The Role of Cation‐Activated ATPases in Transmitter Release from the Rat Iris

Abstract

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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