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Calcium influx in resting conditions in a preparation of peptidergic nerve terminals isolated from the rat neurohypophysis.

1. Calcium accumulation in a preparation of nerve terminals isolated from the rat neurohypophysis was measured both in rapid (10‐60 s) and long‐term (up to 60 min) uptake experiments, by use of 45Ca2+ as radiotracer and ion‐exchange chromatography as separation method. Unless otherwise stated all experiments have been performed in the absence from the incubation media of secretagogues or depolarizing agents. 2. The uptake of 45Ca2+ in nerve terminals was linear up to 30‐45 s, with an apparent initial rate of uptake of 0.98 nmol Ca2+ (mg protein)‐1 min‐1. 3. The level of 45Ca2+ accumulation was sensitive to manipulations of electrochemical gradient for Na+ across the plasma membrane. Alterations of extracellular concentrations of Na+ affected secretory activity to a larger extent than manipulations of internal Na+. These effects were not qualitatively dependent on the nature of the replacement for Na+. 4. Removal of extracellular Na+ induced a significant increase of both the level of 45Ca2+ accumulation and of the apparent initial rate of uptake. The concentration for half‐maximal stimulatory effect was 40 mM‐Na+. 5. The analysis of the stimulatory effect of high extracellular K+ on the 45Ca2+ accumulation reveals at least two components: a depolarization and an intrinsic K+ effect. 6. Sodium channel inhibitors (TTX, 1.25 microM) decreased significantly the level of 45Ca2+ accumulation, an effect which was evident from the first minute of exposure to the drug. 7. A specific L‐type Ca2+ channel blocker (nicardipine) inhibited 45Ca2+ uptake, in a dose‐dependent manner. Simultaneous addition of both TTX and nicardipine (20 microM) decreases the 45Ca2+ uptake up to 50%. 8. In conclusion, the uptake of Ca2+ in isolated peptidergic nerve terminals, incubated in resting conditions, is mediated by at least three pathways: a TTX‐sensitive and a nicardipine (dihydropyrine)‐sensitive pathway and through a Na(+)‐Ca2+ exchange‐dependent mechanism. The principal route of Ca2+ entry appears to be through TTX‐sensitive channels.