Modulation of nickel-induced bursting with 4-aminopyridine in leech Retzius nerve cells

Abstract

Paroxysmal depolarization shift has been identified as a characteristic feature of the cellular basis of epilepsy. On Na+-dependent bursting, 1 mmol/l 4-aminopyridine (4-AP) produced a two-phase effect - a significant depolarization accompanied by an increase in the frequency of bursting, followed by repolarization along with a diminished frequency of bursting. Neither 1 μmol/l apamin nor 150 nmol/l charybdotoxin (ChTX) elicited any significant effect on either bursting or standard conditions. Our results suggest that 4-AP affects the bursting indirectly by altering the excitability of the cell. The lack of effects of apamin and ChTX is probably due to channel insensitivity to these blockers in leech.