A study of synaptic transmission in the absence of nerve impulses was conducted using the axo-axonic giant synapse in the squid's stellate ganglion. When nerve impulses were eliminated with tetrodotoxin, synaptic transfer of potential changes could still occur with brief depolarizing pulses to the presynaptic terminal. These pulses were as effective as normal presynaptic spikes in evoking postsynaptic potentials, with similar synaptic delay and time course. The synaptic transfer (input/output) characteristic was studied under various conditions. Brief current pulses caused detectable postsynaptic responses when presynaptic depolarization exceeded about 30 mV, with the postsynaptic potential increasing tenfold with 10 mV increments. Calcium increased, magnesium reduced the slope of the synaptic transfer curve. The influences of pulse duration, preceding membrane potential, electrode position, and stimulation rate were described. Loading the synaptic terminal with tetraethylammonium ions produced large inside-positive potentials. Raising the internal potential suppressed synaptic transfer during the pulse and delayed the postsynaptic response until the end of the pulse. This observation supports the calcium hypothesis, suggesting that calcium movement is essential for electro-secretory coupling. The study of the squid giant synapse revealed that chemical transmission occurs, with postsynaptic potential changes mediated by quantal release of a transmitter. Previous studies on the neuromuscular junction showed similar features, leading to the conclusion that chemical transmission operates at the giant synapse. The study used tetrodotoxin to eliminate nerve impulses and isolate the synapse. The results showed that a passive potential change matched in size and shape to the normal action potential was equally effective in releasing transmitter and producing postsynaptic responses. The release was not due to regenerative sodium entry but some other event associated with presynaptic depolarization. The calcium hypothesis was supported by findings that calcium influx and magnesium effects on synaptic transfer. The study also showed that depolarization caused inward calcium movement, which facilitated transmitter release. The results demonstrated that raising the internal potential suppressed synaptic transfer and delayed the postsynaptic response. The study concluded that the calcium hypothesis is valid, with calcium movement being essential for electro-secretory coupling. The results also showed that the synaptic transfer characteristic had an S-shape, with calcium and magnesium affecting the slope and postsynaptic response. The study provided insights into the factors regulating presynaptic mechanisms and the effects of various experimental conditions on synaptic transfer. The findings support the idea that chemical transmission occurs at the squid giant synapse, with calcium movement playing a crucial role in transmitter release.A study of synaptic transmission in the absence of nerve impulses was conducted using the axo-axonic giant synapse in the squid's stellate ganglion. When nerve impulses were eliminated with tetrodotoxin, synaptic transfer of potential changes could still occur with brief depolarizing pulses to the presynaptic terminal. These pulses were as effective as normal presynaptic spikes in evoking postsynaptic potentials, with similar synaptic delay and time course. The synaptic transfer (input/output) characteristic was studied under various conditions. Brief current pulses caused detectable postsynaptic responses when presynaptic depolarization exceeded about 30 mV, with the postsynaptic potential increasing tenfold with 10 mV increments. Calcium increased, magnesium reduced the slope of the synaptic transfer curve. The influences of pulse duration, preceding membrane potential, electrode position, and stimulation rate were described. Loading the synaptic terminal with tetraethylammonium ions produced large inside-positive potentials. Raising the internal potential suppressed synaptic transfer during the pulse and delayed the postsynaptic response until the end of the pulse. This observation supports the calcium hypothesis, suggesting that calcium movement is essential for electro-secretory coupling. The study of the squid giant synapse revealed that chemical transmission occurs, with postsynaptic potential changes mediated by quantal release of a transmitter. Previous studies on the neuromuscular junction showed similar features, leading to the conclusion that chemical transmission operates at the giant synapse. The study used tetrodotoxin to eliminate nerve impulses and isolate the synapse. The results showed that a passive potential change matched in size and shape to the normal action potential was equally effective in releasing transmitter and producing postsynaptic responses. The release was not due to regenerative sodium entry but some other event associated with presynaptic depolarization. The calcium hypothesis was supported by findings that calcium influx and magnesium effects on synaptic transfer. The study also showed that depolarization caused inward calcium movement, which facilitated transmitter release. The results demonstrated that raising the internal potential suppressed synaptic transfer and delayed the postsynaptic response. The study concluded that the calcium hypothesis is valid, with calcium movement being essential for electro-secretory coupling. The results also showed that the synaptic transfer characteristic had an S-shape, with calcium and magnesium affecting the slope and postsynaptic response. The study provided insights into the factors regulating presynaptic mechanisms and the effects of various experimental conditions on synaptic transfer. The findings support the idea that chemical transmission occurs at the squid giant synapse, with calcium movement playing a crucial role in transmitter release.