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Evidence for neurological activity of strontium was obtained from a number of in vitro investigations. In a calcium-free medium, strontium ions weakly supported the generation of excitatory postsysnaptic potentials following stimulation of guinea pig cervical ganglia (i.e., the release of acetylcholine was less efficient than when calcium was present) (s_McLachlan_1977). Incubation of vasa deferentia isolated from guinea pigs showed that both strontium and barium cations can substitute for calcium ions in the release of noradrenaline at adrenergic nerve terminals.


It was concluded that all these cations act through the same site at some stage in the process of potassium induced transmitter release (s_Nakazato_1980).Perfusion through acutely denerved cats´ adrenal glandsby strontium in calcium-free Locke´s solution resulted in an intense catecholamine secretion and restored the response to acetylcholine and excess potassium (s_Douglas_1964). Findings that the stimulating effect of strontium also persisted in glands perfused with EDTA led to the conclusion that strontium can substitute for calcium in the secretory process without liberation of endogeneous calcium from some intracellular binding sites. The sequestration of different divalent cations including strontium was examined, in comparison to calcium, by mitochondria and smooth endoplasmic reticulum from isolated presynaptic nerve terminals (s_Rasgado-Flores_1987). Strontium cations were less effective (by about 50 to 60%) than calcium ions.

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