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1. Rohon-Beard cells in the spinal cord of Xenopus laevis tadpoles have been studied in animals 4-days to 2-weeks-old (Nieuwkoop & Faber, 1956, stages 45-49). These neurones have an unusually large resting membrane potential of -88 mV, in Ringer solution containing 3-0 mM K+. 2. Their resting potential (R.) depends on the concentration gradient of K+ across the cell membrane. These cells follow the prediction of the Nernst equation for a K+-selective electrode, down to external K+ concentrations as low as 1-0 mM (R.P. -118 mV). 3. The resting potentials of muscle cells in these animals exhibit the same dependence on external [K+], as has been shown previously. 4. Rohon-Beard cells can be driven antidromically, bu stimulation of the anterior end of the spinal cord with brief current pulses through a suction electrode. Antidromic action potentials fail to invade the cell body with repeated stimulation at 1Hz. 5. Even when impulses fail to invade Rohon-Beard somata, slow depolarizations can be produced by single shocks or trains of shocks which cause impulse activity in other neurones. The response can be observed to a single stimulus or to a train of stimuli. The magnitude of the depolarization is graded, depending on the number of stimuli and the frequency of stimulation. 6. Support is presented for the hypothesis that the slow depolarization in Rohon-Beard cells is mediated by the release of K+ into their environment by the impulse activity of neighbouring neurones. The slow depolarization increases in solutions containing 1-5 mM-K+, and decreases in solutions containing 6-0 mM-K+. The changes are in quantitative agreement with those anticipated by theory. 7. The slow depolarization is unlikely to be due to a conductance change produced by a synaptic transmitter, since hyperpolarization and depolarization of the Rohon-Beard cell with injected current do not change the amplitude of the response. Further, low Ca-high Mg solutions which block neuromuscular transmission do not block the response. 8. The possible role of the slow depolarizing response in the physiological activity of these neurones is discussed.

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