Extracellular potassium and trasmitter release at the giant synapse of squid.

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Abstract
The effects of changes in extracellular K concentration, [K]o, on synaptic transmission were studied at the squid [Loligo pealei] giant synapse with intracellular recording from the presynaptic terminal and post-synaptic axon. The amplitudes of both the presynaptic spike and the EPSP [excitatory postsynaptic potential] varied inversely with [K]o. On the average, a 10 mV change in spike height was accompanied by a 3.1 mV change in EPSP amplitude. The amplitude of the presynaptic spike after-hyperpolarization (AH) varied inversely with [K]o. On the average, increasing [K]o resulted in a 20% change in EPSP amplitude per mV change in presynaptic spike AH. Repetitive antidromic stimulation of the post-synaptic giant axon resulted in an exponential decline in the post-synaptic spike AH, a depolarization of the presynaptic membrane potential and a reduction in the AH of presynaptic spikes. The K+ which accumulates in the extracellular spaces around the post-synaptic axon may also affect the presynaptic terminal. Repetitive antidromic stimulation of the post-synaptic axon resulted in a reduction in EPSP amplitude elicted by stimulation of the presynaptic axon. The EPSP amplitude reduction relative to the change in presynaptic spike AH was quantitatively close to the change produced by increasing [K]o, suggesting that the EPSP amplitude reduction was due to the accumulation of extracellular K+ at the presynaptic terminal. Repetitive stimulation of the presynaptic axon reduced the EPSP amplitude and the presynaptic spike AH. On the average, a 1 mV change in presynaptic spike AH was accompanied by a 204% change in EPSP amplitude, suggesting that K accumulation may only contribute to a small extent, under these conditions, to the depression of transmitter release.