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Sodium‐dependent calcium uptake in membrane vesicles derived from rat brain synaptosomes
Author(s) -
Rahamimoff Hannah,
Spanier Rivka
Publication year - 1979
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(79)81094-7
Subject(s) - hebrew , neurochemistry , medical school , chemistry , philosophy , classics , neurology , psychology , neuroscience , medicine , art , medical education
In presynaptic nerve terminals an increase in the free intracellular Ca*+ concentration leads to an increase in neurotransmitter liberation. This increase in [Cal, is either due to calcium entry via voltage sensitive channels in the presynaptic membrane, or can originate by release of calcium from intracellular stores [ 11. Following synaptic activation a number of processes can participate in lowering of the elevated [Cal, and thus bring the nerve terminal to the resting steady state. One of the major processes regulating [Cal, is the sodium-dependent calcium extrusion process described in squid axons [2], brain slices [3], cardiac muscle [4] and isolated synaptosomes [5]. The synaptosomes are complex structures and therefore the data obtained from them are in some respects ambiguous for interpretation [S]. We report here the isolation of a vesicular membrane system derived from synaptosomes, capable of sodium-dependent calcium transport. In addition, a dependence of *‘Na+ uptake on intravesicular Ca*+ is shown. These membrane vesicles offer a simpler system for studying the molecular properties of the calcium-sodium antiport in synaptosome membranes.