CALCIUM-DEPENDENT RELEASE OF PUTATIVE NEUROTRANSMITTERS IN THE CHICK VISUAL-SYSTEM

The calcium-dependent release of putative neurotransmitters has been studied in the chick brain. Several radioactive compounds were taken up into chick optic lobe homogenates by a high-affinity sodium-dependent transport mechanism. At a concentration of potassium sufficient to cause extensive depolarization, a large proportion of the efflux of the accumulated labeled compounds was calcium dependent. Calcium-stimulated release was antagonized by magnesium. The calcium ionophore, A-23187, enabled calcium-related release to occur in the absence of depolarizing conditions, except after accumulation of [3H]choline. Veratridine was used in order to bring about depolarization in low external potassium concentrations. In this case magnesium was able to replace calcium in inducing the efflux of labeled compounds. Tetrodotoxin inhibited the veratridine-stimulated release of compounds in the presence of calcium. The rate of release of accumulated leucine was affected to a much lesser extent by the presence of calcium. Calcium-stimulated release was also found in homogenates of the optic nerve, indicating that this process is not confined to synapses. Calcium-stimulated release of different compounds varied according to the developmental age and temperature of incubation. This suggests that some dissimilarities in the nature of their release mechanisms exist. Our results suggest that much calcium-dependent efflux is related to presynaptic neurotransmitter release mechanisms. However, a similar release process may exist in non-synaptic regions of the neuron and in glia. Furthermore, the release of non-transmitter compounds under depolarizing conditions can also be enhanced by the presence of calcium. © 1979.