Paroxysmal Depolarization Shift in Leech Retzius Nerve Cells Revisited

The paroxysmal depolarization shift (PDS) is a hallmark of epileptiform activities at cellular level [1-3]. PDS or bursting is characterized by the firing of rapid series of several action potentials with very short (less than ~5ms interspike interval) on the top of the depolarizing membrane envelope [1-4]. Given that the epileptiform activities are identical whether it is lower invertebrates or higher mammalian system, little is known about how the PDS generates, propagates, and terminates. Understanding the number, frequency, and timing of PDS can shed light to dissect epileptiform studies in details [1,5]. At molecular level, recent reports have shown that dysfunction in the particular subtypes of K+ channel are widely implicated in numerous form of seizures [6]. Further electrophysiological analyses have reveal that direct pharmacological blockade of K+ channels like Kv7, Calcium activated K+ channel or persistent sodium current INaP [7,8] may generate bursting. From molecular biology, pharmacology or electrophysiology perspectives, it is anticipated that K+ channel are the key regulator in heighted excitability and hence to PDS or bursting.