Release of noradrenaline (NA) from isolated rat iris during perfusion in K+-free medium was confirmed. Direct The phenomenon of neurotransmitter release in quanta by the process of exocytosis is well accepted [Smith and Winkler, 1972] together with evidence that depolarization produces an increase in Nat and Cat + permeability in the neuronal basal membrane [Katz and Miledi, 1967, 1970]. Studies by Paton, Vizi and Zar [1971] and Vizi [1977] have led to the suggestion in a detailed review by Vizi [1978] that passage of the action potential across the nerve terminal with the accompanying depolarization and influx of Nat ions followed by Ca+ + ions, results in an inhibition of Na+/K+ ATPase activity at the inner side of the presynaptic membrane, producing permeability change in the membrane with transmitter release. He further suggested that release is terminated by stimulation of the membrane ATPase and that a sodium pump inhibition-stimulation cycle enables transmitter release to be quantized.A great deal of experimental evidence was assessed by Vizi [1978] to support this hypothesis. However, there are points requiring clarification. Vizi [1978] himself stressed the important unresolved question of how membrane ATPase inhibition by Ca"+ is terminated. In addition, it is difficult to see how one can reconcile the relatively long turnover time of the sodium pump with the much shorter time involved in transmitter release in response to stimulation.To quote Vizi [1978], most of the supportive evidence for his hypothesis comes from experiments in which application of drugs or conditions known to inhibit or stimulate membrane ATPase activity produce changes in rate of transmitter release, e.g. Nat or Kt deprivation, or ouabain [Paton et al., 1971;

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ATPase activities were studied in erythrocyte membranes prepared from blood of patients suffering from affective disorders. Long‐term (9–12 months) administration of lithium led to an increase in the erythrocyte membrane Na/K ATPase activity (54%) when studied on an age and sex matched basis or when the patients were studied before and after treatment. The Mg ATPase activity was also increased (38%) but there was no consistent effect of lithium treatment on Ca stimulated ATPase activity in the membranes. It is suggested that the effect of lithium treatment on Na/K ATPase was due to recovery of the patients rather than an effect of the drug. MgATPase activity increased regardless of clinical condition. Short‐term lithium treatment (2–4 weeks) led to increased Mg ATPase activity (43%). These results suggest that lithium treatment itself causes an increase in Mg ATPase activity and that this effect is not dependent on changes in protein synthesis. Lithium treatment (long‐term) increased the erythrocyte sodium content by 15%. No effect on plasma sodium, magnesium, potassium or erythrocyte magnesium and potassium was observed.

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