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Synaptosomal tryptophan uptake and efflux following lesion of central 5‐hydroxytryptaminergic neurones
Author(s) -
Wilkinson Lawrence S.,
Collard Keith J.
Publication year - 1990
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1990.tb14192.x
Subject(s) - extracellular , endocrinology , medicine , tryptophan , chemistry , sodium , lesion , depolarization , synaptosome , biology , central nervous system , biochemistry , pathology , organic chemistry , amino acid
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 [ 3 H]‐5‐hydroxytryptamine (5‐HT) in lesioned animals and in sham‐operated controls. [ 3 H]‐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 [ 3 H]‐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 [ 3 H]‐tryptophan in response to extracellular Na + depletion was similar in sham‐operated and lesioned animals. Release expressed as a percentage of tissue [ 3 H]‐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 [ 3 H]‐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.