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The modulation of two motor behaviors by persistent sodium currents in Xenopus laevis tadpoles.

Persistent sodium currents ( I NaP ) are common in neuronal circuitries and have been implicated in several diseases, such as amyotrophic lateral sclerosis (ALS) and epilepsy. However, the role of I NaP in the regulation of specific behaviors is still poorly understood. In this study we have characterized I NaP and investigated its role in the swimming and struggling behavior of Xenopus tadpoles. I NaP was identified in three groups of neurons, namely, sensory Rohon-Beard neurons (RB neurons), descending interneurons (dINs), and non-dINs (neurons rhythmically active in swimming). All groups of neurons expressed I NaP , but the currents differed in decay time constants, amplitudes, and the membrane potential at which I NaP peaked. Low concentrations (1 µM) of the I NaP blocker riluzole blocked I NaP ~30% and decreased the excitability of the three neuron groups without affecting spike amplitudes or cellular input resistances. Riluzole reduced the number of rebound spikes in dINs and depressed repetitive firing in RB neurons and non-dINs. At the behavior level, riluzole at 1 µM shortened fictive swimming episodes. It also reduced the number of action potentials neurons fired on each struggling cycle. The results show that I NaP may play important modulatory roles in motor behaviors. NEW & NOTEWORTHY We have characterized persistent sodium currents in three groups of spinal neurons and their role in shaping spiking activity in the Xenopus tadpole. We then attempted to evaluate the role of persistent sodium currents in regulating tadpole swimming and struggling motor outputs by using low concentrations of the persistent sodium current antagonist riluzole.

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