Journal
EPILEPSIA
Volume 53, Issue -, Pages 21-31Publisher
WILEY
DOI: 10.1111/epi.12032
Keywords
Potassium channel; Sodium channel; Neuron; Subcellular localization; Seizures
Categories
Funding
- NIH [NS34383, NS42225]
- Marie Curie 7th framework program [IRG-2008-239499]
Ask authors/readers for more resources
Voltage-gated ion channels are diverse and fundamental determinants of neuronal intrinsic excitability. Voltage-gated K+ (Kv) and Na+ (Nav) channels play complex yet fundamentally important roles in determining intrinsic excitability. The Kv and Nav channels located at the axon initial segment (AIS) play a unique and especially important role in generating neuronal output in the form of anterograde axonal and backpropagating action potentials. Aberrant intrinsic excitability in individual neurons within networks contributes to synchronous neuronal activity leading to seizures. Mutations in ion channel genes give rise to a variety of seizure-related channelopathies, and many of the ion channel subunits associated with epilepsy mutations are localized at the AIS, making this a hotspot for epileptogenesis. Here we review the cellular mechanisms that underlie the trafficking of Kv and Nav channels found at the AIS, and how Kv and Nav channel mutations associated with epilepsy can alter these processes.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available