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

Wilkinson, Lawrence Stephen ORCID: https://orcid.org/0000-0002-9337-6124 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:	31 Oct 2022 10:36
URI:	https://orca.cardiff.ac.uk/id/eprint/85449

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