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

Wilkinson, Lawrence Stephen and Collard, Keith J. 1990. Synaptosomal tryptophan uptake and efflux following lesion of central 5-hydroxytryptaminergic neurones. British Journal of Pharmacology 101 (4) , pp. 981-985. 10.1111/j.1476-5381.1990.tb14192.x

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Abstract

1 This 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−1) than that observed in sham-operated controls (360.6 ± 30.3 pmol mg−1 protein min−1). However, uptake in the absence of extracellular Na+ was increased to a similar extent in both the sham-operated (539 ± 54.5 pmol mg−1 protein min−1) and lesioned animals (507.2 ± 42.4 pmol mg−1 protein min−1). 4 The efflux of [3H]-tryptophan in response to extracellular Na+ depletion was similar in sham-operated and lesioned animals. Release expressed as a percentage of tissue [3H]-tryptophan released in response to the pulse of Na+-free medium was 6.691 ± 0.585 (n = 4) in sham-operated controls and 8.195 ± 0.906 in lesioned animals. 5 The efflux of [3H]-tryptophan in response to K+ depolarization was also unchanged in lesioned animals when compared with sham-operated controls. Release, expressed as described above was, in sham-operated controls 3.76 ± 0.41 (n = 4) and 4.09 ± 0.30 in lesioned animals. 6 The results of this study show that the tryptophan carrier which is activated by depolarization or by extracellular Na+ depletion is not located exclusively on 5-hydroxytryptaminergic nerve endings. Moreover the contribution made by 5-hydroxytryptaminergic neurones appears to be only minor.

Item Type: Article
Date Type: Publication
Status: Published
Schools: MRC Centre for Neuropsychiatric Genetics and Genomics (CNGG)
Medicine
Neuroscience and Mental Health Research Institute (NMHRI)
Psychology
Subjects: R Medicine > R Medicine (General)
Publisher: Nature Publishing Group
ISSN: 0007-1188
Last Modified: 04 Jun 2017 08:49
URI: http://orca-mwe.cf.ac.uk/id/eprint/85449

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