Abstract
The presence of a mixed Na + Ca 2+ spike along the sensory terminal of the frog muscle spindle was verified. When the terminal was perfused with Ringer's solution containing 0.1–0.5 mM ruthenium red (RuR), the amplitude and duration of the spike were increased, occurring as a prolonged or a long-lasting depolarization of up to 20–30 s duration following individual afferent spikes evoked spontaneously or antidromically by electrical stimulation. In an isotonic TEA solution, the amplitude and duration of the afferent spikes were increased; however, no prolonged depolarization occurred. Adding 0.2 mM RuR to the TEA solution produced the prolonged and long-lasting depolarization. All responses disappeared in the presence of 3 μM TTX or Na +-free Ringer's solution. An impedance decrease along the terminal was observed during the prolonged or long-lasting depolarization. The prolonged depolarization was blocked by the addition of Ca 2+-blockers; the afferent spikes remained. In preparations preincubated with 0.1 mM RuR, increasing CaCl 2 in Ringer's solution from 0.2 mM, resulted in shortening of the duration of individual spikes with prolonged depolarization and in increase in the maximum rate of rise (MMR) of the spikes. Preincubation with higher concentrations of RuR produced higher sensitivities in the modifications of the duration and MRR to the change in [Ca 2+] o. The responses were retained by adding RuR or RuCl 3 to Ca 2+-free Ringer's solution containing 0.1–5 mM EGTA, although all responses disappeared in Ca 2+-free EGTA Ringer's solution. It is concluded that the RuR-induced prolonged response is produced by an influx of Na +.
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