org/record/1233562 }}</ref> This blocks sustained high frequency repetitive firing of [[action potentials]]. This is accomplished by reducing the amplitude of sodium-dependent action potentials through enhancing steady-state inactivation. Sodium channels exist in three main conformations: the resting state, the open state, and the inactive state.

Phenytoin binds preferentially to the inactive form of the sodium channel. Because it takes time for the bound drug to dissassociate from the inactive channel, there is a time-dependent block of the channel. Since the fraction of inactive channels is increased by membrane [[depolarization]] as well as by repetitive firing, the binding to the inactive state by phenytoin sodium can produce voltage-dependent, use-dependent and time-dependent block of sodium-dependent action potentials.<ref>lippincots modern pharmacology with clinical applications pg no:377 5th Edition</ref>

The primary site of action appears to be the [[motor cortex]] where spread of seizure activity is inhibited.<ref>{{cite web | title = Dilantin | date =  2015 | work =  MIMS | url = https://www.mims.com/Hongkong/drug/info/Dilantin/?type=full#Actions | archive-url= https://web.archive.org/web/20140810173319/http://mims.com/Hongkong/drug/info/Dilantin/?type=full | archive-date=10 August 2014 }}</ref> Possibly by promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of [[post-tetanic potentiation]] at synapses which prevents cortical seizure foci from detonating adjacent cortical areas. Phenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of generalized tonic-clonic seizures.<ref name="FDA drug label">{{cite web|title=Parenteral Dilantin (Phenytoin Sodium Injection, USP) | date = October 2011 | work = Parke-Davis | publisher = U.S. Food and Drug Administration |url = http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/010151s036lbl.pdf |access-date=18 April 2014|url-status=live|archive-url= https://web.archive.org/web/20140419011525/http://www.accessdata.fda.gov/drugsatfda_docs/label/2011/010151s036lbl.pdf |archive-date=19 April 2014}}</ref>