Editing Threshold potential (section)

==Clinical significance==
The role of the threshold potential has been implicated in a clinical context, namely in the functioning of the nervous system itself as well as in the cardiovascular system.

===Febrile seizures===
A [[febrile seizure]], or "fever fit", is a convulsion associated with a [[hyperthermia|significant rise in body temperature]], occurring most commonly in early childhood. Repeated episodes of childhood febrile seizures are associated with an increased risk of [[temporal lobe epilepsy]] in adulthood.{{sfn|Wang|Qin|Han|Cai|2011|p=87}}

With [[patch clamp]] recording, an analogous state was replicated ''in vitro'' in rat cortical neurons after induction of febrile body temperatures; a notable decrease in threshold potential was observed. The mechanism for this decrease possibly involves suppression of inhibition mediated by the GABA<sub>B</sub> receptor with excessive heat exposure.{{sfn|Wang|Qin|Han|Cai|2011|p=87}}

===ALS and diabetes===

Abnormalities in neuronal excitability have been noted in [[amyotrophic lateral sclerosis]] and [[diabetes]] patients. While the mechanism ultimately responsible for the variance differs between the two conditions, tests through a response to ischemia indicate a similar resistance, ironically, to ischemia and resulting paresthesias. As ischemia occurs through inhibition of the sodium-potassium pump, abnormalities in the threshold potential are hence implicated.{{sfn|Bostock|Cikurel|Burke|1998|p=141}}

===Arrhythmia===
Since the 1940s, the concept of diastolic depolarization, or "pacemaker potential", has become established; this mechanism is a characteristic distinctive of cardiac tissue.{{sfn|Monfredi|Dobrzyński|Mondal|Boyett|2010|p=1392}} When the threshold is reached and the resulting action potential fires, a heartbeat results from the interactions; however, when this heartbeat occurs at an irregular time, a potentially serious condition known as [[arrhythmia]] may result.

====Use of medications====
A variety of drugs can present prolongation of the [[QT interval]] as a side effect. Prolongation of this interval is a result of a delay in sodium and calcium channel inactivation; without proper channel inactivation, the threshold potential is reached prematurely and thus arrhythmia tends to result.{{sfn|Nelson|Leung|2011|p=292}} These drugs, known as pro-arrhythmic agents, include antimicrobials, antipsychotics, methadone, and, ironically, [[antiarrhythmic agents]].{{sfn|Nelson|Leung|2011|p=291}} The use of such agents is particularly frequent in intensive care units, and special care must be exercised when QT intervals are prolonged in such patients: arrhythmias as a result of prolonged QT intervals include the potentially fatal [[torsades de pointes]], or TdP.{{sfn|Nelson|Leung|2011|p=292}}

====Role of diet====
Diet may be a variable in the risk of arrhythmia. [[Polyunsaturated fatty acids]], found in fish oils and several plant oils,<ref>{{cite web|title=Polyunsaturated Fat|url=https://healthyforgood.heart.org/eat-smart/articles/polyunsaturated-fats|website=American Heart Association|access-date=22 May 2018}}</ref> serve a role in the prevention of arrhythmias.{{sfn|Savelieva|Kourliouros|Camm|2010|p=213}} By inhibiting the voltage-dependent sodium current, these oils shift the threshold potential to a more positive value; therefore, an action potential requires increased depolarization.{{sfn|Savelieva|Kourliouros|Camm|2010|p=213}} Clinically therapeutic use of these extracts remains a subject of research, but a strong correlation is established between regular consumption of fish oil and lower frequency of hospitalization for atrial fibrillation, a severe and increasingly common arrhythmia.{{sfn|Savelieva|Kourliouros|Camm|2010|pp=213–215}}