The control of intracellular calcium and neurotransmitter release in guinea pig-derived cerebral cortical synaptoneurosomes.

Synaptoneurosomes are a simply derived brain vesicular preparation which are believed to contain elements of both presynaptic and postsynaptic material. Inositol phosphates production and neurotransmitter release in the synaptoneurosome have previously been shown to be under the control of a number of receptor agonists. However, there have been few investigations of the role of intracellular calcium ([Ca2+]i) in these events. In this study we report that potassium (K+; 50 mM) was able to increase [Ca2+]i and subsequently release [3H]noradrenaline in guinea pig cerebral cortical synaptoneurosomes via activation of dihydropyridine-insensitive, voltage-sensitive calcium channels. Veratridine (30 microM) produced similar effects but these involved activation of sodium channels which could be blocked by pre-incubation with tetrodotoxin (0.15 microM). A number of agonists were used to investigate possible modulation of these events and to look for agonist-stimulated mobilization of [Ca2+]i. No evidence was found for either receptor-mediated release of calcium from intracellular stores or for modulation of K(+)-induced neurotransmitter release. This might be related to the observed passive entry of calcium through the synaptoneurosomal membrane and the subsequently high levels of [Ca2+]i.