Riluzole suppresses postinhibitory rebound in an excitatory motor neuron of the medicinal leech
Postinhibitory rebound (PIR) is an intrinsic property often exhibited by neurons involved in generating rhythmic motor behaviors. Cell DE-3, a dorsal excitatory motor neuron in the medicinal leech exhibits PIR responses that persist for several seconds following the offset of hyperpolarizing stimuli and are suppressed in reduced Na+ solutions or by Ca2+ channel blockers. The long duration and Na+ dependence of PIR suggest a possible role for persistent Na+ current (INaP). In vertebrate neurons, the neuroprotective agent riluzole can produce a selective block of INaP. This study demonstrates that riluzole inhibits cell DE-3 PIR in a concentration- and Ca2+-dependent manner. In 1.8 mM Ca2+ solution, 50–100 µM riluzole selectively blocked the late phase of PIR, an effect similar to that of the neuromodulator serotonin. However, 200 µM riluzole blocked both the early and late phases of PIR. Increasing extracellular Ca2+ to 10 mM strengthened PIR, but high riluzole concentrations continued to suppress both phases of PIR. These results indicate that riluzole may suppress PIR via a nonspecific inhibition of Ca2+ conductances and suggest that a Ca2+-activated nonspecific current (ICAN), rather than INaP, may underlie the Na+-dependent component of PIR.