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Volume Regulation of Nerve Terminals
Author(s) -
Babila T.,
Atlan H.,
Fromer I.,
Schwalb H.,
Uretzky G.,
Lichtstein D.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb05795.x
Subject(s) - bumetanide , chemistry , tonicity , synaptosome , ouabain , amiloride , dids , stimulation , biophysics , furosemide , sodium , endocrinology , biochemistry , membrane , ion transporter , biology , organic chemistry
Pinched‐off presynaptic nerve terminals (synaptosomes) possess significant regulatory volume increase (RVI) and regulatory volume decrease (RVD) capabilities. Following a swelling induced by a hypotonic challenge, the synaptosomes regulate their volume and adjust it, in 2 min, to within 5% of its initial value (RVD) at an initial rate of ‐0.77 ± 0.10%/s (mean ± SEM). Following a shrinking induced by a hypertonic challenge, the synaptosomes also regulate their volume at an initial rate of 0.18 ± 0.02%/s (RVI), resulting in a new steady state, reached within 5–10 min, with a synaptosomal volume below the original volume. The omission of Na + or K + ions from the extrasynaptosomal medium reduces the initial rate of RVI by 72.5 and 66.5%, respectively. The “loop diureties” bumetanide and furosemide significantly inhibited the RVI of the synaptosomes. In contrast, ouabain, amiloride, or 4,4′‐diisothiocyanatostilbene‐2,2′‐disulfonic acid did not have any significant effect on RVI parameters. Furthermore, bumetanide‐sensitive 86 Rb uptake by rat brain synaptosomes was stimulated threefold by a hypertonic perturbation of 30%. Thus we conclude that the RVI of synaptosomes is mainly due to a stimulation of the Na + , K + , Cl − co‐transport system induced by the synaptosomal shrinking following the hypertonic challenge.