The stimulus-induced release of unmetabolized 5-hydroxytryptamine from superfused rat brain synaptosomes

Collard, Keith J.; Cassidy, Diane; Pye, M.A.; Taylor, Ruth M.

doi:10.1016/0165-0270(81)90051-0

Cited by 18 publications

(19 citation statements)

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“…The involvement of the plasma membrane tryptophan carrier was examined further, by determining the effect of an inhibitor of the carrier on the efflux of tryptophan under both depolarizing and non-depolarizing conditions. wThe Macmillan Press Ltd 1988 Methods Efflux studies Preparation ofsynaptosomes, incubation andperfusion Male Albino Wistar rats weighing between 200 and 250 g were used in all studies. Synaptosomes were prepared from whole forebrain by the method ofGray & Whittaker (1962), as described previously (Collard et al, 1981). The final synaptosomal pellet (P2-B) was resuspended in 20 ml of Krebs solution of the following composition (mM): NaCl 124, KCI 5, KH2PO4 1.2, MgSO4 1.3, CaCl2 0.75, glucose 10, NaHCO3 26.…”

Section: Introductionmentioning

confidence: 99%

“…Incubation was then continued for a further Omin at 370C. Beds of synaptosomes were prepared from 4.5 ml portions of incubated synaptosomes, set up in perfusion chambers (Collard et al, 1981), and perfused at 8.0 ml min-' with oxygenated (95% 02+ 5% C02) Krebs solution of the following composition (mM): NaCl 118, KCl 4.85, KH2PO4 1.15, MgSO4 1.15, CaCl2 2.5, glucose I 1.1, NaHCO3 25. The application of the depolarizing pulses of K+, collection of fractions and processing of the tissue at the end of perfusion were carried out as described previously (Collard et al, 1981;1982).…”

Section: Introductionmentioning

confidence: 99%

“…This was accomplished by ion-exchange chromatography. 5-HT was separated by a modification of the method of Smith et al (1975) with Bio-Rex 70 (Na+ form) as described in detail elsewhere (Collard et al, 1981). The amino acids were separated with Dowex 1-X4 (HCOO-form) (Collard et al, 1982).…”

Section: Introductionmentioning

confidence: 99%

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Studies on the mechanism by which tryptophan efflux from isolated synaptosomes is stimulated by depolarization

Collard¹,

Wilkinson²,

Lewis³

1988

British J Pharmacology

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1 The efflux and influx of tryptophan across the synaptosomal plasma membrane has been studied under a variety of experimental conditions, in order to examine the mechanism by which depolarization enhances the efflux of tryptophan from superfused synaptosomes. 4 Influx of [3H]-tryptophan into synaptosomes was stimulated by extracellular Na+ removal, but the uptake of [3H]-phenylalanine was unaffected by this procedure. 5 Both the induced influx and efflux of tryptophan observed under these experimental conditions was inhibited by immobilizing the plasma membrane carrier with parachlorophenylalanine. This implied that both the enhanced influx and efflux arose as a consequence of the activation of the membrane tryptophan carrier, the direction of the observed effect being dependent upon the manner in which the experiments were conducted. 6 The relationship between depolarization, the activation of the membrane tryptophan carrier and the significance of this to the in vivo situation is discussed.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Studies on the mechanism by which tryptophan efflux from isolated synaptosomes is stimulated by depolarization

Collard¹,

Wilkinson²,

Lewis³

1988

British J Pharmacology

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“…Synaptosomes were prepared from whole forebrain either by the method of Gray & Whittaker (1962) as previously described (Collard et al, 1981), or by the method of Dodd et al (1981). The synaptosomal preparation obtained from either procedure showed almost identical properties with respect to the transport of 5-HT and tryptophan.…”

Section: Preparation Of Synaptosomesmentioning

confidence: 99%

“…Incubation was continued for a further 10min. Beds of synaptosomes were prepared from 5.0 ml portions of the incubated synaptosomes and set up in perfusion chambers (Collard et al, 1981). The perfusion of the synaptosomes, the application of pulses of Na+-deficient, or K'-rich solutions and the separation and measurement of released [3H]-tryptophan were carried out exactly as described previously , except that the K+ was applied for 60 s instead of 38s as in the previous study.…”

Section: Measurement Of [3h]-tryptophan Effluxmentioning

confidence: 99%

Synaptosomal tryptophan uptake and efflux following lesion of central 5‐hydroxytryptaminergic neurones

Wilkinson

Collard

1990

British J Pharmacology

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1This study attempted to determine whether the activation of the tryptophan carrier in rat forebrain synaptosomes caused by depolarization or by extracellular sodium depletion occurred exclusively in 5-hydroxytryptaminergic nerve endings. 2 Ascending 5-hydroxytryptaminergic neurones were lesioned either electrolytically or by intraventricular administration of 5,7-dihydroxytryptamine. The extent of the lesion was assessed by comparing the uptake of [3H]-5-hydroxytryptamine (5-HT) in lesioned animals and in sham-operated controls.[3H]-5-HT uptake was reduced by 85.9 + 1.63% (mean + s.e.mean) in animals receiving electrolytic lesions, and by 87.4 + 4.51% in those receiving 5,7-dihydroxytryptamine. 3 The uptake of [3H]-tryptophan by synaptosomes from lesioned animals incubated in standard Na+-rich media was slightly lower (278.8 + 27.3 pmol mg-1 protein min-') than that observed in shamoperated controls (360.6 + 30.3 pmol mg'-protein min-). However, uptake in the absence of extracellular Na+ was increased to a similar extent in both the sham-operated (539 + 54.5pmolmg-protein min -1) and lesioned animals (507.2 + 42.4 pmol mg-1 protein min -1).

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The regulation of 5-hydroxytryptamine release from superfused synaptosomes by 5-hydroxytryptamine and its immediate precursors

Suter¹,

Collard²

1983

Neurochem Res

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The effect of L-tryptophan, 5-hydroxy-L-tryptophan (5-HTP), and 5-hydroxytryptamine (5-HT) on the K+-evoked release of [3H]5-HT from superfused rat brain synaptosomes was studied. 5-HT at concentrations above 10 nM significantly inhibited the K+-evoked release of [3H]5-HT. A slight enhancement of [3H]5-HT release was observed at a concentration of 5nM. In contrast tryptophan at a concentration of 10 nM significantly enhanced [3H]5-HT release with little effect at higher concentrations. 5-HTP did not significantly effect [3H]5-HT release. The results confirm previous findings that 5-HT inhibits its own release from nerve endings, and demonstrate that low concentrations of tryptophan in the synaptic region may act as a positive feedback regulator of 5-HT release.

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The stimulus-induced release of unmetabolized 5-hydroxytryptamine from superfused rat brain synaptosomes

Cited by 18 publications

References 14 publications

Studies on the mechanism by which tryptophan efflux from isolated synaptosomes is stimulated by depolarization

Studies on the mechanism by which tryptophan efflux from isolated synaptosomes is stimulated by depolarization

Synaptosomal tryptophan uptake and efflux following lesion of central 5‐hydroxytryptaminergic neurones

The regulation of 5-hydroxytryptamine release from superfused synaptosomes by 5-hydroxytryptamine and its immediate precursors

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