RESIDUAL FREE CALCIUM IS NOT RESPONSIBLE FOR FACILITATION OF NEUROTRANSMITTER RELEASE

An increase in internal free calcium ([Ca2+]i) in the presynaptic term inal is often assumed to directly produce facilitation of neurotransmi tter release. Using a Ca2+-activated potassium conductance as a bioass ay for free [Ca2+]i in the presynaptic terminal of the crayfish (Proca mbarus clarkii) opener neuromuscular junction, we now demonstrate that free [Ca2+]i has a decay time constant (tau) of 1-4 msec, whereas fac ilitation of neurotransmitter release has a decay tau of 7-43 msec. In addition, facilitation of neurotransmitter release can be markedly di fferent at times when free [Ca2+]i values and presynaptic membrane vol tages are equal. We conclude that free [Ca2+]i in the presynaptic term inal is not directly responsible for facilitation of neurotransmitter release. Our data suggest that facilitation results from bound Ca2+ or some long-lived consequence of bound Ca2+.