Abstract
The possible involvement of phosphoinositides' turnover in the process of neurotransmitter release in the central nervous system (CNS) was studied using rat brain slices and synaptosomes. A depolarizing concentration of potassium chloride (25 mM) induces an 8.6 ± 0.4% increase of [ 3H]noradrenaline ([ 3H]NA) fractional release in cerebral cortical slices above spontaneous release, and 15 mM KCl induces a 3-fold increase of [ 3H]NA release in rat brain synaptosomes. Neomycin, an aminoglycoside which binds phosphoinositides, inhibits the potassium-induced release in cortical slices with an IC 50 = 0.5 ± 0.07 mM and with IC 50 = 0.2 ± 0.03 mM in synaptosomes. Veratridine, a veratrum alkaloid which increases membrane permeability to sodium ions and causes depolarization of neuronal cells, induces a net 13.4 ± 0.3% increase of [ 3H]NA fractional release above spontaneous release in cortical slices. In analogy to K + stimulation, neomycin inhibits the veratridine-stimulated release in cortical slices with an IC 50 = 0.65 ± 0.1 mM. It appears that the recycling of phospoinositides, which is necessary for Ca 2+ mobilization, participates in the Ca 2+-dependent induced neurotransmitter release in the central nervous system.
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