Abstract
Changes in cytoplasmic free Ca 2+ concentration, [Ca] i elicited by ATP, were studied in neurones cultured from rat hippocampus and thalamus. ATP evoked [Ca] i increases in about 30% of all cells tested and suppressed [Ca] i transients in responsive cells. The number of responses to ATP markedly increased after pretreatment of cells with inhibitors of protein kinase C, H-7 or staurosporine. The potentiation was blocked by a phorbol ester and by dioleylglycerol. In pretreated cells both once peak [Ca] i and the number of successive trials were augmented by an [ATP] increase. The former effect can be described by the Michaelis-Menten equation whereas the latter one has a steeper, leftward-shifted dependence. Both concentration dependences are explained with a model, describing Ca 2+ release as a threshold phenomena. ATP analogues had the rank of potency: ATP ≈ ADP ⪢ AMP > α,β-MeATP. A single ATP application depleted internal Ca 2+ stores which could be replenished by brief membrane depolarization with high-K +. ATP- and caffeine-induced [Ca] i transients were independent, indicating two non-overlapping Ca 2+ storage sites. Only caffeine effects were potentiated at an elevated [Ca] i level, showing a Ca 2+-induced Ca 2+ release. Inhibitors of the Ca 2+ pump in internal stores, ryanodine and sulphydryl reagents suppressed the ATP-induced [Ca] i transients, acting via different mechanisms.
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