<P> 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 receptor with excessive heat exposure . </P> <P> 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 . </P> <P> Since the 1940s, the concept of diastolic depolarization, or "pacemaker potential", has become established; this mechanism is a characteristic distinctive of cardiac tissue . 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 arrythmia may result . </P> <P> 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 . These drugs, known as pro-arrhythmic agents, include antimicrobials, antipsychotics, methadone, and, ironically, antiarrhythmic agents . 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 . </P>

Which membrane potential results in depolarization without a nerve impulse being generated