Uptake of calcium ions by synaptosomes from rat brain

Swanson, Phillip D.; Anderson, Leojean; Stahl, William L.

doi:10.1016/0005-2736(74)90281-8

Cited by 79 publications

(40 citation statements)

References 19 publications

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“…The extent of depolarization, however, remained below the threshold value, which might explain the lack of operation of voltage-dependent Ca2+ channels. A slight enhancement of Ca2+ uptake by synaptosomes by treatment with ouabain has been observed (Stahl & Swanson, 1969;Swanson, Anderson & Stahl, 1974;Goddard & Robinson, 1976) but only after a long incubation time (25-30 min). Pocock (1983) has found that Ca2+ extrusion from adrenal medulla cells is depressed, whereas Ca2+ uptake is not influenced by ouabain.…”

Section: Depolarization By Ouabainmentioning

confidence: 94%

Calcium uptake of rat brain synaptosomes as a function of membrane potential under different depolarizing conditions.

Ádám-Vizi¹,

Ligeti²

1986

The Journal of Physiology

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SUMMARY1. The uptake of 45Ca2+ was measured in brain synaptosomes under conditions designed to depolarize the membranes. Membrane potential was estimated from the distribution of 86Rb+ between the intra-and extracellular compartments.2. K+ depolarization (8-60 mM) only increased Ca2+ uptake beyond a threshold depolarization of about 10 mV, whereas veratridine (5-40 /lM) induced an increased Ca2+ uptake at a concentration which depolarized the membrane less than this threshold. Ouabain did not enhance Ca2+ uptake, but the depolarization it produced did not reach threshold.3. Ca2+ influx already stimulated by K+ depolarization can be further enhanced by veratridine without any parallel change in membrane potential.4. Only the pathway mediating Ca2+ uptake during K+ depolarization can be inactivated: Ca2+ uptake evoked by K+ depolarization is decreased in synaptosomes pre-depolarized in the presence of a high concentration of K+. In contrast, predepolarization does not change Ca2+ uptake evoked by veratridine.5. Ca2+ channel blockers, such as verapamil and diltiazem but not nifedipine, in concentrations of 10-100 /SM, decrease the stimulation of Ca2+ uptake by high K+ concentration without influencing depolarization, whereas the effect of veratridine 6n Ca2+ uptake is only inhibited when its effect on Na+ channels is also prevented. 6. It is concluded that Ca2+ uptake during K+ depolarization proceeds through voltage-dependent Ca2+ channels similar to those of squid axon, whereas veratridine activates an additional Ca2+ entry, possibly via influx through open Na+ channels.7. Different quantitative relationships are found between acetylcholine release of synaptosomes and the amount of Ca2+ taken up by different mechanisms: the same amount of Ca2+ uptake is accompanied by a greater increase of acetylcholine release if the uptake is induced by K+ depolarization rather than veratridine.

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Section: Depolarization By Ouabainmentioning

confidence: 94%

Calcium uptake of rat brain synaptosomes as a function of membrane potential under different depolarizing conditions.

Ádám-Vizi¹,

Ligeti²

1986

The Journal of Physiology

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“…MATERIALS AND METHODS Purified synaptosomes (17) from adult rat cerebrum resuspended in 0.32 M glucose were diluted 1:10 in a Krebs-Ringer medium [128 mM NaCl/5 mM KC1/2.7 mM CaCl2/1.2 mM MgSO4/1 mM Na2HPO4 20 mM N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (Hepes) buffered at pH 7.35], equilibrated for 10 min at 370, and then labeled for another 10 min with 0.5 uM [3H]GABA (New England Nuclear Corp., specific activity 30 Ci/mmol). After the labeling period, a tissue/medium ratio of radioactivity of 70-90 was obtained.…”

mentioning

confidence: 99%

“…caused by the drug is coupled to an influx of Ca2+ (23)(24)(25), while the intracellular K+ decreases (23,26). Potassium deprivation, like ouabain, inhibits the Na+ -K+ -ATPase (27), which causes an accumulation of Na+, a loss of K+ (25,28), and, possibly also an increased influx of Ca2+ (26,29,30). A23187 increases the membrane permeability to Ca2+ and Mg2+ and has no major effect on that of monovalent cations (31).…”

mentioning

confidence: 99%

Modulation of γ-aminobutyric acid transport in nerve endings: Role of extracellular γ-aminobutyric acid and of cationic fluxes

Levi

Raiteri

1978

Proc. Natl. Acad. Sci. U.S.A.

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The aim of the present study was to elucidate the possible functional significance of 'y-aminobutyric acid (GABA) homoexchange at nerve endings. Using synaptosomes from adult rat cerebrum, we found that a number of conditions altering cationic fluxes produced a concomitant change in the stoichiometry of GABA homoexchange, In fact, exogenous GABA (10 AM), while not causing net release of intrasynaptosomal GABA in standard conditions, triggered a large net GABA release in the presence of veratridine, Na+-K+-ATPase inhibitors, or the ionophore A23187, superimposed on that due to the various agents tested alone. This extra release was mediated by the membrane carrier, being largely inhibited by the GABA carrier-blocker L-diaminobutyric acid. The altered stoichiometry of GABA homoexchange observed under these conditions (efflux> influx) appeared to be coupled to the influx of Na+ (or of Ca2+), rather than determined by the establishment of a high intrasynaptosomal [Na+J Under conditions of reversed Na+ flux (Na+ efflux), the GABA outward/inward flux ratio was also reversed, and the stoichiometry of GABA homoexchange was in favor of net influx. The possible contribution of K+ to the effects observed is also discussed. It is concluded that the GABA transport system of nerve endings is susceptible to fine modulation by changes in cationic fluxes similar to those occurring in vivo during depolarization and repolarization. These fluxes may have a prominent role in determining the direction of net GABA transport in GABA-ergic nerve terminals of the living brain.The two essential steps of chemical neurotransmission are the depolarization-induced release of the transmitter from a presynaptic nerve ending and the rapid inactivation of the transmitter by specific biochemical mechanisms. The release of biogenic amines is generally considered to occur through an exocytotic-like process (1-5), and their inactivation mainly through specific reuptake mechanisms present in presynaptic nerve terminals (4, 6, 7). This scheme cannot be easily applied to neurotransmitter amino acids. For example, for 'y-aminobutyric acid (GABA), no evidence for an exocytotic release has been provided, and the mechanism of reuptake is still under discussion (8-15). In fact, several recent studies in vitro have shown that GABA transport consists essentially of a 1:1 homoexchange process in nerve endings incubated in standard media in the presence of low concentrations of the amino acid (9-14). This finding does not seem to fit with the high-affinity reuptake theory for inactivation of synaptically released GABA (4, 6, 16) and raises the question of the functional significance of a transport system that does not result in a net translocation of the substrate in one or the other direction.In the present study we have analyzed the relationship between GABA homoexchange and the processes of release and reuptake of the amino acid. On the basis of our results, we submit a hypothesis for GABA release and reuptake mechanisms and, in particular, we suggest...

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“…Previous investigations (Stahl & Swanson, 1969;1971;Swanson, Anderson & Stahl, 1974;Yoshida & Ichida, 1974) have adequately demonstrated that 100 mM Na+ produces decreased 45Ca uptake and binding in synaptosomes and a loss of 45Ca bound to synaptic membranes. From this information, together with the data presented in the present paper, we would suggest that morphine action induces a Ca2+ dissociated membrane state (analogous to agonist binding in absence of sodium).…”

Section: Preparation Ofsubcellularfractionsmentioning

confidence: 96%

Calcium Depletion of Synaptosomes After Morphine Treatment

Cardenas

Ross

1976

British J Pharmacology

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It was confirmed that morphine administration in vivo produced a selective decrease in the calcium content of synaptosomal fractions prepared from rat cerebral cortices. This effect was prevented by naloxone. After morphine or naloxone, there were no changes in the sodium, potassium and magnesium contents of any of the seven subcellular fractions tested. Since the selective calcium loss was found to occur from fractions similar to those reported to exhibit opiate receptor binding, it is concluded that calcium may play a role in the action of narcotic agonist drugs.

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Uptake of calcium ions by synaptosomes from rat brain

Cited by 79 publications

References 19 publications

Calcium uptake of rat brain synaptosomes as a function of membrane potential under different depolarizing conditions.

Calcium uptake of rat brain synaptosomes as a function of membrane potential under different depolarizing conditions.

Modulation of γ-aminobutyric acid transport in nerve endings: Role of extracellular γ-aminobutyric acid and of cationic fluxes

Calcium Depletion of Synaptosomes After Morphine Treatment

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