Abstract
Electrophysical recordings from opener muscle fibers in the crayfishProcambarus clarkii (Fig. 1) show that pre-synaptic facilitation at terminals of the single excitatory axon usually decays in a dual-exponential fashion after a single pulse or after a train of pulses (Figs. 2, 3, 7, 9), as has been reported for frog neuromuscular junctions (Mallart and Martin, 1967) and squid giant synapses (Charlton and Bittner, 1974, 1976). Furthermore, the second component of decay at crayfish synapses is associated with a break in the monotonic decay of the first component, a result which suggests that the decay of facilitation is not due to the simple diffusion of some substance (such as calcium) from specialized release sites. The growth of facilitation at all opener synapses during trains of equalinterval stimuli could not be predicted by assuming that each pulse contributed an equal amount of facilitation which summed linearly with that remaining from all previous stimuli (Figs. 4, 6; Table 2), as reported for synapses in frog and squid. During high frequency stimulation (>40 Hz), those terminals which facilitate dramatically (highF e synapses) show much greater amounts of facilitation than that predicted by the “linear summation” model (Figs. 4, 8), whereas other terminals (lowF e synapses) show much less facilitation than predicted (Fig. 6). The rate of growth of facilitation was often very constant at various stimulus rates in highF e or mixed type synapses (Figs. 4, 8, 10)-a result not predicted by the linear summation model. Finally, when highF e synapses were stimulated at different frequencies, the rate of growth of facilitation changed dramatically in a fashion not predictable using linear summation (Mallert and Martin, 1967) or power law (Linder, 1974) models. Various measures of facilitation were related such that synapses having a rapid initial time constant of decay (γ1) usually had a large first component of facilitation (F 1.F 1 was positively correlated withF 2 (second component of facilitation) and inversely with γ2 (decay of second component). Furthermore, we noted that these opener synapses formed a continuum with regard to their facilitation properties, although all synapses released a maximum of 70–300 quanta when maximally facilitated. One possible explanation for this latter observation is that the different synapse types in the opener muscle all have a limited number of release sites. After considering all these data, we suggest that there may be a fundamental difference between facilitation mechanisms at synapses which release many quanta per impulse when bathed in normal physiological salines (e.g., many vertebrate neuromuscular junctions, giant fiber synapses in squid) compared to synapses which release transmitter in a more graded fashion (e.g., most crustacean neuromuscular junctions, most CNS synapses).
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