Depolarization and calcium entry in squid giant axons

Abstract

SUMMARY1. Changes in ionized calcium in giant axons were followed by recording the light produced by injected aequorin.2. From the effect of injecting calcium buffers the internal concentration of ionized calcium was found to be about the same as in a mixture of 45 Ca EGTA: 55 free EGTA, i.e. about 04a1sM.3. After an axon had been exposedwto cyanide for 50-100 min the velocity of the aequorin reaction increased about 500 times. This effect, which could be reversed rapidly by removing cyanide, was probably brought about by release of calcium from an internal store.4. Injecting 30 tumole ATP per litre of axoplasm into a cyanide-poisoned axon caused a transient lowering of light intensity; oligomycin blocked the effect.5. Raising external cqicium or replacing external sodium by choline or lithium reversible increased the light produced by axons injected with aequorin.

Membrane fusion of secretory vesicles and liposomes Two different types of fusion

“…It is conceivable that in the adrenal medulla the intracellular Ca2+ concentration rises in a manner similar to that demonstrated in other secretory cells, where free Ca 2 + concentrations have been measured to rise from the resting conditions of less than 10-7 M [25,26] to about 10-5 M du ring secretion [27 ,28]. Mg2+ has been shown to have an inhibitory effect on Ca 2 + induced release, when Ca 2 + and Mg 2 + together are injected in giant synapses [29], which indicates that Mg 2 + has an intracellular target.…”

A free calcium wave traverses the activating egg of the medaka, Oryzias latipes.

“…A correction for magnesium inhibition, based on a study of this effect by Baker et al (6), and estimates of free magnesium in other cells-namely, squid axons (8) and barnacle muscles (4)-shift the "near-independence" level from 10 -r.a to 10 -6.8 M.…”

Effects of veratridine on Ca fluxes and the release of oxytocin and vasopressin from the isolated rat neurohypophysis.

“…Under normal conditions these Na channels are probably responsible for depolarization of the plasmalemma. Such a depolarization leads in turn to activation of"late" calcium channels (Baker et al, 1971) and promotes hormone release.…”