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Calcium buffering in presynaptic nerve terminals. Free calcium levels measured with arsenazo III
Authors:Erik S Schweitzer  Mordecai P Blaustein  
Institution:Department of Physiology and Biophysics, Washington University, School of Medicine, St. Louis, MO 63110 U.S.A.
Abstract:The particulate fraction from osmotically shocked synaptosomes (‘synaptosomal membranes’) sequesters Ca when incubated with ATP-containing solutions. This net accumulation of Ca can reduce the free Ca2+] of the bathing medium to sub-micromolar levels (measured with arsenazo III). Two distinct types of Ca sequestration site are responsible for the Ca2+ buffering. One site, presumed to be smooth endoplasmic reticulum, operates at low Ca2+] (less than 1 μM), and has a relatively small capacity. Ca sequestration at this site is prevented by the Ca2+ ionophore, A-23187, but not by mitochondrial poisons. The second (mitochondrial) site, in contrast, is blocked by the mitochondrial uncoupler, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and oligomycin. Since the intraterminal organelles can buffer Ca2+] to about 0.3–0.5 μM, this may be an upper limit to the normal resting level of Ca2+]i in nerve terminals. In the steady state, total cell Ca and Ca2+]i will be governed principally by Ca transport mechanisms in the plasmalemma; the intracellular organelle transport systems then operate in equilibrium with this Ca2+]. During activity, however, Ca rapidly enters the terminals and Ca2+]i rises. The intracellular buffering mechanisms then come into play and help to return Ca2+]i toward the resting level; the non-mitochondrial Ca sequestration mechanism probably plays the major role in this Ca buffering.
Keywords:Synaptosome  Calcium buffering  Calcium sequestration  Arsenazo III  (Rat brain)
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