The effects of inhalation anesthetics on calcium-stimulated exocytosis in a natural membrane model system

Abstract

Sea urchin egg cortices were used as an in vitro natural membrane model system to determine the effects of inhalation anesthetics on the Ca2+-regulated exocytotic fusion of cortical vesicles with the egg plasma membrane. When Ca2+ was either absent or present in amounts below the threshold for exocytosis, methoxyflurane, halothane, enflurane, isoflurane, chloroform and fluoroxene, at concentrations up to 5 mM, had no effect on the fusion of cortical vesicles with the plasma membrane. However, when Ca2+ was present at or above threshold levels for exocytosis, each of the tested anesthetics caused an inhibition of cortical vesicle fusion. Exocytosis was inhibited most effectively by methoxyflurane (55%), followed by halothane (30%), while fluoroxene consistently had the least effect (less than 5%). These observations support the view that volatile anesthetics can impair the Ca2+-regulated fusogenic activities of natural membranes and are consistent with other data showing that inhalational agents inhibit secretory processes in intact cells.

Sea urchin development: An alternative model for mechanistic understanding of neurodevelopment and neurotoxicity

“…Actually, sea urchin egg was often used as a model of excitable membrane to test the effects of substances such as ionophores (Prestipino et al, 1993b) that act as Ca 21 translocator in artificial and natural membranes, or drugs such as anesthetics (Lederhaas and Hinkley, 1988), where egg and blastomere membranes were used as an in vitro natural membrane model system to check the Ca 21 -regulated exocytotic fusion of cortical vesicles with the egg plasma membrane (Pesando et al, 2003). During the last 30 years, the onset and function of the molecules related to cholinergic neurotransmitter systems have been studied in sea urchin gamete interactions.…”