This feature allows Nav1.6 channels to rapidly recover from inactivation and sustain a high rate of activity.

Similarly, serotonin receptors in the prefrontal cortex are regulated by PKC in order to reduce sodium currents.

The lack of serine residues lead to the channel's ability to consistently and quickly fire following inactivation.

[16] The genome of a child demonstrating epileptic encephalopathy was sequenced and revealed a de novo missense mutation, p.Asn1768Asp.

20% of the initial current persisted 100 ms after hyperpolarization resulting in hyperexcitability of the neuron and increasing the likelihood of premature or unintentional firing.

In addition to epileptic encephalopathy, the patient presented with developmental delay, autistic features, intellectual disability and ataxia.

Sodium channel conversion has been implicated in the demyelination of axons related multiple sclerosis (MS).

This article incorporates text from the United States National Library of Medicine, which is in the public domain.