Calcium released by photolysis of DM‐nitrophen stimulates transmitter release at squid giant synapse.

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Abstract
1. Transmitter release at the squid giant synapse was stimulated by photolytic release of Ca2+ from the ‘caged’ Ca2+ compound DM‐nitrophen (Kaplan & Ellis‐Davies, 1988) inserted into presynaptic terminals. 2. Competing binding reactions cause the amount of Ca2+ released by DM‐nitrophen photolysis to depend on the concentrations of DM‐nitrophen, total Ca2+, Mg+, ATP and native cytoplasmic Ca2+ buffer. Measurements of presynaptic [Ca2+] changes by co‐injection of the fluorescent indicator dye Fura‐2 show that DM‐nitrophen photolysis causes a transient rise in Ca2+ followed by decay within about 150 ms to an increased steady‐state level. 3. Rapid photolysis of Ca2(+)‐loaded nitrophen within the presynaptic terminal was followed in less than a millisecond by depolarization of the postsynaptic membrane. As with action potential‐evoked excitatory postsynaptic potentials (EPSPs), the light‐evoked response was partially and reversibly blocked by 1‐3 mM‐kainic acid which desensitizes postsynaptic glutamate receptors. 4. Release was similar in magnitude and rate to normal action potential‐mediated EPSPs. 5. The release of transmitter by photolysis of Ca2(+)‐loaded DM‐nitrophen was not affected by removal of Ca2+ from the saline or addition of tetrodotoxin. Photolysis of DM‐nitrophen injected into presynaptic terminals without added Ca2+ did not stimulate release of transmitter nor did it interfere with normal action potential‐mediated release. 6. Stimulation of presynaptic action potentials in Ca2(+)‐free saline during the light‐evoked response did not elicit increased release of transmitter if the ganglion was bathed in Ca2(+)‐free saline, i.e. in the absence of Ca2+ influx. Increasing the intensity of the light or stimulating presynaptic action potentials in Ca2(+)‐containing saline increased the release of transmitter. Therefore the failure of presynaptic voltage change to increase transmitter release resulting from release of caged Ca2+ was not due to saturation or inhibition of the release mechanism by light‐released Ca2+. 7. Decreasing the temperature of the preparation increased the delay to onset of the light‐evoked response and reduced its amplitude and rate of rise to an extent similar to that observed for action potential‐evoked EPSPs.