VERATRIDINE-ENHANCED PERSISTENT SODIUM CURRENT INDUCES BURSTING IN CA1 PYRAMIDAL NEURONS

The mechanism of veratridine-induced bursting activity was studied in rat hippocampal CA1 pyramidal neurons. Veratridine (0.1-0.3 mu M) indu ces bursting in previously normal pyramidal neurons. The current-volta ge curves of untreated neurons show a slight deviation from the linear Ohmic relation; this deviation is known as the ''depolarizing rectifi cation''. Veratridine markedly accentuates the depolarizing rectificat ion so that a zero slope or negative slope appears in the current-volt age curve of these neurons. Both the veratridine-induced bursting acti vity and negative slope resistance are blocked by small concentrations of tetrodotoxin or by raising the calcium concentration of the superf usion medium. Under single-electrode voltage clamping, a subthreshold persistent (slowly inactivating) sodium current, which can be recorded in untreated neurons, is found to be enhanced in the veratridine-trea ted neurons. This current is thought to be responsible for the slow de polarizing phase of bursting activity and the development of negative slope resistance in the current-voltage relationship. The present resu lts demonstrate that veratridine enhances the slowly inactivating sodi um current, leading to the development of negative slope resistance an d induction of bursting in rat hippocampal CA1 pyramidal neurons.