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Probing the Endogenous Ca²⁺ Buffers at the Presynaptic Terminals of the Crayfish Neuromuscular Junction

Department of Biology, Boston University, Boston, Massachusetts

Submitted 18 June 2004; accepted in final form 18 March 2005

Ca²⁺ indicators of varying affinity and mobility were pressure injected into the presynaptic axon of the inhibitor of the crayfish neuromuscular junction (NMJ). Fluorescence transients recorded at a 2-kHz resolution were used to probe physiological parameters governing the decay of fluorescence transients within 100 ms after an action potential (early decay). Blocking Ca²⁺ extrusion or Ca²⁺ sequestration processes did not significantly alter early decay, arguing against a role for either mechanism. Fluorescence transients recorded with low mobility or fixed indicators exhibited early decay similar to that recorded with indicators of comparable affinity but high mobility, suggesting that early decay was not due to the rate of Ca²⁺-indicator diffusion. The extent of early decay correlated closely with the affinity, but not mobility, of the Ca²⁺ sensitive dyes tested. These results implicate intrinsic buffers with slow Ca²⁺ binding kinetics as the most likely determinants of early decay. However, computer simulations showed that intrinsic buffers with a slow binding rate are unlikely to be the only ones present in the system because the slow kinetics would be unable to buffer incoming Ca²⁺ during an action potential and would result in momentary indicator saturation. In fact, experimental data show that the peak amplitude of an action potential activated Ca²⁺ transient is about 20% of the maximal fluorescence intensity activated by prolonged Ca²⁺ influx. We conclude that endogenous buffering at the crayfish NMJ includes both fast and slow components, the former being fast enough to compete with fast Ca²⁺ indicators, and the latter dictating the early decay.

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